beta-carotene and Inflammation

The carotenoid pigment astaxanthin has important applications in the nutraceutical, cosmetics, food and feed industries. Haematococcus pluvialis is the richest source of natural astaxanthin and is now cultivated at industrial scale. Astaxanthin is a strong coloring agent and a potent antioxidant - its strong antioxidant activity points to its potential to target several health conditions. This article covers the antioxidant, UV-light protection, anti-inflammatory and other properties of astaxanthin and its possible role in many human health problems. The research reviewed supports the assumption that protecting body tissues from oxidative damage with daily ingestion of natural astaxanthin might be a practical and beneficial strategy in health management.

Topics: Adjuvants, Immunologic; Administration, Oral; Antioxidants; Arteriosclerosis; beta Carotene; Biological Availability; Blindness; Chlorophyta; Diet Therapy; Humans; Inflammation; Macular Degeneration; Neoplasms; Neurodegenerative Diseases; Nutritional Physiological Phenomena; Photosensitivity Disorders; Radiation-Sensitizing Agents; Species Specificity; Xanthophylls

The neutrophil-to-lymphocyte ratio (NLR) is a biomarker that indicates systemic inflammation and can be estimated using array-based DNA methylation data as methylation-derived NLR (mdNLR). We assessed the relationship between prediagnosis mdNLR and lung cancer risk in a nested case-control study in the β-Carotene and Retinol Efficacy Trial (CARET) of individuals at high risk for lung cancer due to heavy smoking or substantial occupational asbestos exposure. We matched 319 incident lung cancer cases to controls based on age at blood draw, smoking, sex, race, asbestos, enrollment year, and time at risk. We computed mdNLR using the ratio of predicted granulocyte and lymphocyte proportions derived from DNA methylation signatures in whole blood collected prior to diagnosis (median 4.4 years in cases). Mean mdNLR was higher in cases than controls (2.06 vs. 1.86,

Topics: Aged; Asbestos; beta Carotene; Carcinoma, Non-Small-Cell Lung; Case-Control Studies; Diterpenes; DNA Methylation; Female; Humans; Inflammation; Lung Neoplasms; Lymphocyte Count; Lymphocytes; Male; Middle Aged; Neutrophils; Occupational Exposure; Oligonucleotide Array Sequence Analysis; Retinyl Esters; Risk Factors; Smokers; Smoking; Vitamin A

The aim of the present study was to determine the beneficial effects of beta-carotene fortified synbiotic food intake on metabolic status in patients with type 2 diabetes mellitus (T2DM).. This randomized double-blinded placebo-controlled crossover clinical trial was conducted among 51 patients with T2DM. Individuals were randomly assigned to take either a beta-carotene fortified synbiotic (n = 51) or control food (n = 51) for 6 weeks. The beta-carotene fortified synbiotic was containing Lactobacillus sporogenes (1 × 10(7) CFU), 0.1 g inulin and 0.05 g beta-carotene. Control food (the same substance without probiotic, inulin and beta-carotene) was packed in identical 9-g packages. Patients were requested to use the beta-carotene fortified synbiotic and control foods three times a day.. Beta-carotene fortified synbiotic food consumption resulted in a significant decrease in insulin (-1.00 ± 7.90 vs. +3.68 ± 6.91 μIU/mL, P = 0.002), HOMA-IR (-0.73 ± 3.96 vs. +1.82 ± vbnm4.09, P = 0.002), HOMA-B (-0.52 ± 19.75 vs. +8.71 ± 17.15, P = 0.01), triglycerides (-2.86 ± 49.53 vs. +20.14 ± 50.10 mg/dL, P = 0.02), VLDL-cholesterol levels (-0.57 ± 9.90 vs. +4.03 ± 10.02 mg/dL, P = 0.02) and total-/HDL-cholesterol ratio (-0.01 ± 1.08 vs. +0.64 ± 0.81, P = 0.001) compared to the control food. In addition, beta-carotene fortified synbiotic food consumption led to elevated plasma nitric oxide (NO) (+6.83 ± 16.14 vs. -3.76 ± 16.47 μmol/L, P = 0.001) and glutathione (GSH) (+36.58 ± 296.71 vs. -92.04 ± 243.05 μmol/L, P = 0.01).. Beta-carotene fortified synbiotic food intake in patients with T2DM for 6 weeks had favorable effects on insulin, HOMA-IR, HOMA-B, triglycerides, VLDL-cholesterol, total-/HDL-cholesterol ratio, NO and GSH levels.

Topics: Adult; Aged; Bacillus coagulans; beta Carotene; Biomarkers; Blood Glucose; Cholesterol; Cross-Over Studies; Diabetes Mellitus, Type 2; Double-Blind Method; Female; Food, Fortified; Glutathione; Humans; Inflammation; Insulin; Inulin; Male; Middle Aged; Nitric Oxide; Oxidative Stress; Synbiotics; Triglycerides

Whereas conventional white cassava roots are devoid of provitamin A, biofortified yellow varieties are naturally rich in β-carotene, the primary provitamin A carotenoid.. We assessed the effect of consuming yellow cassava on serum retinol concentration in Kenyan schoolchildren with marginal vitamin A status.. We randomly allocated 342 children aged 5-13 y to receive daily, 6 d/wk, for 18.5 wk 1) white cassava and placebo supplement (control group), 2) provitamin A-rich cassava (mean content: 1460 μg β-carotene/d) and placebo supplement (yellow cassava group), and 3) white cassava and β-carotene supplement (1053 μg/d; β-carotene supplement group). The primary outcome was serum retinol concentration; prespecified secondary outcomes were hemoglobin concentration and serum concentrations of β-carotene, retinol-binding protein, and prealbumin. Groups were compared by using ANCOVA, adjusting for inflammation, baseline serum concentrations of retinol and β-carotene, and stratified design.. The baseline prevalence of serum retinol concentration <0.7 μmol/L and inflammation was 27% and 24%, respectively. For children in the control, yellow cassava, and β-carotene supplement groups, the mean daily intake of cassava was 378, 371, and 378 g, respectively, and the total daily supply of provitamin A and vitamin A from diet and supplements was equivalent to 22, 220, and 175 μg retinol, respectively. Both yellow cassava and β-carotene supplementation increased serum retinol concentration by 0.04 μmol/L (95% CI: 0.00, 0.07 μmol/L); correspondingly, serum β-carotene concentration increased by 524% (448%, 608%) and 166% (134%, 202%). We found no effect on hemoglobin concentration or serum concentrations of retinol-binding protein and prealbumin.. In our study population, consumption of yellow cassava led to modest gains in serum retinol concentration and a large increase in β-carotene concentration. It can be an efficacious, new approach to improve vitamin A status. This study was registered with clinicaltrials.gov as NCT01614483.

Topics: Analysis of Variance; beta Carotene; Child; Diet; Dietary Supplements; Energy Intake; Female; Food, Fortified; Humans; Inflammation; Kenya; Male; Manihot; Nutritional Status; Plant Roots; Prevalence; Vegetables; Vitamin A; Vitamin A Deficiency

In vitro, ex vivo and animal studies suggest palm-based tocotrienols and carotenes enhance vascular function, but limited data in humans exists. The aim was to examine the effects of palm-tocotrienols (TRF- 80) and palm-carotene (CC-60) supplementation on vascular function and cardiovascular disease (CVD) risk factors in adults at increased risk of impaired vascular function.. Plasma α- and β-carotene and α-, δ- and γ-tocotrienol concentrations increased in CC-60 and TRF-80 groups, respectively, compared to placebo (mean ± SE difference in total plasma carotene change between CC-60 and placebo: 1.5 ± 0.13 μg/ml, p < 0.0001; total plasma tocotrienol change between TRF-80 and placebo: 0.36 ± 0.05 μg/ml, p < 0.0001). Neither FMD (treatment x time effect for CC-60 vs. placebo, p = 0.71; TRF-80 vs. placebo, p = 0.80) nor any other vascular function and CVD outcomes were affected by treatments.. CC-60 and TRF-80 supplementation increased bioavailability of palm-based carotenes and tocotrienols but had no effects, superior or detrimental, on vascular function or CVD risk factors.

Topics: Adolescent; Adult; Aged; beta Carotene; Blood Glucose; Brachial Artery; Cardiovascular Diseases; Carotenoids; Diabetes Mellitus, Type 2; Dietary Supplements; Double-Blind Method; Female; Humans; Inflammation; Insulin; Male; Middle Aged; Oxidative Stress; Palm Oil; Risk Factors; Tocotrienols; Young Adult

Chronic inflammation contributes to the pathophysiology of many chronic diseases. Dietary fibers and antioxidants may exert anti-inflammatory effects. The objective of this study was to determine whether meals with different fibers and antioxidants may elicit a different response in inflammatory markers in healthy volunteers. On 3 separate days, subjects (n = 8) consumed one of three isocaloric meals with different antioxidant (vitamin E, selenium and β-carotene) and fiber content (high, intermediate and low) in a randomized crossover design. Blood samples were collected at different times: 0 min (before the meal), and 30 and 240 min after the meal. Plasma interleukin (IL)-6, IL-10, tumor necrosis factor (TNF)-α, glucose and insulin content were evaluated at each time point. There were no significant differences for any of the parameters at baseline. Furthermore, plasma levels of TNF-α, IL-6 and IL-10 were unchanged at the 30- and 240-min time points whatever meal consumed. Moreover, the cytokine responses to glucose and insulin intake were not significantly different between experimental conditions. In conclusion, isocaloric meals with different fiber, β-carotene, vitamin E and selenium contents do not acutely affect inflammatory markers in healthy young males.

Topics: Adolescent; Antioxidants; beta Carotene; Biomarkers; Blood Glucose; Chronic Disease; Cross-Over Studies; Dietary Carbohydrates; Dietary Fats; Dietary Fiber; Dietary Proteins; Humans; Inflammation; Insulin; Interleukin-10; Interleukin-6; Male; Meals; Selenium; Single-Blind Method; Tumor Necrosis Factor-alpha; Vitamin E; Young Adult

Chronic inflammation contributes to an increased risk for developing chronic conditions such as cardiovascular disease, diabetes, and cancer. A high "inflammatory load" is defined as elevated inflammation markers in blood or other tissues. We evaluated several markers of systemic inflammation from healthy adults and tested the hypothesis that two formulations of encapsulated fruit and vegetable juice powder concentrate with added berry powders (FVB) or without (FV) could impact markers of inflammatory load. Using a double-blind, placebo-controlled approach, 117 subjects were randomly assigned to receive placebo, FV, or FVB capsules. Blood was drawn at baseline and after 60 d of capsule consumption. We measured inflammatory markers (high sensitivity C-Reactive Protein, Monocyte Chemotactic Protein-1, Macrophage Inflammatory Protein 1-β, and Regulated upon Activation, Normal T cell Expressed and Secreted), superoxide dismutase, and micronutrients (β-carotene, vitamin C, and vitamin E). Results showed Monocyte Chemotactic Protein-1, Macrophage Inflammatory Protein 1-β, and RANTES levels were significantly reduced and superoxide dismutase and micronutrient levels were significantly increased in subjects consuming both FV and FVB, relative to placebo. Data suggest a potential health benefit by consuming either formulation of the encapsulated juice concentrates through their anti-inflammatory properties.

Topics: Adult; Anti-Inflammatory Agents, Non-Steroidal; Ascorbic Acid; beta Carotene; Chemokine CCL2; Chemokine CCL4; Chemokine CCL5; Dietary Supplements; Double-Blind Method; Female; Fruit; Humans; Inflammation; Inflammation Mediators; Male; Middle Aged; Superoxide Dismutase; Vegetables; Vitamin E; Young Adult

A cross-sectional observation suggests that total antioxidant capacity (TAC) of the diet positively affects plasma concentrations of beta-carotene independent of beta-carotene intake. This study was carried out to investigate the effect of two dietary strategies, designed to be comparable in fruits, vegetables, fibre, alcohol and beta-carotene intake but substantially different in their TAC, on changes in antioxidant intake and antioxidant status, and in particular in circulating beta-carotene concentrations.. A randomized cross-over intervention trial involving 33 healthy participants and consisting of two 14-day dietary periods (high TAC diet, HT; low TAC diet, LT) with a 14-day washout in between was conducted.. Energy, macronutrient, dietary fibre, alcohol and beta-carotene intake was not significantly different between LT and HT, whereas intake of other carotenoids and dietary TAC was significantly higher in the HT than in the LT (P<0.001). Circulating carotenoids (with the exception of alpha-carotene, which followed an inverse trend) and alpha-tocopherol decreased significantly during the LT and increased during the HT period. Among these, beta-carotene almost doubled its concentration in plasma after the HT diet.. The increase in circulating beta-carotene along with the increase in dietary TAC suggests that plasma beta-carotene could be a marker of TAC intake rather than of beta-carotene intake itself. This may explain, in part, why beta-carotene supplementation alone has shown no benefit in chronic disease prevention and adds to a putative beneficial role of high dietary TAC diets, which merits further investigation.

Topics: Alcohol Drinking; Antioxidants; beta Carotene; Biomarkers; Cross-Over Studies; Dietary Fiber; Female; Free Radical Scavengers; Fruit; Humans; Inflammation; Liver Diseases; Male; Middle Aged; Oxidation-Reduction; Oxidative Stress; Vegetables; Vitamins

The risk of malignant transformation of oral preneoplastic lesion (OPL) is difficult to assess. DeltaNp63 is an early oncoprotein associated with mucosal tumorigenesis. The purpose of this study was to assess DeltaNp63 expression in OPL and its role as a marker of oral cancer risk.. DeltaNp63 expression was determined using immunohistochemistry in 152 OPL patients included in a clinical trial comparing retinyl palmitate alone or plus beta-carotene with low-dose 13-cis-retinoic acid. The associations between DeltaNp63 expression as well as DeltaNp63 expression with other potential risk factors for oral cancer development were analyzed.. DeltaNp63 expression was positive in 41 (27%) patients, clusters of intraepithelial inflammatory cells (EIC) were noted in 37 (26%) patients, and podoplanin (previously reported) was positive in 56 (37%) patients. Significantly more patients whose lesions were DeltaNp63 positive or exhibited EIC developed oral cancers. In the multicovariate analysis including age, treatment, and histologic status as cofactors, positive DeltaNp63 expression was associated with an increased hazard ratio of 3.308 (95% confidence interval, 1.663-6.580; P = 0.0007). Patients whose lesions showed positive DeltaNp63, podoplanin, and EIC had the highest oral cancer risk with a hazard ratio of 4.372 (95% confidence interval, 1.912-9.992; P = 0.0005) and 61% oral cancer development rate at 5 years compared with 15% of other OPL patients (P < 0.0001).. DeltaNp63 overepression in OPL is associated with increased oral cancer risk. Together, DeltaNp63, podoplanin, and EIC may be used as biomarkers to identify OPL patients with substantially high oral cancer risk.

