Effect of vitamin E on monosodium glutamate induced hepatotoxicity and oxidative stress in rats

Monosodium glutamate (MSG), administered to rats (by gavage) at a dose of 0.6 mg/g body weight for 10 days, significantly (P<0.05) induced lipid peroxidation (LPO), decreased reduced glutathione (GSH) level and increased the activities of glutathione-s-transferase (GST), catalase and superoxide dismutase (SOD) in the liver of the animals; these were observed 24 hr after 10 days of administration. The activities of alanine aminotransferase (ALT), aspartate aminotransferase (AST) and gamma glutamyl transferase (GGT) were also significantly increased in the serum, on MSG administration. Vitamin E (0.2 mg/g body wt) co-administered with MSG, significantly reduced the LPO, increased the GSH level and decreased the hepatic activities of GST, catalase and SOD. The activities of ALT, AST and GGT in the serum were also significantly reduced. The results showed that MSG at a dose of 0.6 mg/g body wt induced the oxidative stress and hepatotoxicity in rats and vitamin E ameliorated MSG-induced oxidative stress and hepatotoxicity.     

Effect of oral vitamin E supplementation on oxidative stress in guinea-pigs with short-term hypothermia

Effects of oral vitamin E supplementation on blood malondialdehyde (MDA), glutathione (GSH) and vitamin E levels and superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) enzyme activities in acute hypothermia of guinea-pigs were investigated. Thirty male guinea pigs, weighing 500-800 g were randomly divided into one of three experimental groups: A (control, without cooling), B (hypothermic) and C (hypothermic with vitamin E supplementation). The guinea-pigs of group C received daily oral supplementation of 460 mg kg(-1) bw vitamin E for 4 days before inducing hypothermia. Twenty-four hours after the last vitamin E supplementation, the guinea-pigs of the B and C groups were cooled by immersion into cold water (10-12 degrees C), and the control guinea-pigs were immersed into water of body temperature (37 degrees C) up to the neck for 5 min without using any anaesthetic or tranquilizer. Rectal body temperatures of groups were measured and blood samples for biochemical analysis were collected immediately after the cooling. The body temperature, GSH and vitamin E levels and GSH-Px enzyme activity of hypothermic guinea-pigs were lower (p < 0.05), but SOD enzyme activity was not different (p > 0.05) from those of control animals. Although, the body temperature of hypothermic with vitamin E supplementation group was lower (p < 0.05), all other parameters of this group were not different (p > 0.05) from the controls. It was concluded that oral supplementation of vitamin E can alleviate the lipid peroxidation-induced disturbances associated with hypothermia by increasing the serum vitamin E level to normal. However, more studies are needed to prove whether this vitamin can improve quality of life during the cold seasons.     

Vitamin E supplementation in the mitigation of carbon tetrachloride induced oxidative stress in rats

Oxidative stress is implicated in the pathophysiology of a number of chronic diseases including atherosclerosis, diabetes, cataracts and accelerated aging. The aim of this study was to elucidate the protective role of vitamin E supplementation when oxidative stress is induced by CCl4 administration, using the rat as a model. Rats were fed diets for four weeks either with or without dl-alpha-tocopherol acetate supplementation. Half of the rats (n = 9) from each of the diet groups were then challenged with CCl4 at the completion of the four week diet period. Plasma levels of 8-iso-PGF(2alpha), antioxidant micronutrients and antioxidant enzyme activities were measured to examine changes in oxidative stress subsequent to the supplementation of dl-alpha-tocopherol in the diet. Plasma alpha-tocopherol (vitamin E) concentrations were higher for the groups supplemented with dl-alpha-tocopherol acetate, however the supplemented diet group that was subsequently challenged with CCl4 had significantly lower (p <0.001) plasma alpha-tocopherol concentration than the dl-alpha-tocopherol acetate diet group that was not challenged with CCl4. Total plasma 8-iso-PGF(2alpha) concentration was elevated in diet groups challenged with CCl4, however, the concentration was significantly lower (p <0.001) when the diet was supplemented with dl-alpha-tocopherol acetate. The antioxidant enzymes were not influenced by either dietary alpha-tocopherol manipulation or by the inducement of oxidative stress with CCl4. Plasma concentrations of trans-retinol (vitamin A) were reduced by CCl4 administration in both the dl-alpha-tocopherol acetate supplemented and unsupplemented diet groups. The results of this study indicate that dl-alpha-tocopherol acetate supplementation was protective of lipid peroxidation when oxidative stress is induced by a pro-oxidant challenge such as CCl4.     

