ascorbic-acid and Brain-Diseases

Bacterial bloodstream infection causes septic syndromes that range from systemic inflammatory response syndrome (SIRS) and encephalopathy to severe sepsis and septic shock. Microvascular dysfunction, comprising impaired capillary blood flow and arteriolar responsiveness, precedes multiple organ failure. Vitamin C (ascorbate) levels are low in critically ill patients. The impact of ascorbate administered orally is moderate because of its limited bioavailability. However, intravenous injection of ascorbate raises plasma and tissue concentrations of the vitamin and may decrease morbidity. In animal models of polymicrobial sepsis, intravenous ascorbate injection restores microvascular function and increases survival. The protection of capillary blood flow and arteriolar responsiveness by ascorbate may be mediated by inhibition of oxidative stress, modulation of intracellular signaling pathways, and maintenance of homeostatic levels of nitric oxide. Ascorbate scavenges reactive oxygen species (ROS) and also inhibits the NADPH oxidase that synthesizes superoxide in microvascular endothelial cells. The resulting changes in redox-sensitive signaling pathways may diminish endothelial expression of inducible nitric oxide synthase (iNOS), tissue factor and adhesion molecules. Ascorbate also regulates nitric oxide concentration by releasing nitric oxide from adducts and by acting through tetrahydrobiopterin (BH4) to stimulate endothelial nitric oxide synthase (eNOS). Therefore, it may be possible to improve microvascular function in sepsis by using intravenous vitamin C as an adjunct therapy.

Topics: Animals; Ascorbic Acid; Ascorbic Acid Deficiency; Brain Diseases; Humans; Hypotension; Regional Blood Flow; Sepsis

Topics: Adrenal Cortex Hormones; Adrenocorticotropic Hormone; Ascorbic Acid; Brain Diseases; Collagen Diseases; Cortisone; Glucocorticoids; Humans; Peptic Ulcer; Rheumatic Fever; Water-Electrolyte Balance

We aimed to evaluate the protective effects of Yuk-Mi-Jihwang-Tang (YJT) against acute restraint stress-induced brain oxidative damage. A water extract of YJT was prepared and subjected to high performance liquid chromatography - diode array detector-mass spectrometry (HPLC-DAD-MS). Thirty-six heads of C57BL/6J male mice (7 weeks) were divided into six groups (n = 6/group). The mice were orally administrated YJT (0, 50, 100, or 200 mg/kg) or vitamin C (100 mg/kg) for 5 consecutive days before 6 h of acute restraint stress. In the brain tissue, lipidperoxidation, antioxidant components, and pro-inflammatory cytokines were measured, and the serum corticosterone level was determined. Acute restraint stress-induced notably increased lipid peroxidation in brain tissues, and pretreatment with YJT showed a significant decreased the lipid peroxidation levels (p< 0.05). The levels of antioxidant components including total glutathione contents, activities of SOD and catalase were remarkably depleted by acute restraint stress, whereas these alterations were significantly restored by treatment with YJT (p< 0.05 or p< 0.01). The restraint stress markedly increased pro-inflammatory cytokines, such as TNF-α and IL-6 in the gene expression and protein levels (p< 0.05 or p< 0.01). Pretreatment with YJT significantly attenuated serum corticosterone (200 mg/kg, p < 0.05). YJT drastically attenuated the levels of 4- HNE, HO-1, Nox 2 and iNOSwhich were elevated during acute restraint stress, whereas the Nrf2 level was increased in brain tissue protein levels. Our data suggest that YJT protects the brain tissue against oxidative damage and regulates stress hormones.