Topics: Antineoplastic Combined Chemotherapy Protocols; beta Carotene; Biomarkers, Tumor; Carcinoma, Squamous Cell; Diterpenes; Female; Follow-Up Studies; Gene Expression Regulation, Neoplastic; Genetic Predisposition to Disease; Humans; Inflammation; Isotretinoin; Leukoplakia, Oral; Male; Membrane Glycoproteins; Middle Aged; Mouth Neoplasms; Prognosis; Retinyl Esters; Trans-Activators; Transcription Factors; Tumor Suppressor Proteins; Up-Regulation; Vitamin A

A human study was carried out to investigate whether tomato juice, rich in natural lycopene and fortified with vitamin C, is able to reduce several biomarkers of oxidative stress and inflammation and whether the effect can be attributed to lycopene, vitamin C or any other micronutrient. Following a 2-week depletion phase, volunteers were assigned randomly to ingest either tomato juice with (LC) or without (L) vitamin C fortification for 2 weeks (daily dose 20.6 mg lycopene and 45.5/435 mg vitamin C). Plasma and urine were analysed for carotenoids and vitamin C, lipid status, antioxidant capacity, thiobarbituric acid reactive substances (TBARS) and 8-epi-PGF2alpha, protein carbonyls, cytokines IL-1beta and TNFalpha and C-reactive protein (CRP). The consumption of tomato juice led to a reduction in total cholesterol levels (L: 157.6 v. 153.2 mg/dl, P = 0.008; LC: 153.4 v. 147.4 mg/dl, P = 0.002) and that of CRP (L: 315.6 v. 262.3 microg/l, P = 0.017; LC: 319.2 v. 247.1 microg/l, P = 0.001) in both groups. The vitamin C-fortified juice slightly raised the antioxidant capacity in urine and decreased TBARS in plasma and urine. All other markers were affected to a lesser extent or remained unchanged. Cholesterol reduction was correlated with lycopene uptake (P = 0.003), whereas the other effects could not be related with particular micronutrients. Any beneficial effects of tomato consumption for human health cannot be attributed only to lycopene and, as the additional supplementation with ascorbic acid indicates, a variety of antioxidants might be needed to optimize protection against chronic diseases.

Topics: Adult; Analysis of Variance; Antioxidants; Ascorbic Acid; beta Carotene; Beverages; Biomarkers; C-Reactive Protein; Carotenoids; Cholesterol; Dietary Supplements; Female; Humans; Inflammation; Interleukin-1; Lycopene; Male; Oxidative Stress; Solanum lycopersicum; Thiobarbituric Acid Reactive Substances; Tumor Necrosis Factor-alpha

As evidence of the involvement of inflammation and oxidative damage in pathogenesis of age-related chronic diseases is growing, epidemiologists need to develop measures of both conditions to study their relationships in human populations. One way of searching for appropriate biomarkers is to examine correlations between different inflammatory markers and oxidative indices. We examined cross-sectional correlations between two inflammatory markers, serum C-reactive protein (CRP) and interleukin (IL)-6, and three oxidative indices, plasma levels of alpha-tocopherol and beta-carotene, and urinary levels of 2,3-dinor-5,6-dihydro-15-F2t-isoprostane (F2-IsoP), in 60 individuals at high risk of cardiovascular disease. Correlations between the biomarkers were examined graphically and using the Pearson correlation coefficient. No correlation was found between plasma levels of alpha-tocopherol and either of the inflammatory markers. Plasma beta-carotene inversely correlated with IL-6 (r = -0.46, p=0.0002) and CRP (r = -0.41, p = 0.001). Although urinary F2-IsoP did not correlate with IL-6, this biomarker positively correlated with CRP (r = 0.31, p = 0.002). As only urinary F2-IsoP levels have been validated against known oxidative assaults, their positive association with CRP levels is interpreted as evidence of an interconnection between low-level inflammation and oxidative status. Urinary levels of F2-IsoP and serum levels of CRP represent appropriate biomarkers for future studies of inflammation and oxidative status in humans.

Topics: Aged; alpha-Tocopherol; beta Carotene; Biomarkers; C-Reactive Protein; Cardiovascular Diseases; Dinoprost; Female; Humans; Inflammation; Interleukin-6; Male; Middle Aged; Oxidative Stress; Risk

Regular consumption of tomato and its products is being consistently associated with lower risk of several types of cancer and, to a lesser extent, coronary heart disease. Among the many tomato components credited with healthful properties, carotenoids and particularly lycopene are being actively investigated. Given the recognized role of immune/inflammatory processes in atherogenesis, the effects of a tomato-based drink (Lyc-o-Mato), which was previously shown to afford DNA protection from oxidative stress, on the modulation of immune and inflammatory markers (by enzyme immunoessay), on basal lymphocyte DNA damage (by comet assay), and on F2-isoprostane excretion (by LC-MS/MS), were investigated in 26 healthy young volunteers. In a placebo-controlled, double-blind, crossover study, Lyc-o-Mato (5.7 mg of lycopene, 3.7 mg of phytoene, 2.7 mg of phytofluene, 1 mg of beta-carotene, and 1.8 mg of alpha-tocopherol) or a placebo drink (same taste and flavor, but devoid of active compounds) were given for 26 days, separated by a wash-out period. During the study subjects maintained their habitual, hence unrestricted, diet. TNF-alpha production by whole blood was 34.4% lower after 26 days of drink consumption, whereas the other parameters were not significantly modified by the treatment. In turn, modest effects of the regular intake of a tomato drink, providing small amounts of carotenoids, were found on the production of inflammatory mediators, such as TNF-alpha, in young healthy volunteers. Future intervention trials in subjects with low carotenoid status and/or compromised immune system will resolve the issue of whether carotenoids modulate immune parameters in humans.

Topics: Adult; alpha-Tocopherol; beta Carotene; Beverages; Biomarkers; Carotenoids; Cross-Over Studies; DNA Damage; Double-Blind Method; Female; Humans; Immunity; Inflammation; Interferon-gamma; Lycopene; Lymphocytes; Male; Oxidative Stress; Placebos; Solanum lycopersicum; Tumor Necrosis Factor-alpha

Vitamin A deficiency (VAD) results in intestinal inflammation, increased redox stress and reactive oxygen species (ROS) levels, imbalanced inflammatory and immunomodulatory cytokines, compromised barrier function, and perturbations of the gut microbiome. To combat VAD dietary interventions with β-carotene, the most abundant precursor of vitamin A, are recommended. However, the impact of β-carotene on intestinal health during VAD has not been fully clarified, especially regarding the VAD-associated intestinal dysbiosis. Here we addressed this question by using Lrat

Topics: Animals; beta Carotene; Disease Models, Animal; Dysbiosis; Inflammation; Intestinal Diseases; Mice; Vitamin A; Vitamin A Deficiency

Epidermal growth factor (EGF) has many important biological functions. It plays an important role in regulating the growth, survival, migration, apoptosis, proliferation, and differentiation of intestinal tissues and cells. However, until now, the effect of inflammation on the biological activity of EGF in intestinal cells or tissues is still unclear. For this reason, in the current research, we have conducted a detailed study on this issue. Using the rat small intestinal crypt epithelial cell line (IEC6) was used as an in vitro model, and Confocal laser scanning microscope (CLSM), Flow cytometry (FCM), Indirect immunofluorescence assay (IFA), Western-blotting (WB), and Quantitative real-time RT-PCR (QRT-PCR) methods were used to explore the effects of inflammation on EGF/EGFR biological activity and signal transduction profiles. We found that the EGF/EGFR nuclear signal almost disappeared in the inflammatory state, and the phosphorylation levels of EGFR, AKT, and STAT3 were all significantly down-regulated. In addition, we also studied the effect of β-carotene on the biological activity of EGF, and found that when cells were pretreated with β-carotene, the cellular behavior, biological activity, and nuclear signal of EGF/EGFR under inflammation stimulation were partially restored. In summary, the current study shows that inflammation can disrupt EGF/EGFR-mediated signaling in IEC6 cells, suggesting that inflammation negatively regulates the biological activity of EGF/EGFR. Furthermore, we found that β-carotene not only attenuated lipopolysaccharide (LPS)-induced inflammation but also partially restored the biological activity of EGF in IEC6 cells, laying a solid foundation for studying the biological functions of EGF and β-carotene.

Topics: Animals; beta Carotene; Cell Line, Tumor; Epidermal Growth Factor; ErbB Receptors; Inflammation; Phosphorylation; Rats; Signal Transduction

Genus Melaleuca or tea tree species are well known to be an important source of biological active oils and extracts. The biological significance appears in their usage for treatment of several clinical disorder owing to their traditional uses as anti-inflammatory, antibacterial, antifungal, and cytotoxic activities.. Our study aimed to investigate the metabolic profile of the M. rugulosa polyphenol-rich fraction along with determination of its anti-inflammatory potential, free radical scavenging and antiaging activities supported with virtual understanding of the mode of action using molecular modeling strategy.. The anti-inflammatory activity of the phenolic rich fraction was investigated through measuring its inhibitory activity against inflammatory mediators viz tumor necrosing factor receptor-2 (TNF-α) and cyclooxygenases 1/2 (COX-1/2) in a cell free and cell-based assays. Moreover, the radical scavenging activity was determined using 2,2-diphenyl-1-picrylhydrazyl (DPPH), oxygen radical absorbance capacity (ORAC) and β-carotene assays, while the antiaging activity in anti-elastase, anti-collagenase, and anti-tyrosinase inhibitory assays. Finally, the biological findings were supported with molecular docking study using MOE software.. The chromatographic purification of the polyphenol-rich fraction of Melaleuca rugulosa (Link) Craven afforded fourteen phytoconstituents (1-14). The anti-inflammatory gauging experiments demonstrated inhibition of inflammatory-linked enzymes COX-1/2 and the TNF-α at low μg/mL levels in the enzyme-based assays. Further investigation of the underlying mechanism was inferred from the quantification of protein levels and gene expression in the lipopolysaccharide (LPS)-activated murine macrophages (RAW264.7) in vitro model. The results revealed the reduction of protein synthesis of COX-1/2 and TNF-α with the down regulation of gene expression. The cell free in vitro radical scavenging assessment of the polyphenol-rich fraction revealed a significant DPPH reduction, peroxyl radicals scavenging, and β-carotene peroxidation inhibition. Besides, the polyphenol-rich fraction showed a considerable inhibition of the skin aging-related enzymes as elastase, collagenase, and tyrosinase. Ultimately, the computational molecular modelling studies uncovered the potential binding poses and relevant molecular interactions of the identified polyphenols with their targeted enzymes. Particularly, terflavin C (8) which showed a favorable binding pose at the elastase binding pocket, while rosmarinic acid (14) demonstrated the best binding pose at the COX-2 catalytic domain. In short, natural polyphenols are potential candidates for the management of free radicals, inflammation, and skin aging related conditions.. Natural polyphenols are potential candidates for the management of free radicals, inflammation, and skin aging related conditions.

Topics: Animals; Anti-Inflammatory Agents; Antioxidants; beta Carotene; Free Radicals; Humans; Inflammation; Melaleuca; Mice; Molecular Docking Simulation; Plant Extracts; Polyphenols; Tannins; Tumor Necrosis Factor-alpha

High sodium intake has been linked to the prevalence of non-alcoholic fatty liver disease (NAFLD), but underlying mechanism remains unclear. This study aims to explore the role of chronic inflammation in the association between sodium and NAFLD. We also observed whether β-carotene, which had a strong anti-inflammatory effect, lowers the odds of NAFLD.. We performed mediation analyses to assess the mediating effects of C-reactive protein (CRP) and red cell distribution width (RDW) on the relationship between dietary sodium and NAFLD defined by the hepatic steatosis index (HSI) and the fatty liver index (FLI), respectively.. A total of 6725 participants were included in this study. Compared with the high sodium-low carotene group, participants in the high sodium-high carotene group had 16% and 26% lower odds for HSI and FLI-defined NAFLD, respectively. There were positive indirect effects of dietary sodium intake on the HSI-defined NAFLD (indirect effect: 0.0057, 95% CI: 0.0021-0.0091, P < 0.0001), as well as the FLI defined NAFLD (indirect effect: 0.0081, 95% CI: 0.0024-0.0162, P < 0.0001) when C-reactive protein (CRP) was considered as a mediator. The mediating effects were somewhat attenuated after further adjusting for dietary β-carotene intake. Similar results were found when RDW was considered as a mediator in the HSI-defined NAFLD analysis.. Higher sodium intake increases the odds of NAFLD by upregulating inflammation. Dietary β-carotene may attenuate this association by down regulating inflammation.

Topics: Anti-Inflammatory Agents; beta Carotene; C-Reactive Protein; Carotenoids; Humans; Inflammation; Mediation Analysis; Non-alcoholic Fatty Liver Disease; Sodium; Sodium, Dietary

Research on aging is growing as the elderly make up a greater share of the population, focusing on reversing and inhibiting the aging process. The exhaustion and senescence of stem cells are the fundamental drivers behind aging. β-Carotene has been depicted to have many biological functions, and we speculate that it may have an anti-aging effect.. Firstly, the anti-aging property of β-carotene was investigated in vitro using mesenchymal stem cells (MSCs) induced by H. The in vitro experiment revealed that β-carotene could relieve the aging of MSCs, as evidenced by a series of aging marker molecules such as p16 and p21. β-Carotene appeared to inhibit aging by regulating the KAT7-P15 signaling axis. The in vivo experiment revealed that β-carotene treatment has significantly down-regulated the aging level of tissues and organs.. In this work, we explored the anti-aging effect of β-carotene in vivo and in vitro. The experimental results indicate that β-carotene may be an important potential anti-aging molecule, which can be used as a drug or in functional food to treat aging in the future.