Comparison of vitamin E, L-carnitine and melatonin in ameliorating carbon tetrachloride and diabetes induced hepatic oxidative stress

This study aimed to investigate whether treatments with vitamin E, L-carnitine and melatonin can protect against CCl₄ and diabetes-induced hepatic oxidative stress. Hepatic oxidative stress was performed in rats through 50% v/v carbon tetrachloride (CCl₄) (1 ml/kg/3days, i.p.), and through diabetes mellitus induced by streptozotocin (STZ) (40 mg/kg, i.p.). Vitamin E (100 mg/kg/day, i.p), L-carnitine (300 mg/kg/day, i.p.) and melatonin (10 mg/kg/day, i.p.) were injected for a period of 6 weeks. Thereafter, changes in serum glucose level, liver function tests, hepatic malondialdehyde (MDA) content, hepatic reduced glutathione (GSH) content, hepatic superoxide dismutase (SOD) activity, and serum total antioxidant capacity (TAC) level were evaluated. In CCl₄-induced liver fibrosis, the efficacy order was melatonin > L-carnitine > vitamin E, while in STZ-induced diabetes, the efficacy order was vitamin E ≥ melatonin > L-carnitine. In conclusion, these data indicate that low dose of melatonin is more effective than high doses of vitamin E and L-carnitine in reducing hepatic oxidative stress induced by CCl₄ and diabetes. Moreover, the potent effect of vitamin E in ameliorating diabetes can be linked not only to the antioxidant actions, but also to the superior effect in reducing diabetes-induced hyperglycaemia. Meanwhile, potency of L-carnitine was nearly the same in CCl₄ and diabetes-induced liver damage.     

Adaptations to oxidative stress induced by vitamin E deficiency in rat liver

Vitamin E deficiency in rats led to a sequence of antioxidant defense adaptations in the liver. After three weeks, α-tocopherol concentration was 5% of control, but ascorbate and ubiquinol concentrations were 2- to 3-fold greater than control. During the early phase of adaptation no differences in markers of lipid peroxidation were observed, but the activities of both cytochrome b5 reductase and glucose-6-phosphate dehydrogenase were significantly greater in deficient livers. By nine weeks, accumulation of lipid peroxidation end products began to occur along with declining concentrations of ascorbate, and higher NQO1 activities. At twelve weeks, rat growth ceased, and both lipid peroxidation products and cytosolic calcium-independent phospholipase A2 reached maximum concentrations. Thus, in growing rats the changes progressed from increases in both ubiquinol and quinone reductases through accumulation of lipid peroxidation products and loss of endogenous antioxidants to finally induction of lipid metabolizing enzymes and cessation of rat growth.     

Protection against ischemia-reperfusion induced oxidative stress by vitamin E treatment.

The rat heart protection offered by vitamin E against oxidative stress after ischaemia-reperfusion was studied by using a new methodological approach. Functional recovery of hearts from ischaemia-reperfusion was correlated with a traditional index of oxidative stress such as lipid peroxidation and with antioxidant capacity and susceptibility to oxidants of the tissue evaluated by enhanced chemiluminescence techniques. Rats were treated with ten daily i.m. injections of 100 mg/kg body weight of vitamin E. The functional recovery during reperfusion (20 min, following 45 min ischaemia) of Langendorff preparations from control (vehicle-injected) and vitamin E treated rats was evaluated in terms of heart rate, left ventricular developed pressure (LVDP), double product (= heart rate. LVDP) and coronary flow recovery. Vitamin E treatment significantly improved functional recovery of heart rate, LVDP, double product and coronary flow. It also increased the level of vitamin E and reduced the levels of both malondialdehyde and hydroperoxides in the heart tissue at the end of the ischaemia-reperfusion protocol. In contrast, it did not affect the antioxidant capacity and the response of heart homogenates to in vitro oxidative stress measured after ischaemia-reperfusion. These results show a protective action of vitamin E treatment against lipid peroxidation and cardiac dysfunction associated with ischaemia-reperfusion. Although the precise mechanism of this protection is not evident, our model in part suggests a role of vitamin E other than as a free radical scavenger.     