Topics: Animals; Antioxidants; Ascorbic Acid; Biomarkers; Brain; Brain Diseases; Cytokines; Disease Models, Animal; Dose-Response Relationship, Drug; Drugs, Chinese Herbal; Enzymes; Gene Expression Regulation, Enzymologic; Hydrocortisone; Immobilization; Inflammation Mediators; Lipid Peroxidation; Male; Mice, Inbred C57BL; Nerve Degeneration; Neuroprotective Agents; Oxidative Stress; Stress, Psychological

To determine the effects of vitamins and carotenoids on brain white matter lesions (WMLs), we examined the associations between WMLs with vitamin and carotenoid levels in Japanese middle-aged and elderly subjects.. Four-hundred and sixty-nine healthy participants (male = 317; female = 152) that underwent medical examinations were examined. Deep white matter lesions (DWLs) were detected via magnetic resonance imaging (MRI) in 39 subjects. We evaluated the effects of vitamin and carotenoid levels on DWLs via logistic regression analysis.. Lower gamma-tocopherol levels were significantly associated with DWLs in all subjects. While lower gamma-tocopherol and vitamin C levels were significantly associated with DWLs in males, lower delta-tocopherol levels were associated with DWLs in females. The associations between DWLs and lower gamma- and delta-tocopherol and vitamin C levels were independent of age, hypertension, or smoking. However, the associations between DWLs and lower alfa-tocopherol were not significant following adjustments for smoking.. Lower carotenoid and vitamin levels were independently associated with cerebral DWLs in Japanese subjects.

Topics: Aged; Antioxidants; Ascorbic Acid; Ascorbic Acid Deficiency; Brain; Brain Diseases; Carotenoids; Deficiency Diseases; Female; Geriatric Assessment; Humans; Japan; Male; Middle Aged; Nutrition Assessment; Nutritional Status; Sex Factors; Tocopherols; Vitamin E Deficiency; Vitamins

Transient compression of rat somatosensory cortex has been reported to affect cerebral microvasculature and sensory function simultaneously. However, the effects of long-term cortical compression remain unknown. Here, we investigated whether and to what extent sustained but moderate epidural compression of rat somatosensory cortex impairs somatic sensation and/or cortical microvasculature. Electrophysiological and behavioral tests revealed that sustained compression caused only short-term sensory deficit, particularly at 1 day after injury. Although the diameter of cortical microvessels was coincidentally reduced, no ischemic insult was observed. By measuring Evans Blue and immunoglobulin G extravasation, the blood-brain barrier (BBB) permeability was found to dramatically increase during 1 to 3 days, but this did not lead to brain edema. Furthermore, immunoblotting showed that the BBB component proteins occludin, claudin-5, type IV collagen, and glial fibrillary acidic protein were markedly upregulated in the injured cortex during 1 to 2 weeks when BBB regained integrity. Conversely, treatment of ascorbic acid prevented compression-induced BBB disruption and sensory impairment. Together, these data suggest that sustained compression of the somatosensory cortex compromises BBB integrity and somatic sensation only in the early period. Ascorbic acid may be used therapeutically to modulate cortical compression and/or BBB dysfunction.

Topics: Animals; Antioxidants; Ascorbic Acid; Blood-Brain Barrier; Brain Diseases; Claudin-5; Collagen Type IV; Glial Fibrillary Acidic Protein; Male; Membrane Proteins; Nerve Tissue Proteins; Occludin; Rats; Rats, Sprague-Dawley; Sensation Disorders; Somatosensory Cortex; Up-Regulation