Topics: Aging; Animals; beta Carotene; Cell Proliferation; Cellular Senescence; Hydrogen Peroxide; Inflammation; Mice; Oxidative Stress

Topics: Animals; Anti-Inflammatory Agents; bcl-2-Associated X Protein; beta Carotene; Bile Acids and Salts; Carotenoids; Caspase 3; Cholesterol; Cytokines; Diet, High-Fat; Dyslipidemias; Fatty Acids; Focal Adhesion Kinase 2; Inflammation; Inflammation Mediators; Interleukin-6; Lipopolysaccharides; Lipoproteins, HDL; Lipoproteins, LDL; Liver; Mice; Mice, Inbred C57BL; Mice, Obese; Nerve Growth Factors; PPAR alpha; Proteomics; Signal Transduction; Triglycerides; Tumor Necrosis Factor-alpha

Topics: Animals; Anti-Inflammatory Agents; beta Carotene; Calcium; Calcium Channels; Calcium Signaling; Cattle; Epithelial Cells; Female; Inflammation; Lipopolysaccharides; NF-kappa B

Carotenoids are natural lipophilic pigments with substantial health benefits. Numerous studies have demonstrated the anti-inflammatory activities of carotenoids, especially toward lipopolysaccharide-induced inflammatory responses. As such, there are few reports on the evaluation and comparison of the anti-inflammatory activities of carotenoids against inflammation induced by other stimuli. In this study, we used pathogen-associated molecular patterns, proinflammatory cytokines, degenerated proteins, and chemical irritants as inflammatory inducers to evaluate the anti-inflammatory activities of eight different carotenoids. Each carotenoid showed characteristic anti-inflammatory activities; thus, we conducted a multivariate analysis to clarify the differences among them. Unsubstituted β-ring (i.e., provitamin A) and C8-keto structures of carotenoids were found to be crucial for their inhibitory effects on the activation of nuclear factor-kappa B and interferon regulatory factors, respectively. Furthermore, we found that β-carotene and echinenone treatment increased intracellular retinoid levels in monocytes and that the retinoids showed the similar activities to β-carotene and echinenone. Taken together, the intake of both provitamin A and C8-keto carotenoids (e.g., siphonaxanthin and fucoxanthin) might be effective in improving the inflammatory status of individuals. A multivariate analysis of anti-inflammatory activities is a useful method for characterizing anti-inflammatory compounds.

Topics: Anti-Inflammatory Agents; beta Carotene; Carotenoids; Cell Count; Cell Death; Cytokines; Humans; Inflammation; Interferon Regulatory Factors; Intracellular Space; Ligands; Lipopeptides; Lipopolysaccharides; Multivariate Analysis; NF-kappa B; Principal Component Analysis; Retinoids; Structure-Activity Relationship; THP-1 Cells; Toll-Like Receptors

As the precursor of vitamin A, β-carotene has a positive effect on reproductive performance. Our previous study has shown that β-carotene can increase antioxidant enzyme activity potentially through regulating gut microbiota in pregnant sows. This study aimed to clarify the effect of β-carotene on reproductive performance and postpartum uterine recovery from the aspect of inflammation and gut microbiota by using a mouse model. Twenty-seven 6 weeks old female Kunming mice were randomly assigned into 3 groups (n=9), and fed with a diet containing 0, 30 or 90 mg/kg β-carotene, respectively. The results showed that dietary supplementation of β-carotene reduced postpartum uterine hyperemia and uterine mass index (

Topics: Animals; Animals, Outbred Strains; beta Carotene; Diet; Female; Gastrointestinal Microbiome; Inflammation; Mice; Postpartum Period; Pregnancy; Random Allocation; Uterus

Hypothalamic inflammation has been linked to various aspects of central metabolic dysfunction and diseases in humans, including hyperphagia, altered energy expenditure, and obesity. We previously reported that loss of β-carotene oxygenase 2 (BCO2), a mitochondrial inner membrane protein, causes the alteration of the hypothalamic metabolome, low-grade inflammation, and an increase in food intake in mice at an early age, e.g., 3-6 weeks. Here, we determined the extent to which the deficiency of BCO2 induces hypothalamic inflammation in BCO2 knockout mice. Mitochondrial proteomics, electron microscopy, and immunoblotting were used to assess the changes in hypothalamic mitochondrial dynamics and mitochondrial DNA sensing and signaling. The results showed that deficiency of BCO2 altered hypothalamic mitochondrial proteome and respiratory supercomplex assembly by enhancing the expression of NADH:ubiquinone oxidoreductase subunit A11 protein and improved cardiolipin synthesis. BCO2 deficiency potentiated mitochondrial fission but suppressed mitophagy and mitochondrial biogenesis. Furthermore, deficiency of BCO2 resulted in inactivation of mitochondrial MnSOD enzyme, excessive production of reactive oxygen species, and elevation of protein levels of stimulator of interferon genes (STING) and interferon regulatory factor 3 (IRF3) in the hypothalamus. The data suggest that BCO2 is essential for hypothalamic mitochondrial dynamics. BCO2 deficiency induces mitochondrial fragmentation and mitochondrial oxidative stress, which may lead to mitochondrial DNA release into the cytosol and subsequently sensing by activation of the STING-IRF3 signaling pathway in the mouse hypothalamus.

Topics: Animals; beta Carotene; Dioxygenases; DNA, Mitochondrial; Energy Metabolism; Humans; Hypothalamus; Inflammation; Interferon Regulatory Factor-3; Male; Membrane Proteins; Metabolome; Mice; Mice, Knockout; Mitochondria; Mitochondrial Dynamics; Oxidative Stress; Reactive Oxygen Species

Inflammation is a protective response of the immune defense system and inflammatory response could be regulated by autophagy. β-Carotene has shown anti-inflammatory potential. However, whether β-carotene could alleviate rat intestinal inflammation by modulating autophagy and its anti-inflammation underlying mechanisms remain unknown. In this study, we found that β-carotene significantly reduced (p < .05) the production of nitric oxide (NO), prostaglandin (PG)E2, tumor necrosis factor (TNF)-α, and interleukin-1β (IL-1β) levels by the Griess reaction and enzyme-linked immunosorbent assay (ELISA), and we found that β-carotene significantly suppressed (p < .05) the mRNA expression levels of IL-1β and TNF-α by RT-PCR. In addition, H&E staining revealed that β-carotene could improve intestinal morphology and cell morphology. Furthermore, the levels of signaling proteins of microtubule-associated protein light chain 3 (LC3), AKT, Janus kinase 2/signal transducers and activators of transcription 3 (JAK2/STAT3), nuclear factor-kappa B (NF-κB), and c-Jun N-terminal kinase (JNK)/p38 mitogen-activated protein kinase (MAPK) were detected by Western blot analysis. We found that β-carotene significantly attenuated (p < .05) the related signaling proteins activated by lipopolysaccharide (LPS) stimulation in rats. Moreover, this conclusion was also verified in intestinal epithelial cell (IEC)-6. 3-Methyladenine (3-MA) is widely used as inhibitor of autophagy via its inhibitory effect on class III PI3K. Simultaneously, pretreatment of 3-MA suppressed the inhibiting effects of β-carotene on the related signaling proteins. This study demonstrates that β-carotene could attenuate the LPS-induced intestinal inflammation in rats via modulating autophagy and regulating the JAK2/STAT3 and JNK/p38 MAPK signaling pathways. We also found the same phenomenon when we verified the results with the IEC-6 cells. These findings provide new insights into improving the nutritional value of basic diets and enhancing immune performance. PRACTICAL APPLICATIONS: β-Carotene is a generally acknowledged natural carotenoid nutrient that exhibits provitamin A activity, and it is widely found in fruits or vegetables. Our study provide a new insight into the anti-inflammatory mechanism of β-carotene. Treatment with β-carotene can be used for the beneficial effect against LPS-induced inflammation damage. This study not only lays the foundation for the related research on the anti-inflammatory properties

Topics: Animals; Autophagy; beta Carotene; Cytokines; Inflammation; Janus Kinase 2; Lipopolysaccharides; p38 Mitogen-Activated Protein Kinases; Rats; Signal Transduction

β-Apocarotenoids are the cleavage products of β-carotene. They are found in plants, carotenoid-containing foods, and animal tissues. However, limited information is available regarding the health benefits of β-apocarotenoids. Here, we prepared seco-type β-apocarotenoids through the chemical oxidation of β-carotene and investigated their anti-inflammatory effects against activated macrophages. Oxidation of β-carotene with potassium permanganate produced seco-β-apo-8'-carotenal, in which one end-group formed an "open" β-ring and the other was cleaved at the C-7',8' position. In lipopolysaccharide-stimulated murine macrophage-like RAW264.7 cells, seco-β-apo-8'-carotenal inhibited the secretion and mRNA expression of inflammatory mediators such as nitric oxide, interleukin (IL)-6 and IL-1β, and monocyte chemoattractant protein-1. Furthermore, seco-β-apo-8'-carotenal suppressed phosphorylation of c-Jun N-terminal kinase and the inhibitor of nuclear factor (NF)-κB as well as the nuclear accumulation of NF-κB p65. Notably, since seco-β-apo-8'-carotenal exhibited remarkable anti-inflammatory activity compared with β-apo-8'-carotenal, its anti-inflammatory action could depend on the opened β-ring structure. These results suggest that seco-β-apo-8'-carotenal has high potential for the prevention of inflammation-related diseases.

Topics: Animals; Anti-Inflammatory Agents; beta Carotene; Carotenoids; Chemokine CCL2; Gene Expression; Inflammation; Inflammation Mediators; Interleukin-1beta; Interleukin-6; Macrophage Activation; Mice; NF-kappa B; Nitric Oxide; Oxidation-Reduction; RAW 264.7 Cells; RNA, Messenger; Structure-Activity Relationship

This study was conducted to investigate the β-carotene status in osteoarthritis (OA) patients and examine its relationships with the risk of inflammation and metabolic syndrome. OA patients were stratified by obesity based on body fat percentage (obese OA,

Topics: Aged; beta Carotene; Female; Humans; Inflammation; Male; Metabolic Syndrome; Middle Aged; Osteoarthritis

In recent years, microalgae have drawn increasing attention as a valuable source of functional food ingredients. Intriguingly,

Topics: Animals; Anti-Inflammatory Agents; beta Carotene; Cell Line; Cell Survival; Cyclooxygenase 2; Diatoms; Dinoprostone; Heme Oxygenase-1; Inflammation; Interleukin-6; Lipopolysaccharides; Membrane Proteins; Mice; Microglia; NAD(P)H Dehydrogenase (Quinone); NADPH Oxidases; Nitric Oxide; Nitric Oxide Synthase Type II; Tumor Necrosis Factor-alpha

The NLRP3 inflammasome is closely linked to the pathophysiology of a wide range of inflammatory diseases. This study was undertaken to identify small molecules that directly bind to NLRP3 in order to develop pharmacologic interventions for NLRP3-related diseases.. A structure-based virtual screening analysis was performed with ~62,800 compounds to select efficient NLRP3 inhibitors. The production of caspase 1-p10 and interleukin-1β (IL-1β) was measured by immunoblotting and enzyme-linked immunosorbent assay to examine NLRP3 inflammasome activation. Two gouty arthritis models and an air pouch inflammation model induced by monosodium urate monohydrate (MSU) crystal injection were used for in vivo experiments. Primary synovial fluid cells from gout patients were used to determine the relevance of NLRP3 inflammasome inhibition in human gout.. Beta-carotene (provitamin A) suppressed the NLRP3 inflammasome activation induced by various activators, including MSU crystals, in mouse bone marrow-derived primary macrophages (P < 0.05). Surface plasmon resonance analysis demonstrated the direct binding of β-carotene to the pyrin domain (PYD) of NLRP3 (K. Our results present β-carotene as a selective and direct inhibitor of NLRP3, and the binding of β-carotene to NLRP3 PYD as a novel pharmacologic strategy to combat NLRP3 inflammasome-driven diseases, including gouty arthritis.

Topics: Animals; Arthritis, Gouty; beta Carotene; Caspase 1; Disease Models, Animal; Enzyme-Linked Immunosorbent Assay; Gout; Humans; Inflammasomes; Inflammation; Interleukin-1beta; Macrophages; Mice; Molecular Docking Simulation; NLR Family, Pyrin Domain-Containing 3 Protein; Provitamins; Pyrin Domain; Surface Plasmon Resonance; Synovial Fluid

Topics: Arthritis, Gouty; beta Carotene; Humans; Inflammasomes; Inflammation; NLR Family, Pyrin Domain-Containing 3 Protein; Pyrin Domain

Palmitoylethanolamide (PEA) is an endogenous lipid mediator with powerful anti-inflammatory and analgesic functions. PEA can be hydrolyzed by a lysosomal enzyme N-acylethanolamine acid amidase (NAAA), which is highly expressed in macrophages and other immune cells. The pharmacological inhibition of NAAA activity is a potential therapeutic strategy for inflammation-related diseases. Fucoxanthinol (FXOH) is a marine carotenoid from brown seaweeds with various beneficial effects. However, the anti-inflammatory effects and mechanism of action of FXOH in lipopolysaccharide (LPS)-stimulated macrophages remain unclear. This study aimed to explore the role of FXOH in the NAAA-PEA pathway and the anti-inflammatory effects based on this mechanism. In vitro results showed that FXOH can directly bind to the active site of NAAA protein and specifically inhibit the activity of NAAA enzyme. In an LPS-induced inflammatory model in macrophages, FXOH pretreatment significantly reversed the LPS-induced downregulation of PEA levels. FXOH also substantially attenuated the mRNA expression of inflammatory factors, including inducible nitric oxide synthase (iNOS), interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-α), and markedly reduced the production of TNF-α, IL-6, IL-1β, and nitric oxide (NO). Moreover, the inhibitory effect of FXOH on NO induction was significantly abolished by the peroxisome proliferator-activated receptor α (PPAR-α) inhibitor GW6471. All these findings demonstrated that FXOH can prevent LPS-induced inflammation in macrophages, and its mechanisms may be associated with the regulation of the NAAA-PEA-PPAR-α pathway.

