ascorbic-acid and Aortic-Diseases

Cardiovascular disease (CVD) is the leading cause of mortality, and vascular calcification has been highly correlated with CVD events. Abdominal aortic calcification (AAC) has been shown to predict subclinical CVD and incident CVD events. However, the relationship between vitamin C and abdominal aortic calcification remains unclear.. To investigate the relationship of dietary vitamin C with AAC among the adult population in the US.. The National Health and Nutrition Examination Survey (NHANES) 2013-2014 provided the data for the cross-sectional study. 2297 subjects (1089 males) were included in the study. Two scoring systems, AAC 24-point scale (Kauppila) and AAC 8-point scale (Schousboe), were used for the measurement of AAC score. Dietary vitamin C intake was calculated as the average of two rounds of 24-h interview recall data and classified in tertiles for analysis. We applied weighted multiple regression analyses to assess the relationship of dietary vitamin C with AAC score and the risk of having AAC. To ensure the robustness of the findings, subgroup and sensitivity analyses were performed. Additionally, smooth curve fittings, using generalized additive models (GAM) were employed to visualize potential nonlinear relationships. Furthermore, an exploratory analysis on the relationship of vitamin C supplements with AAC was also conducted.. The results showed that higher dietary vitamin C intake was related to a reduction in AAC score (AAC-24: β = -0.338, 95% confidence interval [CI] -0.565, -0.111, P = 0.004; AAC-8: β = -0.132, 95%CI -0.217, -0.047, P = 0.002), and lower risk of AAC (odds ratio [OR] = 0.807, 95%CI 0.659, 0.989, P = 0.038). However, the relationship of vitamin C supplements with AAC was not identified.. The study revealed that higher intake of dietary vitamin C rather than vitamin C supplements was related to reduced AAC score and lower risk of AAC, indicating that diets rich in vitamin C are recommended due to its potential benefits for protecting against vascular calcification and CVD among the adult population in the US.

Topics: Adult; Aorta, Abdominal; Aortic Diseases; Ascorbic Acid; Cardiovascular Diseases; Cross-Sectional Studies; Diet; Humans; Male; Nutrition Surveys; Risk Factors; Vascular Calcification; Vitamins

To assess the role of combined deficiencies of vitamins C and E on the earliest stages of atherosclerosis (an inflammatory condition associated with oxidative stress), 4 combinations of vitamin supplementation (low C/low E, low C/high E, high C/low E, and high C/high E) were studied in atherosclerosis-prone apolipoprotein E-deficient mice also unable to synthesize their own vitamin C (gulonolactone oxidase(-/-)); and to evaluate the effect of a more severe depletion of vitamin C alone in a second experiment using gulonolactone oxidase(-/-) mice carrying the hemizygous deletion of SVCT2 (the vitamin C transporter).. After 8 weeks of a high-fat diet (16% lard and 0.2% cholesterol), atherosclerosis developed in the aortic sinus areas of mice in all diet groups. Each vitamin-deficient diet significantly decreased liver and brain contents of the corresponding vitamin. Combined deficiency of both vitamins increased lipid peroxidation, doubled plaque size, and increased plaque macrophage content by 2- to 3-fold in male mice, although only plaque macrophage content was increased in female mice. A more severe deficiency of vitamin C in gulonolactone oxidase(-/-) mice with defective cellular uptake of vitamin C increased both oxidative stress and atherosclerosis in apolipoprotein E(-/-) mice compared with littermates receiving a diet replete in vitamin C, again most clearly in males.. Combined deficiencies of vitamins E and C are required to worsen early atherosclerosis in an apolipoprotein E-deficient mouse model. However, a more severe cellular deficiency of vitamin C alone promotes atherosclerosis when vitamin E is replete.

Topics: Animals; Aortic Diseases; Apolipoproteins E; Ascorbic Acid; Ascorbic Acid Deficiency; Atherosclerosis; Brain; Dietary Supplements; Disease Models, Animal; Disease Progression; Female; L-Gulonolactone Oxidase; Lipid Peroxidation; Liver; Macrophages; Male; Mice; Mice, Inbred C57BL; Mice, Knockout; Myocardium; Organic Anion Transporters, Sodium-Dependent; Oxidative Stress; Severity of Illness Index; Sex Factors; Sodium-Coupled Vitamin C Transporters; Symporters; Time Factors; Vitamin E; Vitamin E Deficiency; Vitamins

Periodontitis has been causally linked to cardiovascular disease, which is mediated through the oxidative stress induced by periodontitis. Since vitamin C has been suggested to limit oxidative damage, we hypothesized that vitamin C intake may reduce endothelial oxidative stress induced by periodontitis in the aorta. The aim of this study was to investigate the effects of vitamin C intake on the initiation of atherosclerosis in a ligature-induced rat periodontitis model.. Eighteen 8-week-old-male Wistar rats were divided into three groups of six rats and all rats received daily fresh water and powdered food through out the 6-week study. In the vitamin C and periodontitis groups, periodontitis was ligature-induced for the first 4 weeks. In the vitamin C group, rats were given distilled water containing 1 g/L vitamin C for the 2 weeks after removing the ligature.. In the periodontitis group, there was lipid deposition in the descending aorta and significant increases of serum level of hexanoyl-lysine (HEL), and aortic levels of nitrotyrosine expression, HEL expression and 8-hydroxydeoxyguanosine (8-OHdG) compared to the control group. Vitamin C intake significantly increased plasma vitamin C level and GSH:GSSG ratio (178% and 123%, respectively), and decreased level of serum HEL and aortic levels of nitrotyrosine, HEL and 8-OHdG (23%, 87%, 84%, and 38%, respectively).. These results suggest that vitamin C intake attenuates the degree of experimental atherosclerosis induced by periodontitis in the rat by decreasing oxidative stress.