Fish oil and vitamin E supplementation in oxidative stress at rest and after physical exercise

Sen, Chandan K., Mustafa Atalay, Jyrki Ågren,David E. Laaksonen, Sashwati Roy, and Osmo Hänninen. Fishoil and vitamin E supplementation in oxidative stress at rest and afterphysical exercise. J. Appl. Physiol.83(1): 189-195, 1997.Fish oil supplementation and physicalexercise may induce oxidative stress. We tested the effects of 8 wk of-tocopherol (vitamin E) and fish oil (FO) supplementation on resting and exercise-induced oxidative stress. Rats(n = 80) were divided into groupssupplemented with FO, FO and vitamin E (FOVE), soy oil (SO), and SO andvitamin E (SOVE), and for FOVE and SOVE they were dividedinto corresponding exercise groups (FOVE-Ex and SOVE-Ex). Lipidperoxidation [thiobarbituric acid-reacting substances(TBARS)] was 33% higher in FO compared with SO in the liver, butoxidative protein damage (carbonyl levels) remained similar in bothliver and red gastrocnemius muscle (RG). Vitamin E supplementation,compared with FO and SO, markedly decreased liver and RG TBARS, butliver TBARS remained 32% higher in FOVE vs. SOVE. Vitamin E alsomarkedly decreased liver and RG protein carbonyl levels, althoughlevels in FOVE and SOVE were similar. Exercise increased liver and RGTBARS and RG protein carbonyl levels markedly, with similar levels inFOVE-Ex and SOVE-Ex. FO increased lipid peroxidation but not proteinoxidation in a tissue-specific manner. Vitamin E markedly decreasedlipid peroxidation and protein oxidation in both FOVE and SOVE,although liver lipid peroxidation remained higher in FOVE. Despitehigher levels of hepatic lipid peroxidation at rest in FOVE comparedwith SOVE, liver appeared to be relatively less susceptible toexercise-induced oxidative stress in FOVE.

     

Oxidative stress and serum paraoxonase activity in experimental hypothyroidism: effect of vitamin E supplementation

Thyroid hormones are associated with the oxidative and antioxidative status of the organism. Since data on the oxidative status of hypothyroidism are limited and controversial, we investigated the oxidant and antioxidant status and serum paraoxonase/arylesterase activities in propylthiouracil-induced hypothyroidism and examined the effect of vitamin E supplementation on this experimental model. Forty male Sprague Dawley rats were randomly divided into four groups (group 1, control; group 2, control + vitamin E; group 3, propylthiouracil; group 4, propylthiouracil + vitamin E). Plasma, red blood cell, liver, heart and skeletal muscle malondialdehyde levels were increased in the propylthiouracil-treated group compared with the control rats and were decreased in propylthiouracil + vitamin E group compared with the propylthiouracil-treated group. Vitamin E supplementation also significantly increased liver and kidney reduced glutathione levels in propylthiouracil treated animals. Serum paraoxonase and arylesterase activities were decreased in propylthiouracil treated group and vitamin E supplementation caused significant increase in serum paraoxonase activity compared with the propylthiouracil-treated rats. These findings suggest that hypothyroidism is accompanied with increased oxidative stress and vitamin E supplementation exerts beneficial effects on this situation.     