Topics: Amides; Amidohydrolases; Animals; Anti-Inflammatory Agents; beta Carotene; Cytokines; Enzyme Inhibitors; Ethanolamines; Inflammation; Lipopolysaccharides; Mice; Nitric Oxide; Oxazoles; Palmitic Acids; PPAR alpha; RAW 264.7 Cells; Tyrosine

BACKGROUND Excessive reactive oxygen species (ROS) stimulate mitochondrial damage that causes degenerative diseases such as cardiovascular disease (CVD). ß-carotene (BC), a natural antioxidant able to counteract free radicals, acts as a cytoprotective agent. However, knowledge of the role of BC on cardiomyoblasts is limited. In this study, we explored its role on COX4, Tom20, Nfr1, Nrf2, Nf-kappaB, LC3, p62, caspase 3, and caspase 9 and its association with cardiomyoblast viability and survival. MATERIAL AND METHODS H9C2 cell lines were seeded, cultivated until 90% to 100% confluency, and treated with various doses of BC: 10 µM, 1 µM, 0.1 µM, and 0.01 µM. After 24 h, the cells were harvested, lyzed, and tested for specific related protein expressions from each dose. RESULTS Low-dose BC induced autophagy most effectively at 1 µM, 0.1 µM, and 0.01 µM, as indicated by a decrease of LC3II and p62 levels. We observed that Nf-kB protein levels were suppressed; Nrf2 was stimulated, but Nrf1 was not altered significantly. Further, low-dose BC might stimulate cell viability by reducing apoptotic signals of caspase 3 and 9. Notably, low-dose BC also showed potential to increase Tom20 protein levels. CONCLUSIONS Low-dose BC supplementation shows beneficial effects, especially at 0.01 µM, by reducing inflammation through the suppression of Nf-kappaB and increase of Nrf2 level. Autophagy as a cellular maintenance mechanism was also stimulated, and the amount of the mitochondria marker Tom20 increased. Taken together, results showed that specific low-dose BC is effective and might improve cell viability by stimulating autophagy, inhibiting proinflammatory factors, and suppressing apoptosis.

Topics: Animals; Autophagy; beta Carotene; Biomarkers; Caspases; Cell Line; Cell Shape; Inflammation; Microtubule-Associated Proteins; Mitochondria; Myocytes, Cardiac; NF-E2-Related Factor 2; NF-kappa B; Nuclear Respiratory Factor 1; Rats; Signal Transduction

Previous research has shown that nutrition can influence cognitive abilities in older adults. We examined whether nutritional factors or inflammatory biomarkers moderate the age-cognition association.. Analyses included 1,308 participants (age ≥60) from the National Health and Nutrition Examination Survey III. Macronutrients (% of calories from fat, protein, and carbohydrates), micronutrients/amino acids (blood serum values: Vitamins B12, C, D, E, folate, iron, homocysteine, and β-carotene), and inflammatory biomarkers (serum C-reactive protein, plasma fibrinogen, and serum ferritin) were examined as moderators with cognition. Cognition was measured by six tasks: immediate and delayed story recall, immediate and delayed word memory, digit subtraction, and questions about place/orientation.. Higher values of serum folate were significantly associated with better cognitive scores. Specifically, the interaction between age-cognition and folate indicated the associations of higher age and lower global cognition and lower immediate story recall were weaker in those with higher folate values (p's < .05). A significant interaction between age and plasma fibrinogen indicated that the association between age and worse digit subtraction was stronger with values >3.1 g/L.. Folate and fibrinogen were significant moderators between age and cognition. Further research into the relationship between nutrition, inflammation, and cognitive aging is needed.

Topics: Age Factors; Aged; beta Carotene; Biomarkers; C-Reactive Protein; Cognition; Cognitive Dysfunction; Diet; Female; Ferritins; Fibrinogen; Folic Acid; Homocysteine; Humans; Inflammation; Iron; Male; Middle Aged; Neuropsychological Tests; Nutrition Surveys; Nutritional Status; Vitamins

β-carotene is one of the most abundant carotenoids, has potential anti-inflammatory effect, it has been reported that β-carotene could suppress LPS-induced inflammatory responses by inhibiting nuclear factor kappa B (NF-κB) translocation, but the more detailed molecular mechanisms underlying the anti-inflammatory action of β-carotene remain to be fully understood. In this study, we investigated the influence of β-carotene on the activation of JAK2/STAT3, MAPK, and NF-κB signaling pathway induced by LPS in RAW264.7 cells and peritoneal macrophages. Cells were treated with different concentrations of β-carotene for 3 hr after LPS treatment for 24 hr. The mRNA expression and the release of IL-1β, IL-6, and TNF-α were evaluated by RT-PCR and ELISA, and the level of signaling proteins of JAK2/STAT3, MAPK, and NF-κB signaling pathway were detected by Western blot. The results showed that β-carotene significantly suppressed (p < 0.05) LPS-induced release of IL-1β, IL-6, and TNF-α and their mRNA expression. LPS-induced JAK2/STAT3, IκB/NF-κB p65, JNK/p38 MAPK signal activation were significantly attenuated (p < 0.05) by β-carotene in a dose-dependent manner. In conclusion, β-carotene could attenuate LPS-induced inflammation via inhibition of the NF-κB, JAK2/STAT3, and JNK/p38 MAPK signaling pathways in macrophages.

Topics: Animals; beta Carotene; Cell Survival; Cytokines; Dose-Response Relationship, Drug; Gene Expression; Inflammation; Inflammation Mediators; Janus Kinase 2; Lipopolysaccharides; Macrophage Activation; Macrophages, Peritoneal; MAP Kinase Signaling System; Mice; NF-kappa B; RAW 264.7 Cells; RNA, Messenger; Signal Transduction; STAT3 Transcription Factor

β-Carotene has been reported to alleviate hepatic steatosis (SS), inflammation, and fibrosis in vivo and vitro studies. However, the clinical relevance of serum β-carotene and β-carotene-to-retinol (SC/SR) ratio with histological severity in nonalcoholic fatty liver disease (NAFLD) patients is unknown. This case-control study enrolled 24 control subjects and 62 NAFLD patients. Liver biopsies were collected and histological characteristics were assessed. Information with regard to demographic, anthropometric and dietary intake was assessed by face-to-face interviews with questionnaire. Serum β-carotene and retinol concentrations were determined by the HPLC method. Serum β-carotene and SC/SR levels in NAFLD patients were significantly lower than these in controls (0.23 ± 0.01 vs. 0.35 ± 0.04 μmol/L, 0.38 ± 0.03 vs. 0.84 ± 0.10). Compared with individuals without SS, both β-carotene and SC/SR levels were significantly decreased in those with moderate SS (0.34 ± 0.03 vs. 0.21 ± 0.02 μmol/L, 0.76 ± 0.09 vs. 0.37 ± 0.05). Subjects with mild inflammation had a significantly lower β-carotene and SC/SR levels than those without inflammation (0.23 ± 0.01 vs. 0.33 ± 0.04 μmol/L, 0.77 ± 0.09 vs. 0.38 ± 0.03). Serum SC/SR was significantly lower in patients with mild fibrosis than those without fibrosis (0.45 [0.27-0.83] vs. 0.34 [0.26-0.51]). According to the NAFLD Activity Scoring score, both β-carotene and SC/SR gradually decreased with disease progression from normal liver, simple SS to steatohepatitis borderline (ptrend ≤ 0.001). These results show that NAFLD patients have lower circulating β-carotene concentration and SC/SR ratio, which are associated with the histological severity of NAFLD.

Topics: Adult; beta Carotene; Case-Control Studies; Female; Humans; Inflammation; Liver; Male; Middle Aged; Non-alcoholic Fatty Liver Disease; Vitamin A

Atopic dermatitis (AD) is a cutaneous condition characterized by itchy, swollen, and dry skin, which is mediated by T helper cell-related cytokines. β-Carotene, a natural red pigment found in plants, exhibits antioxidant activity that has been shown to promote an inflammatory response. Because it is not clear whether β-carotene suppresses inflammation in AD skin tissues, we examined the effects of oral administration of β-carotene in mice induced by a low zinc/magnesium diet (HR-AD diet). Our studies found that AD-like inflammation was remarkably reduced by β-carotene. In addition, β-carotene significantly suppressed protein expression of TNF-α, IL-1β, and MCP-1 and mRNA expression of TSLP, IL-6, IL-1β, IL-4, IL-5, and Par-2 in AD-like skin tissues. It was also found that mRNA and protein expression of filaggrin (a major structural protein in epidermis) in AD-like skin was significantly elevated by β-carotene administration. Furthermore, β-carotene treatment significantly reduced the activity and/or mRNA expression of matrix metalloproteinases (MMPs), degradation of the extracellular matrix and regulation of chemokines. These results suggest that β-carotene reduces skin inflammation through the suppressed expression of inflammatory factors or the activity of MMPs as well as the promotion of filaggrin expression in AD-like skin. β-Carotene is a potent anti-inflammatory agent, which improves AD-like skin by enhancing the skin barrier function.

Topics: Administration, Oral; Animals; beta Carotene; Cytokines; Dermatitis, Atopic; Diet; Epidermis; Extracellular Matrix; Filaggrin Proteins; Gene Expression; Inflammation; Intermediate Filament Proteins; Male; Mice, Hairless

Although α- and γ-tocopherol are co-consumed antioxidants, circulating γ-tocopherol concentrations were paradoxically found to be inversely associated with total vitamin E intake and circulating α-tocopherol concentrations. There are limited data on this apparent paradox or on determinants of circulating γ-tocopherol concentrations.. To help clarify possible determinants of circulating γ-tocopherol concentrations, we investigated associations of circulating γ-tocopherol concentrations with various dietary and lifestyle factors and biomarkers of oxidative stress and inflammation.. We pooled cross-sectional data from 2 outpatient, adult, elective colonoscopy populations (pooled n = 419) on whom extensive dietary, lifestyle, and medical information was collected, and the following plasma concentrations were measured: α- and γ-tocopherol (via HPLC), F2-isoprostanes (FiPs; via gas chromatography-mass spectrometry), and high-sensitivity C-reactive protein (hsCRP; via latex-enhanced immunonephelometry). Multivariable general linear models were used to assess mean γ-tocopherol differences across quantiles of plasma antioxidant micronutrients, FiPs, and hsCRP; an oxidative balance score [OBS; a composite of anti- and pro-oxidant dietary and lifestyle exposures (a higher score indicates higher antioxidant relative to pro-oxidant exposures)]; and multiple dietary and lifestyle factors.. Adjusted for serum total cholesterol, mean γ-tocopherol concentrations among those in the highest relative to the lowest tertiles of circulating α-tocopherol and β-carotene, the OBS, and total calcium and dietary fiber intakes were 31.0% (P < 0.0001), 29.0% (P < 0.0001), 27.6% (P = 0.0001), 29.7% (P < 0.0001), and 18.6% (P = 0.008) lower, respectively. For those in the highest relative to the lowest tertiles of circulating FiPs and hsCRP, mean γ-tocopherol concentrations were 50% (P < 0.0001) and 39.0% (P < 0.0001) higher, respectively.. These findings support the conclusion that circulating γ-tocopherol concentrations are inversely associated with antioxidant exposures and directly associated with systemic oxidative stress and inflammation in adults. Additional research on possible mechanisms underlying these findings and on whether circulating γ-tocopherol may serve as a biomarker of oxidative stress, inflammation, or both is needed.

Topics: Aged; alpha-Tocopherol; Antioxidants; beta Carotene; Cross-Sectional Studies; Diet; Female; gamma-Tocopherol; Humans; Inflammation; Life Style; Male; Middle Aged; Oxidative Stress; Vitamin E

High-fat diet (HFD)-induced leaky gut syndrome combined with low-grade inflammation increase reactive oxygen species (ROS) in the intestine and may contribute to dysbiosis and metabolic syndrome (MetS). Poorly bioavailable and only partially metabolizable dietary polyphenols, such as proanthocyanidins (PACs), may exert their beneficial effects on metabolic health by scavenging intestinal ROS. To test this hypothesis, we developed and validated a novel, noninvasive, in situ method for visualizing intestinal ROS using orally administered ROS-sensitive indocyanine green (ICG) dye. C57BL/6J mice fed HFD for 10 weeks accumulated high levels of intestinal ROS compared to mice fed low-fat diet (LFD). Oral administration of poorly bioavailable grape polyphenol extract (GPE) and β-carotene decreased HFD-induced ROS in the gut to levels comparable to LFD-fed mice, while administration of more bioavailable dietary antioxidants (α-lipoic acid, vitamin C, vitamin E) did not. Forty percent of administered GPE antioxidant activity was measured in feces collected over 24 h, confirming poor bioavailability and persistence in the gut. The bloom of beneficial anaerobic gut bacteria, such as Akkermansia muciniphila, associated with improved metabolic status in rodents and humans may be directly linked to protective antioxidant activity of some dietary components. These findings suggest a possible mechanistic explanation for the beneficial effects of poorly bioavailable polyphenols on metabolic health.