The protective effect of diphenyl diselenide, (PhSe)(2), on oxidative stress induced by cigarette smoke exposure in brains of rat pups was evaluated. Animals were exposed to passive cigarette smoke (15 min/day) in two different experimental protocols: P1 (1, 2, and 3 cigarettes) and P2 (4, 5, and 6 cigarettes) for 3 weeks. Before each period of smoke exposure, animals received an oral administration of (PhSe)(2) (0.5 mg/kg). A number of toxicological parameters in the brain were examined, such as lipid peroxidation, delta-aminolevulinate dehydratase (delta-ALA-D) activity, and components of enzymatic (superoxide dismutase and catalase activities) and non-enzymatic antioxidant defenses (ascorbic acid and non-protein thiol levels). In P1, smoke exposure induced an inhibition of catalase activity and an increase of ascorbic acid levels. (PhSe)(2) treatment was able to protect catalase activity but not ascorbic acid levels. In P2, an augmentation of lipid peroxidation, a reduction of enzymatic and non-enzymatic antioxidant status, and an inhibition of delta-ALA-D activity caused by smoke exposure were found. (PhSe)(2) protected the brains of rat pups against oxidative damage induced by smoke exposure. The results are consistent with the antioxidant effect of (PhSe)(2) demonstrated by the reduction of oxidative changes caused by smoke exposure in the brains of pups.

Topics: Animals; Antioxidants; Ascorbic Acid; Benzene Derivatives; Body Weight; Brain; Brain Diseases; Catalase; Lipid Peroxidation; Magnetic Resonance Spectroscopy; Organoselenium Compounds; Oxidative Stress; Porphobilinogen Synthase; Rats; Rats, Wistar; Sulfhydryl Compounds; Superoxide Dismutase; Tobacco Smoke Pollution; Weight Gain

The oxidative stress-induced changes and feasibility of prevention of these changes with an aid of vitamines E and C were investigated in cultured brain cortex of the newborn albino rats. Modeling the oxidative stress was achieved with addition of H(2)O(2) into the nutrient medium. In order to prevent an oxidative stress-induced cytotoxic effect, concomittantly with H(2)O(2), vitamines E and C were added into the nutrient medium. The data, obtained in our study revealed inhibition of the glial cells'- and axonal migration into the growth zone resulting from the oxidative stress. These changes were attenuated following action of vitamines E and C, which points at feasibility of their use against oxidative impact from the free radicals emerging during neurodegenerative disorders.

Topics: Animals; Ascorbic Acid; Brain; Brain Diseases; Drugs, Chinese Herbal; Glucosides; Iridoid Glucosides; Iridoids; Oxidative Stress; Rats; Vitamin E

Bisphenol A (BPA), nonylphenol (NP) and octylphenol (OP) are endocrine-disrupting chemicals that has been shown to exert both toxic and estrogenic effects on mammalian cells. The aim of this study was to investigate if BPA, NP and OP induce oxidative stress on the brain tissue of male rats and if co-administration of vitamin C, an antioxidant, can prevent any possible oxidative stress. The male rats were divided into seven groups as control (vehicle), BPA, NP, OP, BPA+C, NP+C, OP+C. BPA, OP and NP (25 mg/(kg day)) were administrated orally to male Wistar rats for 45 days. In vitamin C co-administration groups (BPA+C, NP+C, OP+C), vitamin C (60 mg/(kg day)) were administrated orally along with BPA, OP and NP (25 mg/(kg day)) treatments. The rats in the control group received olive oil orally. The final body and absolute organ weights of treated rats did not show any significant difference when compared with the control group. Also, there were no significant difference in relative organ weights of BPA, NP, OP, BPA+C and NP+C groups when compared with control group. Only, relative organ weights were increased significantly in OP+C group compared with control group. Decreased levels of reduced glutathione (GSH) were found in the brains of BPA, NP, OP treated rats. The end product of lipid peroxidation, malondialdehyde (MDA), appeared at significantly higher concentrations in the BPA, NP, and OP treated groups when compared to the control group. On the other hand, there were no changes in the brain MDA and GSH levels of BPA+C, NP+C and OP+C groups compared with BPA, NP and OP treatment groups, respectively. In histopathologic examination, the vitamin C co-administrated groups had much more hyperchromatic cells in the brain cortex than that observed in the groups treated with only BPA, NP, and OP. The results of this study demonstrate that BPA, NP and OP generate reactive oxygen species that caused oxidative damage in the brain of male rats. In addition, vitamin C co-administration along with BPA, NP, and OP aggravates this oxidative damage in the brain of rats.