Protective effect of vitamin E, beta-carotene and N-acetylcysteine from the brain oxidative stress induced in rats by lipopolysaccharide

The major goal of this study was to examine the ability of several antioxidants namely, vitamin E, beta-carotene and N-acetylcysteine, to protect the brain from oxidative stress induced by lipopolysaccharide (LPS, endotoxin). LPS, a component of the bacterial wall of gram-negative bacteria, has been recognized as one of the most potent bacterial products in the induction of host inflammatory responses and tissue injury and was used in this study to mimic infections. LPS injection resulted in a significant increase in the stress indices, plasma corticosterone and glucose concentration, a significant alteration of the brain oxidative status observed as elevation of the level of malondialdehyde (MDA, index of lipid peroxidation) and reduction of reduced glutathione (GSH), and a disturbance in the brain energy metabolism presented as a reduction in the ATP/ADP ratio and an increase in the mitochondrial/cytosolic hexokinase ratio. However, the activities of brain superoxide dismutase and Na+, K+-ATPase and contents of cholesterol and phospholipids were not altered. Administration of the aforementioned antioxidants prior to LPS injection ameliorated the oxidative stress by reducing levels of MDA, restoring GSH content and normalizing the mitochondrial/cytosolic hexokinase ratio in the brain in addition to lowering levels of plasma corticosterone and glucose. In conclusion, this study showed the increased free radical generation during infections and LPS-induced stress. It also suggests that brain oxidative status and energy is disturbed.     

The effect of taurine supplementation on oxidative stress in experimental hypothyroidism

The purpose of this study was to investigate the oxidative status in experimental hypothyroidism and the antioxidant effect of taurine supplementation. Forty male Sprague Dawley rats were randomly divided into four groups (group 1, control; group 2, control + taurine; group 3, propylthiouracil (PTU); group 4, PTU + taurine). Hypothyroidism was induced by giving 0.05% PTU in drinking water for 8 weeks. Taurine was supplemented in drinking water at a concentration of 1% for 5 weeks. Plasma (p < 0.05), red blood cell (p < 0.01), liver (p < 0.001) and kidney tissue (p > 0.05) malondialdehyde levels were increased in the PTU group compared with those of the control rats and were decreased in the PTU + taurine group compared with the PTU alone group. No significant changes were observed in glutathione levels of kidney and liver in the PTU group, but taurine supplementation significantly increased the glutathione levels of these tissues. Paraoxonase and arylesterase activities were decreased in the PTU group while taurine supplementation caused no significant changes in paraoxonase and arylesterase activities. These findings suggest that taurine supplementation may play a protective role against the increased oxidative stress resulting from hypothyroidism.     

Protective effect of vitamin E in dimethoate and malathion induced oxidative stress in rat erythrocytes

Organophosphate (OP) pesticides such as dimethoate and malathion intoxication has been shown to produce oxidative stress due to the generation of free radicals and alter the antioxidant defense system in erythrocytes. It is possible that vitamin E being present at the cell membrane site may prevent OP-induced oxidative damage. In the present study, rats were pretreated orally with vitamin E (250 mg/kg body wt, twice a week for 6 weeks) prior to oral administration of a single low dose of dimethoate and/or malathion (0.01% LD(50)). The result showed that treatment with OP increased lipid peroxidation (LPO) in erythrocytes, however, vitamin E pretreated rats administered OP's showed decreased LPO in erythrocytes. The increase in the activities of superoxide dismutase (SOD) and catalase (CAT) and total-SH content in erythrocytes from dimethoate and/or malathion treated rats as compared to control appears to be a response towards increased oxidative stress. Vitamin E pretreated animals administered OP's showed a lowering in these parameters as compared to OP treated rats which indicates that vitamin E provide protection against OP-induced oxidative stress. The glutathione-S-transferase (GST) activity in erythrocytes was inhibited in OP intoxicated rats which partially recovered in vitamin E pretreated animals administered OP's. Inhibition in erythrocyte and serum acetylcholinesterase (AChE) activity was not relieved in vitamin E pretreated rats administered OP's probably due to the competitive nature of enzyme inhibition by OP's. The results show that vitamin E may amelierate OP-induced oxidative stress by decreasing LPO and altering antioxidant defense system in erthrocytes.     