Topics: Administration, Oral; Animals; Antioxidants; beta Carotene; Diet, High-Fat; Dysbiosis; Feces; Gastrointestinal Microbiome; Indocyanine Green; Inflammation; Intestines; Male; Metabolic Syndrome; Mice; Mice, Inbred C57BL; Mice, Obese; Plant Extracts; Polyphenols; Reactive Oxygen Species; Spectrometry, Mass, Electrospray Ionization; Tandem Mass Spectrometry; Vitis

To examine the correlation between inflammatory biomarkers and plasma β-carotene levels in children.. A total of 564 Spanish schoolchildren aged 9-12 were observed and studied. Plasma β-carotene levels were assessed by HPLC. A β-carotene level <4.83 µg/dL (0.09 µmol/L) was considered deficient. Plasma tumour necrosis factor-α (TNF-α) and interleukin-6 (IL-6) were measured by immunoenzyme assays. Serum high-sensitivity C-reactive protein (hs-CRP) was tested by immunonephelometry.. Subjects who were β-carotene-deficient (23.1% of the studied children) had higher IL-6 levels than subjects with normal β-carotene concentrations. The log-IL-6 and log-hs-CRP concentrations, but not the log-TNF-α level, were strongly and inversely related to the plasma log-β-carotene level (taking into account log-age, energy intake, log-triglycerides, gender, log-body mass index, log-β-carotene intake, energy from lipids and cholesterol as covariables). When the 3 inflammatory biomarkers were introduced into the regression model along with the corresponding covariables, only the log-IL-6 level was related to the plasma log-β-carotene level (β = -0.505 ± 0.078; p < 0.001).. Inflammatory status, in particular IL-6 levels, appears to be negatively associated with plasma β-carotene levels in schoolchildren.

Topics: beta Carotene; Biomarkers; Body Mass Index; C-Reactive Protein; Child; Cholesterol; Cross-Sectional Studies; Diet Surveys; Exercise; Female; Health Surveys; Humans; Inflammation; Interleukin-6; Male; Nutritional Status; Sensitivity and Specificity; Spain; Triglycerides; Tumor Necrosis Factor-alpha

We have previously shown that quercetin modulates the proinflammatory effect of β-carotene (BC) induced by oral benzo[a]pyren (Bap) partly through the regulation of the JNK pathway. In the present study, we determined whether the combination of BC and quercetin regulates the antioxidant enzymes and the activation of NF-κB in Mongolian gerbils exposed to Bap. We also compared the combined effects of BC+ quercetin with that of BC+ ascorbic acid (C)+ α-tocopherol (E).. The gerbils were given BC (10 mg/kg) alone or in combination with quercetin (50 or 100 mg/kg) or C (13 mg/kg)+E (92 mg/kg) by gavage 3 times/week for 6 months. During the first 2 months, the gerbils were exposed to Bap by intratracheal instillation once/week. The levels of proinflammatory cytokines, thiobarbituric acid reactive substances, antioxidant enzymes and NF-κB activation in the plasma or the lungs were determined.. Bap increased the level of proinflammatory cytokines and oxidative stress in the plasma or lungs, while it decreased the antioxidant systems. Bap also increased nuclear NF-κB levels in the lungs. BC partly recovered the Bap-induced decrease in antioxidant activity, antioxidant enzyme activities and glutathione levels but had no effect on proinflammatory cytokines and NF-κB translocation. BC in combination with quercetin or C+E suppressed all the harmful effects induced by Bap. All the effects of quercetin at 100 mg/kg were similar to the effect of C+E.. BC in combination with quercetin or C+E rather than BC alone similarly suppresses the Bap-induced inflammatory reaction that was accompanied by the regulation of antioxidant enzymes and the translocation of NF-κB in vivo.

Topics: alpha-Tocopherol; Animals; Antioxidants; Ascorbic Acid; Benzo(a)pyrene; beta Carotene; Catalase; Gerbillinae; Glutathione; Glutathione Peroxidase; Inflammation; Interleukin-1beta; Lipid Peroxidation; Lung; Male; NF-kappa B; Oxidative Stress; Quercetin; Superoxide Dismutase; Thiobarbituric Acid Reactive Substances; Tumor Necrosis Factor-alpha

Ulcerative colitis (UC), a chronic gastrointestinal disorder, is a debilitating disease affecting many people across the globe. Research suggests that the levels of several antioxidants, including β-carotene (β-CAR), decrease in the serum of patients with UC. The present study was aimed at elucidating the molecular mechanisms involved in β-CAR-mediated protection against UC in mice.. UC was induced in mice using 3%w/v dextran sulfate sodium in drinking water for two cycles; one cycle comprised of 7 days of dextran sulfate sodium-treated water followed by 14 days of normal drinking water. β-CAR was administered at the doses of 5, 10 and 20 mg/kg bw/day, po throughout the experiment. The effect of β-CAR in mice with UC was evaluated using biochemical parameters, histological evaluation, comet and micronucleus assays, immunohistochemistry and Western blot analysis.. The results indicated that β-CAR treatment ameliorated the severity of UC by modulating various molecular targets such as nuclear factor-kappa B, cyclooxygenase-2, interleukin 17, signal transducer and activator of transcription 3, nuclear erythroid 2-related factor 2, matrix metalloproteinase-9 and connective tissue growth factor. Further, β-CAR treatment maintained the gut integrity by increasing the expression of a tight junction protein, occludin, which was decreased in the colon of mice with UC. Also β-CAR treatment significantly reduced UC-associated elevated plasma lipopolysaccharide level, systemic inflammation and genotoxicity.. β-CAR ameliorated UC-associated local and systemic damage in mice by acting on multiple targets.

Topics: Animals; Antioxidants; beta Carotene; Colitis, Ulcerative; Comet Assay; Connective Tissue Growth Factor; Cyclooxygenase 2; Dextran Sulfate; Disease Models, Animal; DNA Damage; Dose-Response Relationship, Drug; Glutathione; Inflammation; Interleukin-17; Interleukin-6; Lipid Peroxidation; Lipopolysaccharides; Male; Matrix Metalloproteinase 9; Mice; NF-E2-Related Factor 2; NF-kappa B; Occludin; Oxidative Stress; STAT3 Transcription Factor; Tight Junction Proteins; Tumor Necrosis Factor-alpha

Anemia of chronic disease is frequently seen in chronic inflammatory conditions. Its hallmark is disrupted iron homeostasis, with increased uptake and retention of iron in cells of the reticuloendothelial system. Using the Caco-2 cell line as an in vitro model for iron absorption, local intestinal iron-related protein dynamics were evaluated during interleukin (IL)1β/iron-induced inflammation, confirmed by IL8 release, and following β-carotene and vitamin A supplementation. Time- and dose-dependent iron administration to the cells was then studied. The effects on heavy and light ferritin, ferroportin, transferrin receptor and intracellular iron levels were compared in inflamed Caco-2 cells with and without application of the anti-inflammatory agents β-carotene and vitamin A. IL1β treatment led to IL8 release, a surge in both ferritins' expressions and suppression of ferroportin and transferrin receptor expression. β-Carotene significantly reduced IL8 (1,306.2-253.75 pg/ml), decreased light and heavy ferritin by 77.8 and 45.8%, respectively, and increased ferroportin by 59.9% (P < 0.05). Increasing iron concentrations and incubation periods resulted in increased IL8 release. A strong correlation was found between the levels of IL8 and the ferritins. Intracellular iron sequestration was induced by IL1β and iron and alleviated by β-carotene. β-Carotene normalized the main iron-related proteins' levels, reduced IL8 production, and released intracellular trapped iron. These results highlight local mucosal control of iron regulation and suggest that by applying anti-inflammatory compounds, less iron is locked in inflamed intestinal epithelial cells, leading to its increased bioavailability. This suggests a possible approach to combating anemia associated with chronic inflammatory conditions.

Topics: Anti-Inflammatory Agents; beta Carotene; Caco-2 Cells; Carotenoids; Carrier Proteins; Cation Transport Proteins; Dose-Response Relationship, Drug; Ferritins; Humans; Inflammation; Interleukin-1beta; Interleukin-8; Intracellular Space; Iron; Protein Binding; Receptors, Transferrin

The aim of the present study was to examine the association between intake of five common antioxidative nutrients from supplements and medications (vitamin E, vitamin C, carotenoids, Se, and Zn) and levels of high-sensitivity C-reactive protein (hs-CRP) in the general population. For this purpose, a total of 2924 participants of the population-based Cooperative Health Research in the Region of Augsburg (KORA) F4 study (2006-8) were investigated cross-sectionally. Intake of dietary supplements and medication during the last 7 d was recorded in a personal interview, when participants were asked to show product packages of ingested preparations. Linear regression models were calculated; first, the exposure to regular nutrient intake was treated with a binary response (yes/no); then regularly ingested amounts were divided into quartiles to examine dose-response relationships. Effect of single v. combined supplementation of antioxidants was assessed through the inclusion of interaction terms into the models. Regular intake of any of the five investigated antioxidants per se was not associated with hs-CRP levels. However, dose-response analyses revealed that participants who regularly ingested more than 78 mg vitamin E/d, which corresponds to the upper quartile, had 22% lower hs-CRP levels (95% CI 0·63, 0·97) compared to those of persons who were not exposed to any vitamin E supplementation. Stratified analyses showed that this association was found only in persons who took vitamin E in combination with other antioxidants. The combined supplementation of vitamin E with other antioxidants could thus be a promising strategy for the prevention of inflammation-related diseases in the general population, if further studies could confirm that the proposed association is causal.

Topics: Adult; Aged; Aged, 80 and over; Antioxidants; Ascorbic Acid; beta Carotene; Body Mass Index; C-Reactive Protein; Cross-Sectional Studies; Dietary Supplements; Dose-Response Relationship, Drug; Female; Humans; Inflammation; Male; Middle Aged; Motor Activity; Selenium; Vitamin E; Zinc

Fucoxanthin (Fx) is a marine carotenoid found in edible brown seaweeds. We previously reported that dietary Fx metabolite into fucoxanthinol (FxOH), attenuates the weight gain of white adipose tissue of diabetic/obese KK-Ay mice. In this study, to evaluate anti-diabetic effects of Fx, we investigated improving the effect of insulin resistance on the diabetic model of KK-Ay mice. Furthermore, preventing the effect of FxOH on low-grade chronic inflammation related to oxidative stress was evaluated on 3T3-L1 adipocyte cells and a RAW264.7 macrophage cell co-culture system. A diet containing 0.1% Fx was fed to diabetic model KK-Ay mice for three weeks, then glucose tolerance was observed. Fx diet significantly improved glucose tolerance compared with the control diet group.  In in vitro studies, FxOH showed suppressed tumor necrosis factor-α (TNF-α), and monocyte chemotactic protein-1 (MCP-1) mRNA expression and protein levels in a co-culture of adipocyte and macrophage cells. These findings suggest that Fx ameliorates glucose tolerance in the diabetic model mice. Furthermore, FxOH, a metabolite of Fx, suppresses low-grade chronic inflammation in adipocyte cells.

Topics: 3T3-L1 Cells; Adipocytes; Adipose Tissue, White; Animals; beta Carotene; Blood Glucose; Cell Line; Chemokine CCL2; Diabetes Mellitus, Experimental; Diet; Disease Models, Animal; Inflammation; Insulin Resistance; Macrophages; Mice; Obesity; RNA, Messenger; Tumor Necrosis Factor-alpha; Weight Gain; Xanthophylls

Periodontitis is a chronic inflammatory disease and a significant risk factor for tooth loss. Although a link between diet and periodontal health exists, the relation between diet and healing after periodontal therapy has yet to be investigated.. The objective was to determine whether higher intakes of fruits and vegetables or nutrients with antioxidant or anti-inflammatory activity are associated with greater healing, measured as reduced probing depth (PD), after scaling and root planing (SRP), a cost-effective treatment to manage periodontal disease and prevent tooth loss.. Patients (63 nonsmokers, 23 smokers) with chronic generalized periodontitis who were undergoing SRP participated. Healing was evaluated based on PD, assessed at baseline and 8-16 wk after SRP. Intakes of fruits, vegetables, β-carotene, vitamin C, α-tocopherol, α-linolenic acid (ALA), eicosapentaenoic acid (EPA), and docosahexaenoic acid (DHA) were estimated using the Block 2005 food frequency questionnaire and a supplement questionnaire. Serum 25-hydroxyvitamin D concentrations were also measured. PD (% sites >3 mm) was modeled in multiple linear regression and analysis of covariance by tertile of intake and adjusted for age, sex, body mass index (BMI), baseline PD, examiner, gingival bleeding, and study duration.. In nonsmokers, PD was associated with fruit and vegetable, β-carotene, vitamin C, α-tocopherol, EPA, and DHA intakes (P < 0.05). PD was not significantly associated with ALA intake or serum 25-hydroxyvitamin D concentration. Significant associations that included supplements (β-carotene, vitamin C, α-tocopherol) were attenuated or lost, depending on the statistical model used. There were no significant associations within the group of smokers.. Dietary intakes of fruits and vegetables, β-carotene, vitamin C, α-tocopherol, EPA, and DHA are associated with reduced PD after SRP in nonsmokers, but not smokers, with chronic generalized periodontitis. These findings may lead to the development of dietary strategies to optimize healing after periodontal procedures. This trial was registered at clinicaltrials.gov as NCT02291835.

Topics: Adult; Aged; Aged, 80 and over; alpha-Linolenic Acid; alpha-Tocopherol; Antioxidants; Ascorbic Acid; beta Carotene; Body Mass Index; Chronic Disease; Cross-Sectional Studies; Dietary Supplements; Docosahexaenoic Acids; Eicosapentaenoic Acid; Energy Intake; Female; Fruit; Humans; Inflammation; Linear Models; Male; Middle Aged; Nutrition Assessment; Periodontitis; Risk Factors; Smoking; Surveys and Questionnaires; Vegetables; Vitamin D

Using archival data, we conducted a secondary analysis to examine race differences in the relation of serum vitamins A, C, E and β-carotene to insulin resistance (IR), fasting insulin and glucose, high sensitivity C-reactive protein (hs-CRP), and leukocyte count in 176 non-smoking, healthy, white, and African American (AA) adults aged 18 to 65 years (48% women, 33% AA). We hypothesized that micronutrient concentrations would be associated with early risk markers of cardiometabolic diseases in a race-dependent manner. Fasting blood samples were analyzed for micronutrients, insulin, glucose, hs-CRP, and leukocyte count. Insulin resistance was estimated using the homeostatic model assessment. After adjusting for age, body mass index, gender, educational level, use of vitamin supplements, alcohol intake, leisure time physical activity, menopausal status, and total cholesterol, we observed that β-carotene was significantly associated with insulin resistance and fasting insulin in a race-dependent manner. Among AA, lower β-carotene levels were associated with higher estimates of insulin resistance and fasting insulin; whereas, these same associations were not significant for whites. Race also significantly moderated the relation of vitamin C to leukocyte count, with lower vitamin C being associated with higher leukocyte count only in AA but not whites. For all subjects, lower β-carotene was associated with higher hs-CRP. In AA, but not whites, lower levels of β-carotene and vitamin C were significantly associated with early risk markers implicated in cardiometabolic conditions and cancer. Whether or not lower levels of micronutrients contribute uniquely to racial health disparities is a worthwhile aim for future research.