Topics: Administration, Oral; Animals; Antioxidants; Ascorbic Acid; Benzhydryl Compounds; Body Weight; Brain; Brain Diseases; Drug Antagonism; Estrogens, Non-Steroidal; Glutathione; Lipid Peroxidation; Male; Malondialdehyde; Organ Size; Oxidative Stress; Phenols; Rats; Rats, Wistar; Reactive Oxygen Species

This study was designed to examine if diphenyl diselenide (PhSe)(2), an organoselenium compound, attenuates pulmonar and cerebral oxidative stress caused by sub-chronic exposure to CdCl(2). Male adult Swiss albino mice received CdCl(2) (10 micromol/kg, subcutaneously), 5 times/week, for 4 weeks. (PhSe)(2) (10 micromol/kg or 20 micromol/kg, orally) was given concomitantly with CdCl(2) to mice. A number of toxicological parameters in lung and brain of mice were examined including delta-aminolevulinic acid dehydratase (delta-ALA-D), superoxide dismutase (SOD) and catalase activities, lipid peroxidation, non-protein thiols (NPSH) and ascorbic acid content. Na(+),K(+)-ATPase activity, acetylcholinesterase (AChE) activity, [(3)H]glutamate uptake and [(3)H]glutamate release were also carried out in brain. Cadmium concentration and histopathological analysis were carried out in lung tissue. (PhSe)(2) at the dose of 20 micromol/kg protected the inhibition of delta-ALA-D, SOD and CAT activities, the reduction of vitamin C content and the increase of lipid peroxidation levels caused by CdCl(2) in lungs. At 10 micromol/kg, (PhSe)(2) protected cerebral AChE and CAT activities inhibited by CdCl(2). There were no histopathological alterations in the lung of mice after CdCl(2) exposure. The pulmonary cadmium concentration was higher (2.8-fold) in the group exposed to CdCl(2) than in control mice. (PhSe)(2) at dose of 20 micromol/kg reduced cadmium concentration towards the control level. The results suggest that oral administration of (PhSe)(2) attenuated the oxidative damage induced by CdCl(2) in lung and brain of mice.

Topics: Acetylcholinesterase; Animals; Antioxidants; Ascorbic Acid; Benzene Derivatives; Brain; Brain Diseases; Cadmium Chloride; Catalase; Disease Models, Animal; Dose-Response Relationship, Drug; Glutamic Acid; Lipid Peroxidation; Lung; Lung Diseases; Male; Mice; Organoselenium Compounds; Oxidative Stress; Porphobilinogen Synthase; Sodium-Potassium-Exchanging ATPase; Sulfhydryl Compounds; Superoxide Dismutase

Septic encephalopathies rapidly affect brain function without the involvement of a specific area causing a broad range of reversible neurologic symptoms. Capillary leakage including dysfunction of the blood-brain barrier has been proposed as a potential pathogenic mechanism in this entity. We tested the hypothesis that oxidative stress measured in plasma and cerebrospinal fluid (CSF) of patients suffering from septic encephalopathy could be linked to the neurologic symptoms of the disease. The neurologic symptoms of eleven patients with septic encephalopathy were described semiquantitatively through a score system. The ascorbate levels were significantly lower in both plasma and CSF from patients with septic encephalopathy than controls, and in CSF but not plasma this decrease correlated with the severity of neurologic symptoms. No significant changes were found for alpha-tocopherol. Our findings suggest that the short-term oxidative stress may be an important factor in the development of septic encephalopathy, possibly through dysregulation of the blood-brain barrier.