Topics: 8-Hydroxy-2'-Deoxyguanosine; Animals; Antioxidants; Aorta, Thoracic; Aortic Diseases; Ascorbic Acid; Atherosclerosis; Deoxyguanosine; Endothelium, Vascular; Glutathione; Lysine; Male; Oxidative Stress; Periodontitis; Random Allocation; Rats; Rats, Wistar; Tyrosine; Vitamins

It has been suggested that iron plays an important role in the pathogenesis of atherosclerosis, primarily by acting as a catalyst for the atherogenic modification of LDL. Although some epidemiological data suggest that high stored iron levels are an independent risk factor for coronary artery disease and that iron has been detected in both early and advanced atherosclerotic lesions, the evidence is often contradictory and inconclusive. We used the New Zealand White rabbit to investigate the effects of iron overload (FeO) and iron deficiency (FeD) on atherosclerosis. Groups of 7 rabbits were either iron loaded by injections of iron dextran (FeO group), iron depleted by phlebotomy (FeD group), or given injections of saline (control group) for a total of 9 weeks. All rabbits were fed a chow diet containing 1% (wt/wt) cholesterol for the last 6 weeks of the study. Iron and antioxidant status and cholesterol levels were assayed in plasma before cholesterol feeding (week 3) and at the time that the rabbits were killed (week 9). In addition, the susceptibility of LDL to oxidation was measured and pathological examination of the aortic arch and thoracic aorta performed at the end of the study. FeD significantly decreased the levels of blood hemoglobin, serum iron, and transferrin saturation compared with controls. Conversely, FeO significantly increased transferrin Fe saturation. FeO but not FeD decreased plasma cholesterol levels compared with control animals both before (P < .05) and after (P = .055) cholesterol feeding. Neither FeO nor FeD had a significant effect on the levels of antioxidants and lipid peroxidation products in plasma and aortic tissue or on the susceptibility of LDL to ex-vivo oxidation. FeO significantly decreased aortic arch lesion formation by 56% compared with controls (P < .05), whereas FeD had no significant effect. These results indicate that in this animal model, FeO decreases rather than increases atherosclerosis, likely because iron dextran exerts a hypocholesterolemic effect. Our data do not support the hypotheses that elevation of Fe stores increases or that a reduction of Fe stores by phlebotomy decreases the risk of coronary artery disease.

Topics: Animals; Antioxidants; Aorta; Aortic Diseases; Arteriosclerosis; Ascorbic Acid; Diet, Atherogenic; Hypercholesterolemia; Iron; Iron Deficiencies; Iron Overload; Lipid Peroxidation; Lipids; Lipoproteins, LDL; Male; Phlebotomy; Prostaglandins F; Rabbits; Risk Factors; Vitamin E

Rabbits were randomly assigned to two groups. Age and body weight distribution were equal in both groups. All animals were placed on a high cholesterol diet for 9 wk, then returned to a normal diet for 1 wk. At the end of this dietary regimen, one group of animals received subcutaneous injections of psysiological saline 3 times/day, 5 days/wk for 10 wk, and the other group recieved L-ascorbate 2-sulfate (0.37 mmole) according to the same timetable. On alternate weeks, the serum levels of total and free cholesterol were determined. After 10 wk of treatment the animals were killed; the plaques were excised from the aortas and examined for total mass and cholesterol content. We observed that, under these dietary conditions, L-ascorbate 2-sulfate does not mobilize cholesterol or its esters from preformed aortic plaque. However, we did observe that animals showing high cholesterol levels in their sera died prematurely when injected with L-ascorbate 2-sulfate. Gross and histopathological investigations of organs and tissues did not reveal any significant differences among the animals that died prematurely and those that survived to the termination of the experiment.

Topics: Animals; Aortic Diseases; Arteriosclerosis; Ascorbic Acid; Cholesterol; Diet, Atherogenic; Drug Evaluation, Preclinical; Injections, Subcutaneous; Male; Rabbits; Saline Solution, Hypertonic

Effects of intravenously injected L-ascorbic acid or L=ascorbic acid 2-sulfate on aortic intimal thickening were examined histologically, qualitatively, and quantitatively in the upper, middle and lower thoracic aortic positions of cholesterol-induced atherosclerotic rabbits. A means of evaluating the degree of pathology of the aortic positions was developed employing five descriptive statistics of intimal thickening. Both L-ascorbic acid and L-ascorbic acid 2-sulfate inhibited intimal thickening. The most significant reductions were observed in the upper thoracic aorta.

Topics: Adrenal Glands; Animals; Aorta, Thoracic; Aortic Diseases; Arteriosclerosis; Ascorbic Acid; Cholesterol; Injections, Intravenous; Liver; Male; Rabbits; Spleen; Sulfates

Topics: Animals; Aorta; Aortic Diseases; Arteriosclerosis; Ascorbic Acid; Collagen; Epinephrine; Hydroxyproline; Iron; Ketoglutaric Acids; Kinetics; Liver; Male; Mixed Function Oxygenases; Organ Specificity; Proline; Rabbits; Rats; Species Specificity; Stimulation, Chemical; Thyroxine; Tritium; Water

Topics: Aging; Aortic Diseases; Arteriosclerosis; Ascorbic Acid; Atherosclerosis; Calcium; Hexosamines; Histocytochemistry; Hydroxyproline; Lipidoses; Lipids; Pathology; Research