Topics: Adiposity; Adolescent; Adult; Aged; Ascorbic Acid; beta Carotene; Biomarkers; Black or African American; Blood Glucose; C-Reactive Protein; Female; Humans; Inflammation; Insulin; Insulin Resistance; Leukocyte Count; Male; Metabolic Diseases; Middle Aged; Racial Groups; Risk Factors; Vitamin A; Vitamin E; Vitamins; White People

The present study was designed to compare the anti-inflammatory effects of several agents applied in vivo, namely, a synthetic inhibitor of the NF-κB cascade, fat-soluble antioxidants, and the thymic peptide thymulin. Cytokine response in LPS-treated mice was analysed in tandem with the following parameters: the synthesis of inducible forms of the heat shock proteins HSP72 and HSP90α; activity of the NF-κB and SAPK/JNK signalling pathways; and TLR4 expression. Inflammation-bearing Balb/c male mice were pretreated with an inhibitor of IKK-α/β kinases (IKK Inhibitor XII); with thymulin; with dietary coenzyme Q9, α-tocopherol, and β-carotene; or with combinations of the inhibitor and peptide or antioxidants. Comparable anti-inflammatory effects were observed in inflammation-bearing mice treated separately with thymulin or with dietary antioxidants administered daily for two weeks before LPS treatment. When LPS-injected mice were treated with the inhibitor and antioxidants together, neither plasma cytokines, signal proteins, nor heat shock proteins recovered more efficiently than when mice were treated with these agents separately. In contrast to antioxidant diet, the thymulin was shown to increase the effect of IKK Inhibitor XII in preventing IKK activation in LPS-treated mice.

Topics: Animals; Anti-Inflammatory Agents; Antioxidants; beta Carotene; Inflammation; Lipopolysaccharides; Male; Mice; Mice, Inbred BALB C; Serine Proteinase Inhibitors; Thymic Factor, Circulating; Tocopherols

The aim of the present study was to evaluate the potential association between dietary nutrients and alterations in DNA methylation in a set of five candidate genes, including CD14, Et-1, iNOS, HERV-w and TNFα, in a population of overweight/obese subjects. We evaluated possible associations between gene methylation and clinical blood parameters, including total cholesterol (TC), low- and high-density lipoprotein cholesterol (LDL-C and HDL-C), triglyceride and homocysteine levels. We employed validated methods to assess anthropometric, clinical and dietary data, as well as pyrosequencing to evaluate DNA methylation of the five candidate genes in 165 overweight/obese subjects. There was no association between body mass index and DNA methylation of the five candidate genes in this group of subjects. Positive associations were observed between TNFα methylation and blood levels of LDL-C (β = 0.447, p = 0.002), TC/HDL-C (β = 0.467, p = 0.001) and LDL-C/HDL-C (β = 0.445, p = 0.002), as well as between HERV-w methylation and dietary intakes of β-carotene (β = 0.088, p = 0.051) and carotenoids (β = 0.083, p = 0.029). TNFα methylation showed negative associations with dietary intakes of cholesterol (β = -0.278, p = 0.048), folic acid (β = -0.339, p = 0.012), β-carotene (β = -0.332, p = 0.045), carotenoids (β = -0.331, p = 0.015) and retinol (β = -0.360, p = 0.008). These results suggest a complex relationship among nutrient intake, oxidative stress and DNA methylation.

Topics: Adult; Aged; beta Carotene; Body Mass Index; Carotenoids; Cholesterol; Cholesterol, HDL; DNA Methylation; Eating; Endothelin-1; Energy Intake; Female; Folic Acid; Gene Products, env; Humans; Inflammation; Lipopolysaccharide Receptors; Lipoproteins, LDL; Male; Middle Aged; Nitric Oxide Synthase Type II; Nutritional Status; Obesity; Overweight; Pregnancy Proteins; Triglycerides; Tumor Necrosis Factor-alpha; Vitamin A

Low-grade inflammation is an independent risk factor for cardiovascular disease. Relationships between the antioxidant status and inflammatory biomarkers could give new insights into cardiovascular disease prevention. We investigated long-term associations between the antioxidant nutrient (vitamin C, α-tocopherol, β-carotene) status and C-reactive protein (CRP) in a population-based cohort.. Subjects included in the French SU.VI.MAX trial study who had available data on baseline (1994-1995) blood nutrient concentrations and CRP measurements 12 years later (2007-2009) were included. Associations between baseline antioxidant circulating concentrations and elevated CRP (>3 mg/l) were investigated in multivariate logistic regression models. Subgroup analyses were performed according to gender, supplementation group of the initial trial, smoking status, and alcohol intake.. Serum α-tocopherol (n = 2,060) and vitamin C (n = 1,719) concentrations [odds ratio (OR) and 95% confidence interval (95% CI) quintile 5 vs. 1: OR 1.10 (95% CI 0.71-1.73), p for trend = 0.533, vs. OR 0.79 (95% CI 0.48-1.29), p for trend = 0.121, respectively] were not associated with elevated CRP concentrations. The β-carotene status (n = 2,048) was inversely associated with elevated CRP [adjusted OR quintile 5 vs. 1: OR 0.61 (95% CI 0.38-0.98), p for trend = 0.01]. Subgroup analyses showed that associations were stronger in women (p for trend = 0.004), never smokers (p for trend = 0.009) and subjects in the supplementation group (p for trend = 0.002).. Our results suggest that the β-carotene status may be inversely associated with low-grade inflammation in the long term.

Topics: alpha-Tocopherol; Antioxidants; Ascorbic Acid; beta Carotene; C-Reactive Protein; Cohort Studies; Female; France; Humans; Inflammation; Male; Middle Aged; Randomized Controlled Trials as Topic; Risk Factors

Carotene-15,15'-monooxygenase (CMO-I) cleaves β-carotene to form vitamin A, whereas carotene-9',10'-monooxygenase (CMO-II) preferentially cleaves non-provitamin A carotenoids. Recent reports indicate that β-carotene metabolites regulate dietary lipid uptake, whereas lycopene regulates peroxisome proliferator-activated receptor expression. To determine the physiologic consequences of carotenoids and their interactions with CMO-I and CMO-II, we characterized mammalian carotenoid metabolism, metabolic perturbations, and lipid metabolism in female CMO-I(-/-) and CMO-II(-/-) mice fed lycopene or tomato-containing diets for 30 days. We hypothesized that there would be significant interactions between diet and genotype on carotenoid accumulation and lipid parameters. CMO-I(-/-) mice had higher levels of leptin, insulin, and hepatic lipidosis but lower levels of serum cholesterol. CMO-II(-/-) mice had increased tissue lycopene and phytofluene accumulation, reduced insulin-like growth factor 1 levels and cholesterol levels, but elevated liver lipids and cholesterol compared with wild-type mice. The diets did not modulate these genotypic perturbations, but lycopene and tomato powder significantly decreased serum insulin-like growth factor 1. Tomato powder also increased hepatic peroxisome proliferator-activated receptor expression, independent of genotype. These data point to the pleiotropic actions of CMO-I and CMO-II supporting a strong role of these proteins in regulating tissue carotenoid accumulation and the lipid metabolic phenotype as well as tomato carotenoid-independent regulation of lipid metabolism.

Topics: Adipose Tissue; Animals; beta Carotene; beta-Carotene 15,15'-Monooxygenase; Carotenoids; Cholesterol; Diet; Fatty Acid Desaturases; Female; Genotype; Hormones; Inflammation; Insulin-Like Growth Factor I; Lipid Metabolism; Liver; Lycopene; Mice; Mice, Inbred C57BL; Mice, Knockout; Organ Size; Phenotype; Powders; RNA, Messenger; Solanum lycopersicum

Dietary patterns and biomarkers of inflammation have been scarcely associated. The aim was to assess dietary factors associated with subclinical inflammation among girls.. Fasting blood samples were collected from 12- to 17-year old girls (n=219) to measure adiponectin, leptin, tumor necrosis factor-alpha, plasminogen activator inhibitor 1 (PAI-1), interleukin-6 (IL-6) and high-sensitivity C-reactive protein (hs-CRP) levels. Body mass index (BMI) and waist-to-height ratio (WHtR), and food intake were also measured. Western (WDP) and Mediterranean (MDP) dietary patterns were identified.. BMI and WHtR were associated with adiponectin, leptin and hs-CRP (the last, only associated with BMI). Intakes of β-carotene equivalents and vitamin C were associated with adiponectin; saturated fatty acids (SFA), vitamin A, manganese and selenium with leptin; linoleic acid with PAI-1; and oleic acid and vitamin E with IL-6. Selenium was inversely associated with adiponectin, whereas magnesium was positively associated with IL-6. MDP was associated with higher plasma concentrations of adiponectin (β=0.174, P<0.05); after adjustment for BMI, associations were not significant (β=0.144, P=0.076). WDP was negatively associated with adiponectin (β=-0.177, P<0.05) and positively with IL-6 (β=0.183, P<0.05).. Subclinical inflammation is detectable with increasing BMI and also WHtR. Measures of adiposity (BMI and WHtR) are significant predictors of adiponectin, leptin and hs-CRP. Dietary patterns per se have a small role in affecting inflammatory markers among adolescents.

Topics: Adiponectin; Adolescent; Ascorbic Acid; beta Carotene; Biomarkers; Body Height; Body Mass Index; C-Reactive Protein; Child; Diet; Fatty Acids; Female; Humans; Inflammation; Interleukin-6; Leptin; Linoleic Acid; Manganese; Oleic Acid; Plasminogen Activator Inhibitor 1; Selenium; Tumor Necrosis Factor-alpha; Vitamin A; Vitamin E; Waist Circumference

Eryngium foetidum (EF) has long been used as a medicinal plant and culinary spice in tropical regions. Phytochemicals in its leaves have been proposed to be responsible for the anti-inflammatory and antioxidant activities. The present study used in vitro digestion coupled with Caco-2 cells to assess such activities. Caco-2 cells were incubated with aqueous fraction from simulated digestion (bioaccessible fraction) of EF leaves with/without bile extract prior to stimulation with interleukin-1 beta (IL-1β). Monocyte chemoattractant protein-1 (MCP-1) and IL-8 in culture media and the intracellular reactive oxygen species (ROS) were measured. Approximately 24% β-carotene and 35% lutein of leaves were present in the aqueous fraction. The transfer of caffeic and chlorogenic acids to the aqueous fraction was 76%-81%, while that of kaempferol was 48%. Prior incubation of Caco-2 cells with the bioaccessible fraction suppressed IL-1β activated IL-8 and MCP-1 by 33%, but the fraction lacking mixed micelles decreased IL-8 and MCP-1 levels only by 11%. The pretreatment of Caco-2 cells with the bioaccessible fraction of EF reduced ROS by 34%; the fraction lacking mixed micelles decreased ROS by 28%. These data suggest that bioactive compounds partitioning in mixed micelles play a significant role to suppress the proinflammatory insult but with a modest antioxidant effect.

Topics: Anti-Inflammatory Agents; Antioxidants; beta Carotene; Caco-2 Cells; Chemokine CCL2; Eryngium; Gene Expression Regulation; Humans; Inflammation; Interleukin-1beta; Interleukin-8; Lutein; Plant Extracts; Plant Leaves; Reactive Oxygen Species

Antioxidants are widely used for prevention of diseases associated with oxidative stress and ischemic disorder. We investigated the hypothesis of antioxidants (α-tocopherol and β-carotene) can suppress the renal disorder in apo E-/-mice. Renal damage induced by chronic infusion of Angiotensin II (Ang II) into 4 month old male apo E-/-mice. After that the mice were treated with diet enriched α tocopherol and β carotene (800 mg/kg) for 150 days. Ang II treated kidney showed polycystic appearance with accumulation of clear fluid and constriction of renal artery and renal vein was noticed. Vacuolar/cystic degeneration as well as inflammatory reactions was noticed in the tubules/glomerulus of Ang II treated mice. β carotene treated mice showed enormous numbers of regenerated tubules in the kidney and over expression of ICAM proteins in the regenerated tubules. CD 45.2, MAC 3 proteins were over expressed in the inflammatory cells infiltrated into the tubular region of Ang II treated kidney. Gene expression studies revealed up regulation of Renin 1 (Ren 1) and PPARγ genes in the kidney of Ang II treated animals, but the β carotene treatment controlled the expression of these genes in the regenerated kidneys. β carotene may have protective effective on chronic renal disorder. It may repress the inflammatory genes (Ren 1, PPARγ) to achieve the protective effect on Ang II induced renal damage.

Topics: Angiotensin II; Animals; Apolipoproteins E; beta Carotene; Cell Movement; Female; Inflammation; Kidney Glomerulus; Kidney Tubules, Proximal; Male; Mice; Mice, Knockout; Polycystic Kidney Diseases; PPAR gamma; Renal Insufficiency, Chronic; Renin

In vitro studies have shown that quercetin modulates the effects of β-carotene induced by stimulants. Whether these reactions happen in vivo, however, is unclear. Thus, we investigated whether quercetin supplementation suppresses the harmful effects of benzo[a]pyrene (BaP) alone or combined with β-carotene in the lungs of Mongolian gerbils. The gerbils were given quercetin (100 mg/kg body wt, 3 times/week), β-carotene (10 mg/kg body wt, 3 times/week), and BaP (8 mmol, 2 times/week) alone or in combination by gavage for 6 months. β-Carotene supplementation enhanced the pro-inflammatory effects of BaP in the lungs of gerbils. In contrast, quercetin supplementation significantly decreased the infiltration of inflammatory cells as well as the levels of TNF-α and IL-1β in the bronchoalveolar lavage fluid and plasma of gerbils exposed to BaP or BaP+β-carotene (P<.05). Such effects of quercetin supplementation were accompanied by a down-regulation of the expression of phospho-c-Jun and phospho-JNK induced by BaP or BaP+β-carotene in the lungs of gerbils. Furthermore, in the ex vivo study, we found that quercetin-metabolite-enriched plasma (QP) obtained from gerbils acted like a JNK inhibitor to significantly suppress the secretion of pro-inflammatory cytokines induced by BaP or BaP+β-carotene in A549 cells (P<.05). QP also suppressed the activation of the JNK pathway in the A549 cells. These results suggest that supplemental quercetin suppress the pro-inflammatory effect of β-carotene induced by BaP in vivo and ex vivo. The regulation of the JNK pathway by the metabolites of quercetin contributes, at least in part, to such effects of quercetin in vivo.