Topics: alpha-Tocopherol; Antioxidants; Ascorbic Acid; Brain Diseases; Case-Control Studies; Female; Humans; Lipids; Male; Middle Aged; Oxidation-Reduction; Oxidative Stress; Sepsis

A method is presented for evaluating the concentration of ascorbic acid in 10 microliters samples of cerebrospinal fluid (CSF) with just ultraviolet (UV) scanning in the 220-300 nm range. The method assumes that the two main UV absorbing CSF components are proteins (with a peak at 280 nm) and ascorbic acid (with a peak at 264 nm). On this basis, the absorbances at those wavelengths are the starting points for a calculation that evaluates the sheer contribution of ascorbic acid to the absorbance at 264 nm. The rapidity of the UV analysis (just a few min), together with the precaution of keeping the samples under argon, along the short preparatory procedure, is especially suitable in the analysis of an air labile substance, such as ascorbic acid. The results of the UV procedure have been checked with parallel HPLC determinations for 19 test CSF samples and the results have shown an excellent correspondence. Finally, data are presented about the evaluation of ascorbic acid concentrations in CSF samples from various neurological pathologies in comparison with normal cases. These data show the interesting result of a significant reduction in the average ascorbic acid CSF level in patients suffering from Alzheimer's disease. However, a decrease in that parameter is found also for a few other pathologies.

Topics: Ascorbic Acid; Brain; Brain Diseases; Chromatography, High Pressure Liquid; Culture Techniques; Humans; Models, Biological; Spectrophotometry, Ultraviolet

The protective effect of selenium on the neurotoxicity of vanadium in different brain regions of rats was investigated. The lipid peroxidation was significantly accentuated after intraperitoneal (i.p.) administration of vanadium (1.5 mg kg-1 b.wt) for a period of 12 consecutive days to rats. The increase in lipid peroxidation was inhibited by selenium treatment (0.02 mg kg-1 b.wt., i.p.) for 12 consecutive days. Vanadium exposure produced a decrease in nonprotein sulfhydryl group. Selenium treatment prevented the depression in nonprotein sulfhydryl group in all the brain regions of the vanadium exposed rats. The concentration of ascorbic acid was decreased after co-administration of selenium and vanadium. These results suggest that selenium protects neuronal cells against neurotoxic effects of vanadium by maintaining the availability of antioxidant nonprotein sulfhydryl groups. The decrease in ascorbic acid levels may have been due to its consumption in forming complexes with vanadium.

Topics: Animals; Ascorbic Acid; Body Weight; Brain; Brain Diseases; Drug Interactions; Lipid Peroxidation; Male; Rats; Rats, Sprague-Dawley; Selenium; Vanadium

In this study, the protective effect of melatonin against kainate (KA)-induced neurotoxicity was evaluated in vitro and in vivo. In rat brain synaptosomes, KA-induced oxidative stress was measured as shown by significant increases in both the basal generation of reactive oxygen species (ROS), assessed by a fluorescent method, and lipid peroxidation, evaluated as malondialdehyde (MDA) levels. Melatonin decreased, in a concentration-dependent manner, KA-induced lipid peroxidation. The intrinsic fluorescence of melatonin molecule hindered the evaluation of its protective effect against KA-induced ROS generation. However, melatonin was able to reduce FeSO4/ascorbate-induced ROS generation. The melatonin protective effect was confirmed by in vivo experiments: 73% of rats injected with KA (10 mg/kg i.p.) died within 5 days; melatonin administration i.p. significantly reduced mortality of the animals. The present results suggest that melatonin might be considered a pharmacological agent for the treatment of neurodegenerative pathologies.

Topics: Animals; Ascorbic Acid; Brain; Brain Diseases; Dose-Response Relationship, Drug; Ferric Compounds; Kainic Acid; Lipid Peroxidation; Male; Melatonin; Oxidative Stress; Rats; Rats, Wistar; Reactive Oxygen Species; Synaptosomes

Topics: Antioxidants; Ascorbic Acid; Brain Diseases; Cardiovascular Diseases; Cells; Free Radical Scavengers; Free Radicals; Humans; Ischemia; Phagocytes; Reactive Oxygen Species; Reperfusion Injury; Respiratory Tract Diseases; Superoxide Dismutase

Preliminary data of a postmortem brain study in a single case with Rett syndrome compared to a single control case showed a severe reduction of ascorbic acid and reduced glutathione in most brain regions studied. These findings suggest a secondary disturbance of ascorbic acid and glutathione metabolism in the Rett syndrome.