Topics: Animals; Benzo(a)pyrene; beta Carotene; Bronchoalveolar Lavage Fluid; Cell Line, Tumor; Cytokines; Dietary Supplements; Gene Expression Regulation; Gerbillinae; Humans; Inflammation; Interleukin-1beta; JNK Mitogen-Activated Protein Kinases; Liver; Lung; Male; MAP Kinase Kinase 4; Quercetin; Tumor Necrosis Factor-alpha

Cardiovascular disease (CVD) is associated with vascular oxidative imbalance and inflammation. Increased reactive oxygen species (ROS) generation is associated with a functional inactivation of nitric oxide (NO) due to the reaction with O₂⁻, leading to peroxynitrite (ONOO⁻) formation and subsequent reduction in the beneficial effect of vascular NO bioavailability. Carotenoids'-rich diets have been associated with decreased risk of CVD, but the underlying mechanism is still unknown.. In human umbilical vein endothelial cells (HUVECs), both β-carotene (BC) or lycopene (Lyc) significantly affected tumor necrosis factor-α (TNF-α)-induced inflammation, being associated with a significant decrease in the generation of ROS (spectrofluorometry) and nitrotyrosine (an index of ONOO⁻ formation, cytofluorimetry), an increased NO/cGMP (cyclic guanosine monophosphate) levels (EIA), and a down-regulation of NF-κB-dependent adhesion molecule expression (Western blot and EMSA) and monocyte-HUVEC interaction (adhesion assay). Our results indicate that BC or Lyc treatment reduce the inflammatory response in TNF-α-treated HUVECs. This is due to the redox balance protection and to the maintenance of NO bioavailability.. Our observations provide background for a novel mechanism for carotenoids' anti-inflammatory activity in the vasculature and may contribute to a better understanding of the protective effects of carotenoid-rich diets against CVD risk.

Topics: Anti-Inflammatory Agents, Non-Steroidal; beta Carotene; Biological Availability; Carotenoids; Cell Adhesion; Cell Adhesion Molecules; Cyclic GMP; Human Umbilical Vein Endothelial Cells; Humans; Inflammation; Lycopene; Monocytes; NF-kappa B; Nitric Oxide; Oxidative Stress; Reactive Oxygen Species; Tumor Necrosis Factor-alpha; Tyrosine

This study examined the effect of weight loss after 3, 6 and 12 months of Roux-en-Y Gastric Bypass (RYGB) on energy intake and on several biomarkers of oxidative stress such as levels of vitamin C, beta-carotene, vitamin E (diet/blood), nitric oxide metabolites (NOx), myeloperoxidase (MPO), thiobarbituric acid reactive substances (TBARS), reduced glutathione (GSH) and activity of catalase (CAT).. Study with a control group (CG), assessed once, and a bariatric group (BG) assessed at the basal period as well as at 3, 6 and 12 months post-surgery; both groups were composed of 5 men and 31 women (n=36). Age was 38.7 ± 9.4 and 39.6 ± 9.2 years old and body mass index (BMI) was 22.2 0 ± 2.1 and 47.6 ± 9.1 kg/m(2), respectively. The variance measure quoted was SEM.. The body weight at 12 months was 35.8 ± 1.0% (P<0.001) lower than that of the basal period. At the basal period BG showed higher levels of NOx (P=0.007) and TBARS (P<0.001) and lower levels of vitamins C and E (P<0.001) compared with CG. After 3 months the activity of MPO was decreased (P<0.001). Six months after surgery GSH levels were decreased (P=0.037), whereas CAT activity was increased (P=0.029). After 12 months levels of NOx (P=0.004), TBARS (P<0.001), beta-carotene (P<0.001) and vitamin E (P<0.001) were decreased, whereas those of vitamin C (P<0.001) were increased compared with controls.. RYGB followed by a daily vitamin supplement apparently attenuated pro-inflammatory and oxidative stress markers 1 year after surgery, but additional antioxidant supplementation appears necessary.

Topics: Adult; Antioxidants; Ascorbic Acid; beta Carotene; Biomarkers; Body Mass Index; Case-Control Studies; Catalase; Diet; Dietary Supplements; Energy Intake; Female; Follow-Up Studies; Gastric Bypass; Glutathione; Humans; Inflammation; Male; Middle Aged; Oxidative Stress; Peroxidase; Prospective Studies; Thiobarbituric Acid Reactive Substances; Vitamin E; Weight Loss

Recent findings have implicated the gut microbiota as a contributor of metabolic diseases through the modulation of host metabolism and inflammation. Atherosclerosis is associated with lipid accumulation and inflammation in the arterial wall, and bacteria have been suggested as a causative agent of this disease. Here we use shotgun sequencing of the gut metagenome to demonstrate that the genus Collinsella was enriched in patients with symptomatic atherosclerosis, defined as stenotic atherosclerotic plaques in the carotid artery leading to cerebrovascular events, whereas Roseburia and Eubacterium were enriched in healthy controls. Further characterization of the functional capacity of the metagenomes revealed that patient gut metagenomes were enriched in genes encoding peptidoglycan synthesis and depleted in phytoene dehydrogenase; patients also had reduced serum levels of β-carotene. Our findings suggest that the gut metagenome is associated with the inflammatory status of the host and patients with symptomatic atherosclerosis harbor characteristic changes in the gut metagenome.

Topics: Actinobacteria; Aged; Atherosclerosis; beta Carotene; Case-Control Studies; Eubacterium; Female; Gastrointestinal Tract; Humans; Inflammation; Male; Metagenome; Oxidoreductases; Peptidoglycan

This study was conducted to evaluate blood concentrations of inflammatory cytokines and oxidative stress-related biomarkers as risk factors of breast cancer and to determine the relation between these markers and antioxidant nutrient intake.. Study subjects were 134 patients with breast cancer and 149 controls. Total antioxidant capacity and concentrations of 8-isoprostane, 8-hydroxy-2'-deoxyguanosine, interleukin (IL)-1β, IL-6, and IL-8 of blood samples were determined. A food-frequency questionnaire was used to assess nutrient intake.. Patients with breast cancer had significantly higher blood levels of oxidative stress markers compared with control subjects. Plasma concentrations of IL-1β and IL-6 were significantly higher in patients with breast cancer compared with those of control subjects. In the pooled analysis, total antioxidant capacity was significantly decreased with increasing quartiles of carbohydrate intake but was increased with increasing quartiles of total vitamin A intake and vitamin C intake. In addition, 8-hydroxy-2'-deoxyguanosine concentration was decreased with increasing quartiles of vitamin A and β-carotene. No significant association was found between nutrient intake and cytokine concentrations.. These results suggest that oxidative stress and inflammation may be associated with the risk of breast cancer. Total vitamin A intake was negatively related to oxidative stresses, possibly modifying the risk of breast cancer.

Topics: 8-Hydroxy-2'-Deoxyguanosine; Adult; Antioxidants; Ascorbic Acid; beta Carotene; Biomarkers; Breast Neoplasms; Case-Control Studies; Deoxyguanosine; Diet; Diet Surveys; Dietary Carbohydrates; Female; Humans; Inflammation; Inflammation Mediators; Interleukin-1beta; Interleukin-6; Middle Aged; Oxidative Stress; Risk Factors; Surveys and Questionnaires; Vitamin A; Vitamins

The association between aluminum (Al), essential trace metals, oxidative stress, and inflammation status was evaluated in hemodialysis patients.. Biochemical parameters in blood were determined in long-term hemodialysis patients (n=69) and age- and sex-matched healthy individuals (n=30).. Compared with healthy subjects, patients had significantly higher concentrations of plasma Al. Elevated Al was negatively associated with the essential metals zinc, selenium, and iron. Al concentrations were strongly and positively correlated with contents of the oxidation products malondialdehyde and protein carbonyl. Inverse relationships were observed between Al concentrations and reduced concentrations of glutathione, β-carotene, vitamin C, and vitamin E. Patients were also observed to have significantly increased production values of plasma high-sensitivity C-reactive protein, tumor necrosis factor-α, and interleukin-5.. An increased plasma Al concentration is associated with disturbed concentrations of essential metals, increased oxidative stress, and increased inflammation status in hemodialysis patients.

Topics: Aluminum; Antioxidants; Ascorbic Acid; beta Carotene; C-Reactive Protein; Case-Control Studies; Female; Glutathione; Humans; Inflammation; Interleukin-5; Iron; Male; Malondialdehyde; Middle Aged; Oxidative Stress; Renal Dialysis; Risk Factors; Selenium; Trace Elements; Tumor Necrosis Factor-alpha; Vitamin E; Zinc

Reactive oxygen species (ROS) including hydrogen peroxide (H(2)O(2)) are involved in the pathogenesis of gastric inflammation. Interleukin-8 (IL-8) is a potent mediator of the inflammatory response by activating and recruiting neutrophils to the site of infection. Oxidant-sensitive transcription factor NF-κB regulates the expression of IL-8 in the immune and inflammatory events. Carotenoids (carotenes and oxygenated carotenoids) show antioxidant and anti-inflammatory activities. Low intake of β-carotene leads to high risk of gastric cancer. Oxygenated carotenoid lutein inhibited NF-κB activation in experimental uveitis. The present study aims to investigate whether β-carotene and lutein inhibit H(2)O(2)-induced activation of NF-κB and expression of IL-8 in gastric epithelial AGS cells. The cells were treated with carotenoids 2 h prior to the treatment of H(2)O(2). mRNA expression was analyzed by reverse transcription-polymerase chain reaction (RT-PCR) and real time RT-PCR analyses. IL-8 level in the medium was determined by enzyme-linked immunosorbent assay. NF-κB activation was assessed by electrophoretic mobility shift assay. ROS levels of the cells were detected by confocal microscopic analysis for fluorescent dichlorofluorescein. As a result, H(2)O(2 )induced the activation of NF-κB and expression of IL-8 in AGS cells time-dependently. β-Carotene and lutein showed inhibitory effects on H(2)O(2)-induced increase in intracellular ROS levels, activation of NF-κB, and IL-8 expression in AGS cells. In conclusion, supplementation of carotenoids such as β-carotene and lutein may be beneficial for the treatment of oxidative stress-mediated gastric inflammation.

Topics: Anti-Inflammatory Agents; Antioxidants; beta Carotene; Cell Line, Tumor; Epithelial Cells; Gastric Mucosa; Humans; Hydrogen Peroxide; Inflammation; Inflammation Mediators; Interleukin-8; Lutein; NF-kappa B; Reactive Oxygen Species; RNA, Messenger; Stomach

Emerging evidence suggests a role of lycopene in the primary prevention of cardiovascular disease. This study aimed to investigate the association of serum lycopene concentration with brachial-ankle pulse wave velocity (baPWV), a marker of arterial stiffness and markers of oxidative stress and inflammation.. healthy women (n=264, 31-75 yrs) were classified into tertiles according to serum lycopene concentration. Multivariate linear regression analyses were used to assess the relationship between serum lycopene and baPWV.. Subjects in middle tertile (T2) and upper tertile (T3) had lower baPWV (1263+/-23 and 1265+/-14 cm/s vs. 1338+/-21 cm/s; p=0.009) and lower oxidized LDL (oxLDL) (53+/-3 and 55+/-3 U/L vs. 66+/-3 U/L; p<0.001) than those in lower tertile (T1). Subjects in T3 showed higher LDL particle size (24.3+/-0.08 nm vs. 24.0+/-0.07 nm, p=0.005) and lower C-reactive protein (hs-CRP) (0.80+/-0.25mg/dL vs. 1.27+/-0.24 mg/dL, p=0.015), compared with those in T1. Logistic regression analysis showed that baPWV decreased with the increment of lycopene concentration; log baPWV decreased by 0.21 cm/s (95% CI -0.168;-0.045, p=0.001) per unit change in lycopene. After adjustment for age, BMI, smoking, drinking, menopause and blood pressure, the estimated effect was attenuated by 35%, but remained statistically significant [-0.13 cm/s (95% CI -0.112;-0.018, p=0.006)]. Further adjustment for beta-carotene, alpha-tocopherol, oxLDL, LDL particle size, and hs-CRP increased the strength of the association [beta=-0.221 (95% CI -0.215;-0.012, p=0.029)].. This study supports the presence of an independent inverse relationship between circulating lycopene and baPWV. Additionally, reduced oxidative modification of LDL may be one of mediators on the mechanisms how lycopene reduces arterial stiffness.

Topics: Adult; Aged; alpha-Tocopherol; Arteries; beta Carotene; Cardiovascular Diseases; Carotenoids; Female; Humans; Inflammation; Lipoproteins, LDL; Lycopene; Middle Aged; Oxidative Stress; Oxygen; Regression Analysis

beta-Carotene (BC) intake has been shown to enhance lung cancer risk in smokers and asbestos-exposed subjects (according to the ATBC and CARET studies), but the mechanism behind this procarcinogenic effect of BC is unclear. Both smoking and asbestos exposure induce an influx of inflammatory neutrophils into the airways, which results in an increased production of reactive oxygen species and formation of promutagenic DNA lesions. Therefore, the aim of our study was to investigate the effects of BC and its metabolites (BCM) on neutrophil-induced genotoxicity. We observed that the BCM vitamin A (Vit A) and retinoic acid (RA) inhibited the H(2)O(2)-utilizing enzyme myeloperoxidase (MPO), which is released by neutrophils, thereby reducing H(2)O(2) conversion. Moreover, BC and BCM were able to increase (.)OH formation from H(2)O(2) in the Fenton reaction (determined by electron spin resonance spectroscopy). Addition of Vit A and RA to lung epithelial cells that were co-incubated with activated neutrophils resulted in a significant increase in the level of oxidized purines assessed by the formamidopyrimidine DNA glycosylase-modified comet assay. These data indicate that BCM can enhance neutrophil-induced genotoxicity by inhibition of MPO in combination with subsequent increased formation of hydroxyl radicals.

Topics: beta Carotene; Cell Line, Tumor; Cell Movement; DNA Damage; Electron Spin Resonance Spectroscopy; Epithelial Cells; Humans; Hydrogen Peroxide; Inflammation; Inflammation Mediators; Lung; Mutagenicity Tests; Neutrophil Activation; Neutrophils; Oxidation-Reduction; Oxidative Stress; Peroxidase; Purines; Tretinoin; Vitamin A

Fruit and vegetable consumption has been associated with a reduced risk of several diseases including CVD. A part of these effects seen could be linked to anti-inflammatory and antioxidative effects, although this has not been thoroughly investigated. The present study was designed to investigate the effects of the dietary intake of beta-carotene, alpha-tocopherol and ascorbic acid on in vivo biomarkers of inflammation (PGF2alpha, high-sensitive C-reactive protein (hsCRP) and IL-6 formation) and oxidative stress (F2-isoprostane formation), the two important factors associated with accelerated atherosclerosis. The dietary intake of 704 participants in the Uppsala Longitudinal Study of Adult Men (ULSAM) at age 70 years was registered and inflammatory and oxidative stress biomarkers were quantified 7 years later. The registered dietary intakes of ascorbic acid and alpha-tocopherol were negatively associated linearly and in quartiles with both PGF2alpha, hsCRP, IL-6 and F2-isoprostanes, where ascorbic acid intake generally was more strongly associated. Dietary intake of beta-carotene was only significantly negatively associated with F2-isoprostanes. In conclusion, the present study is the first to suggest that the intake of food rich in antioxidants is associated with reduced cyclo-oxygenase- and cytokine-mediated inflammation and oxidative stress at 7 years of follow-up. These associations could be linked to the beneficial effects of fruit and vegetables observed on CVD.

Topics: Aged; alpha-Tocopherol; Ascorbic Acid; beta Carotene; Biomarkers; C-Reactive Protein; Creatinine; Diet; Dinoprost; Humans; Inflammation; Interleukin-6; Linear Models; Longitudinal Studies; Male; Oxidative Stress; Vitamins

Acute ischemic stroke is a clinical condition accompanied by inflammation and oxidative stress. In this study, we compared levels of plasma lipophilic antioxidants and inflammation markers between patients with stroke and healthy controls and assessed the associations of antioxidants, inflammation markers, and neurologic deficits among patients with stroke.. We measured plasma levels of lipophilic antioxidant vitamins (retinol, lycopene, alpha-carotene, beta-carotene, alpha-tocopherol, and gamma-tocopherol), inflammation markers (high-sensitivity C-reactive protein [hs-CRP], fibrinogen, erythrocyte sedimentation rate, and white blood cell count), and neurologic deficits (indicated by the score of the National Institute of Health Stroke Scale) in 68 patients with acute ischemic stroke within 48 h after stroke onset in comparison with 41 normal controls.. Plasma alpha- and beta-carotene concentrations were lower and levels of inflammation markers were higher among patients with acute ischemic stroke compared with normal controls. Levels of alpha- and beta-carotene in patients with stroke were negatively associated with hs-CRP level (R = -0.29 and -0.41, respectively, P < 0.01) and with neurologic deficits (R = -0.28 and -0.27, respectively, P < 0.05). The negative association between neurologic deficits and combined plasma levels of alpha- and beta-carotene remained after adjustment for age and sex (P = 0.04). However, the magnitude of association decreased after adjustment of hs-CRP (P = 0.08).. Plasma concentrations of alpha- and beta-carotene are lower in patients with acute ischemic stroke than in healthy controls and are negatively correlated with hs-CRP level and neurologic deficits. The negative association between neurologic deficits and combined plasma alpha- and beta-carotene levels is confounded by hs-CRP.

Topics: Acute Disease; Aged; Antioxidants; beta Carotene; Biomarkers; Brain Ischemia; C-Reactive Protein; Carotenoids; Case-Control Studies; Disease Progression; Female; Humans; Inflammation; Lipid Peroxidation; Male; Middle Aged; Nutritional Status; Oxidative Stress; Severity of Illness Index; Vitamin A; Vitamins

It remains unclear to what extent the associations between low serum beta-carotene concentration and increased risk for cardiovascular disease and cancers are attributable to inflammation. The objective of this study was to evaluate simultaneously the effects of serum beta-carotene concentration and inflammation on the subsequent all-cause mortality risk in high-functioning older persons.. The authors conducted a prospective cohort study using information from 672 participants from the MacArthur Studies of Successful Aging. Baseline information was obtained for serum concentrations of beta-carotene, C-reactive protein, interleukin-6, cholesterols, and albumin; body mass index; waist:hip ratio; prevalent medical conditions; health behaviors; and medications. Sex-specific univariate and multivariate logistic regression analyses were used to study the effects of low beta-carotene, high inflammation burden, or both on 7-year all-cause mortality rates while adjusting for other confounders.. The serum beta-carotene concentration was inversely associated with C-reactive protein and interleukin-6 levels. After adjustment for inflammation markers and other covariates, the relative risks for low beta-carotene for the 7-year all-cause mortality risk were 2.30 (95% confidence interval [CI], 1.23 to 4.31) in men and 0.85 (95% CI, 0.42 to 1.75) in women. Compared with men with high beta-carotene levels and low inflammation, the multiply adjusted relative risk for low beta-carotene and high inflammation burden was 3.78 (95% CI, 1.69 to 8.47) in men.. Low levels of serum beta-carotene are independently associated with an increased all-cause mortality risk in older men, even after adjustment for the effects of inflammation and other risk factors. In men, but not women, a synergistic effect occurs between low beta-carotene concentration and high inflammation burden in predicting higher mortality rates.

Topics: Aged; beta Carotene; C-Reactive Protein; Female; Humans; Inflammation; Interleukin-6; Male; Mortality; Prospective Studies

The exact pathogenesis of liver injury and fibrosis in chronic hepatitis C (CHC) is unclear. Free radicals play a role in CHC liver damage. Antioxidants (AO) (enzymatic and nonenzymatic) scavenge free radicals and prevent tissue injury. The aims of our study were to estimate serum levels of malondialdehyde (MDA), serum and liver levels of nonenzymatic fat-soluble AO, and to correlate the liver AO levels with the degree of inflammation and fibrosis on biopsy.. AO levels were estimated by high-pressure liquid chromatography in the pretreatment serum and liver biopsy specimen of 20 treatment-naïve patients with CHC who were not on vitamin supplements. Serum levels of MDA were measured as a marker of increased oxidative stress. Twenty-two healthy individuals with no history of vitamin supplementation served as controls. AO analyzed were: retinol, alpha- and gamma-tocopherol, lutein, beta-cryptoxanthin, lycopene, and alpha- and beta-carotene.. Twenty CHC patients (11 men, nine women, mean age 48.5 +/- 7.9 yr) were studied. Patients and controls were comparable in age and sex. Serum MDA levels were significantly higher in CHC patients compared with controls (1.62 +/- 0.57 vs 0.23 +/- 0.15 micromol/L, p = < 0.0000). Serum levels of all AO except lutein were significantly decreased in CHC patients, and their levels were two to ten times lower than serum levels in controls. Liver levels of alpha-carotene (p = 0.0004), beta-carotene (p = 0.006), and lutein (p = 0.002) correlated with the serum levels, whereas the levels of retinol, alpha-tocopherol, lycopene, and beta-cryptoxanthin showed no correlation. Serum MDA levels were significantly higher in patients with moderate-to-severe inflammation or fibrosis compared with those with mild inflammation or fibrosis. The levels of all liver AO except alpha-carotene were significantly lower in patients with moderate-to-severe fibrosis. The severity of inflammation (portal or lobular) did not affect liver AO levels.. Our findings suggest that increased oxidative stress is present in patients with CHC. Micronutrient AO are severely depleted in serum and liver tissue of patients with CHC, and liver levels of some AO appear to reflect serum levels. Increasing fibrosis is associated with decreased liver AO levels indicating that severe disease may be a consequence of AO depletion or decreased liver storage resulting from fibrosis.

Topics: Adult; Antioxidants; beta Carotene; Carotenoids; Cryptoxanthins; Female; Fibrosis; Hepatitis C, Chronic; Humans; Inflammation; Liver; Lutein; Lycopene; Male; Malondialdehyde; Micronutrients; Middle Aged; Oxidative Stress; Tocopherols; Vitamin A; Xanthophylls

The aim of this study was to examine the influence of lycopene and beta-carotene on the inflammatory status in a rat model of induced-colitis. Using the 2,4,6-trinitrobenzenesulfonic acid (TNBS) model, colitis was induced in thirty-two male Wistar rats divided into four groups. Each group received a different diet regime in parallel with the induction of colitis and was sacrificed after seven days. The groups were divided as follows: Group A: without colitis and fed a normal chow diet; Group B: induced with colitis and fed a diet supplemented with lycopene (300 micrograms/rat/day); Group C: induced with colitis and fed a diet supplemented with beta-carotene (300 micrograms/rat/day); Group D: induced with colitis and fed a normal chow diet. Colonic inflammation following TNBS induction was characterized by hemorrhagic necrosis and fibrosis of the mucosa, increased colonic wall thickness, infiltration of inflammatory cells, and increased myeloperoxidase (MPO) activity. Supplementation of lycopene in the diet had a beneficial effect on the various macroscopic parameters examined including: colonic thickness, colon weight, and total area of inflammation. Furthermore, the level of myeloperoxidase (MPO) was significantly lower in the lycopene-treated group compared to the control group. In terms of microscopic changes, a more attenuated inflammatory reaction was observed in the group fed a diet supplemented with lycopene. No significant effect was noted in the beta-carotene-supplemented group. Therefore, we propose that the dietary supplementation of lycopene may be an effective approach for reducing the level of oxidative stress and improving the inflammatory status of colitis.

Topics: Analysis of Variance; Animals; Antioxidants; beta Carotene; Carotenoids; Colitis; Colon; Inflammation; Lycopene; Male; Peroxidase; Rats; Rats, Wistar; Trinitrobenzenesulfonic Acid

One explanation for discrepant results between epidemiologic studies and randomized trials of beta-carotene and cardiovascular disease may be a failure to consider inflammation as a confounder. To evaluate the potential for such confounding, the authors relate the serum concentrations of five carotenoids (alpha-carotene, beta-carotene, beta-cryptoxanthin, lycopene, and lutein/zeaxanthin) to levels of three inflammatory markers (C-reactive protein, fibrinogen, and white blood cell count) measured during the Third National Health and Nutrition Survey, 1988-1994. The analysis included 4,557 nonsmoking participants aged 25-55 years. Adjusted concentrations of all five carotenoids were significantly lower in those with C-reactive protein levels above 0.88 mg/dl (p = 0.001). There was a trend toward lower adjusted beta-cryptoxanthin concentrations with increasing level of fibrinogen (p value test for trend = 0.01), but other carotenoids were not related. Many of the carotenoid concentrations were lower among participants with high white blood cell counts. After log transformation, only adjusted mean beta-carotene levels were significantly lower in those with white blood cell counts above 7.85 x 10(9)/liter (p < 0.01). These cross-sectional data do not clarify the biologic relation between carotenoids and C-reactive protein but, to the extent that the carotenoids are associated with C-reactive protein levels, a carotenoid-heart disease association may be, in part, an inflammation-heart disease association.

Topics: Acute-Phase Proteins; Adult; beta Carotene; Biomarkers; C-Reactive Protein; Cardiovascular Diseases; Carotenoids; Cross-Sectional Studies; Effect Modifier, Epidemiologic; Female; Fibrinogen; Humans; Inflammation; Leukocyte Count; Male; Risk

Vitamin C status and possible associations with the disease process in cystic fibrosis (CF) patients were investigated. Plasma vitamin C concentrations in patients from two different mid-European populations (Swiss, n = 62; Austrian, n = 60) taking no or low-dose vitamin C from multivitamin supplements did not differ from each other or from control subjects (n = 34). Vitamin C concentrations decreased with age (5.05 mumol.L-1, y-1). When followed up for 12 mo, patients had the highest plasma vitamin C concentrations in February and the lowest in May and August (P < 0.01); the decrease in vitamin C was accompanied by increases in plasma malondialdehyde (P < 0.001) and tumor necrosis factor alpha concentrations (P < 0.01). During supplementation with vitamin E for 2 mo or beta-carotene for 12 mo vitamin C concentrations did not change. They correlated inversely with white blood cell count (r = -0.36, P = 0.008), bands (r = -0.36, P = 0.02), alpha 1-acid glycoprotein (r = -0.45, P = 0.002), interleukin 6 (r = -0.46, P = 0.0006), and neutrophil elastase/alpha 1-proteinase inhibitor complexes (r = -0.34, P = 0.02). In patients with vitamin C concentrations < 40 mumol/L, all indexes of inflammation were relatively high, whereas those with concentrations > 80 mumol/L (upper quartile of control subjects) showed clearly lower values. These results are consistent with the hypothesis that by scavenging oxygen free radicals vitamin C interacts with an inflammation-amplifying cycle of activation of alveolar macrophages and neutrophils, release of proinflammatory cytokines and oxygen free radicals, and inactivation of antiproteases.

Topics: Adolescent; Adult; Ascorbic Acid; beta Carotene; Child; Child, Preschool; Cohort Studies; Cystic Fibrosis; Cytokines; Dose-Response Relationship, Drug; Female; Humans; Infant; Inflammation; Interleukin-6; Leukocyte Elastase; Lipid Peroxidation; Lung Diseases; Male; Malondialdehyde; Nutritional Status; Orosomucoid; Seasons; Tumor Necrosis Factor-alpha; Vitamin E