Topics: Ascorbic Acid; Brain Chemistry; Brain Diseases; Child; Female; Glutathione; Humans; Intellectual Disability; Syndrome

The uptake of 99mTc-pertechnetate (TcO4), 99mTc-iron-ascorbic acid (Feasc), 99mTc-Solcocitran (Solcocitran), 99mTc-diphosphonate (HEDP) and 67Ga-citrate (Ga) in various brain lesions was compared. Influence of time from injection was also studied on the first three compounds. A rank correlation method was used to compare the scans which were judged visually by three independent observers. There was good agreement between the observers, as measured by Kendall's tau, but the concordance between rankings within the same type of lesion, as measured by Kendall's W, was rather poor. There was no significant difference in the uptake of TcO4, Feasc and Solcocitran. Ga showed generally poor uptake and its uptake in tumours and infarcts did not differ significantly. However, when HEDP and TcO4 were compared in two groups (I: Infarcts, haemorrhages and bone invading meningiomas, and II: Tumours not invaded into bone) a highly significant difference was obtained with much higher uptake of HEDP in Group I.

Topics: Adult; Ascorbic Acid; Brain Diseases; Brain Neoplasms; Cerebral Hemorrhage; Cerebral Infarction; Citrates; Diphosphonates; Gallium Radioisotopes; Humans; Organotechnetium Compounds; Radionuclide Imaging; Sodium Pertechnetate Tc 99m; Technetium; Technetium Compounds

Topics: Age Factors; Ascorbic Acid; Brain Diseases; Dietary Carbohydrates; Food Hypersensitivity; Pellagra; Vitamin B 12; Vitamin B Complex

Topics: Adult; Ascorbic Acid; Brain; Brain Diseases; Cerebrovascular Circulation; Dermatologic Agents; Electroencephalography; Humans; Hypothalamus; Plethysmography, Impedance; Tannins

Topics: Ascorbic Acid; Brain Diseases; Cerebral Ventricles; Chemical Phenomena; Chemistry; Drug Stability; Humans; Injections, Spinal; Iron; Radionuclide Imaging; Serum Albumin; Sulfites; Technetium

Topics: Animals; Ascorbic Acid; Blood Pressure; Brain Diseases; Brain Edema; Dehydration; Glycerol; Hematuria; Injections, Intravenous; Intracranial Pressure; Male; Rabbits

Topics: Ascorbic Acid; Brain Diseases; Humans; Iron; Kidney Diseases; Radionuclide Imaging; Technetium

Topics: Adolescent; Ascorbic Acid; Brain Diseases; Electroencephalography; Emaciation; Female; Humans; Psychotic Disorders; Puberty; Pyridoxine; Riboflavin; Thiamine; Vitamin B 12

Topics: 17-Hydroxycorticosteroids; Adolescent; Adrenal Cortex Hormones; Adrenal Gland Diseases; Adrenocorticotropic Hormone; Adult; Aged; Ascorbic Acid; Brain Diseases; Brain Neoplasms; Female; Humans; Hypertension; In Vitro Techniques; Male; Middle Aged; Pituitary Diseases; Thyroid Diseases; Urine

Topics: Animals; Ascorbic Acid; Brain; Brain Diseases; Chickens; Diet; Encephalomalacia; Fatty Acids; Inositol; Nutrition Assessment; Peroxides; Proteins; Vitamin E Deficiency

Topics: Ascorbic Acid; Brain; Brain Diseases; Carbohydrate Metabolism; Cerebrospinal Fluid; Ear Diseases; Humans; Vitamins