Effect of methanol-induced oxidative stress on the neuroimmune system of experimental rats

It is well known that the nervous system has increased susceptibility to methanol intoxication. The present study reveals the effect of methanol intoxication on antioxidant status, lipid peroxidation and DNA integrity in hypothalamic-pituitary-adrenal (HPA) axis organs and spleen. Non-specific and specific immune functions were analyzed. In addition, open field behavior, plasma corticosterone level and blood methanol level were estimated. Male Wistar albino rats were intoxicated with methanol (2.37 g/kg b.wt., i.p.) for 1 day, 15 and 30 days. Administration of methanol showed significant increase in enzymatic (superoxide dismutase, catalase, glutathione peroxidase), non-enzymatic (reduced glutathione and Vitamin C) antioxidants and lipid peroxidation (LPO) in hypothalamus and adrenal gland of day 1 group. However, decrease in enzymatic and non-enzymatic antioxidants with concomitant increase in LPO level were observed in 15 and 30 days groups. Plasma corticosterone level was significantly increased in day 1 and 15 days groups whereas, 30 days methanol intoxication group showed considerable decrease in corticosterone level compared with control animals. Cell-mediated immune response of footpad thickness was significantly decreased with an increased leukocyte migration inhibition. Humoral immune response of antibody titers was elevated in methanol-intoxicated groups. Neutrophil functions, adherence and phagocytic index (PI) were found to be significantly decreases. Furthermore, significant increase in the avidity index and nitro blue tetrozolium reduction was observed in the methanol exposed animals. Day 1 methanol exposed group showed increased PI compared to the control ones. Methanol exposure for 30 days showed an increased DNA fragmentation in the hypothalamus, adrenal glands, and spleen. In conclusion, exposure to methanol-induced oxidative stress disturbs the HPA-axis function altering the level of corticosterone, which lead to varied non-specific and specific immune response in experimental rats.     

Protective effects of selenium, vitamin C and vitamin E against oxidative stress of cigarette smoke in rats

Cataractous lenses have been found to have an altered distribution of the intracellular ionic environment: the concentrations of potassium and magnesium being decreased and the concentrations of sodium and calcium increased. These changes arise as a result of changes to lens membrane characteristics causing an increase in lens membrane permeability. In this study flame atomic absorption spectroscopy (AAS) was used for calcium, magnesium, iron and zinc determination, and flame atomic emission spectroscopy (AES) was used for sodium and potassium contents in normal and cigarette smoke-exposed rat lenses. The methods are sensitive enough to detect quantitatively all six cations in a single rat lenses. In this work, six elements, including Ca2+, K+, Na+, Zn2+, Fe2+ and Mg2+ in experimental rat eye lenses and normal transparent lenses were determined. It was found that the concentrations of Ca2+, Na+, Zn2+, and Fe2+ were increased dramatically while K+ and Mg2+ decreased in smoke-exposed rat lenses when compared to the control rat lenses. There were no significant changes between 'smoked' rats supplied with vitamin C and control groups. A positive correlation was found also in the other two groups of 'cigarette smoked' animals supplemented with selenium plus vitamin E and selenium when compared with 'cigarette smoked' without any supplements. These data provide support for the hypothesis that cigarette smoking increases the risk of cataract formation. We investigated whether vitamin C is the most important antioxidant in the body. The roles of diet with optimum amounts of antioxidant vitamins C and vitamin E and the antioxidant mineral selenium are discussed.     

Effect of vitamin E and menadione supplementation on riboflavin production and stress parameters in Ashbya gossypii

Ashbya gossypii is a filamentous fungus which overproduces riboflavin as a pseudo-secondary metabolite. Vitamin E supplemented at 1, 2.5 and 5 μM levels in the growth medium of A. gossypii increased the extracellular secretion of riboflavin and at 50, 100 and 240 μM levels reduced the biomass and riboflavin yield. With 2.5 μM vitamin E total riboflavin production and extracellular riboflavin secretion on day 2 was higher than non-supplemented control. By day 3 the production in supplemented was nearly the same as in non-supplemented, but the intracellular riboflavin levels were lower and extracellular levels higher. Supplemented cells showed increased levels of catalase, glutathione peroxidase, lipid peroxides and membrane lipid peroxides, and decreased glutathione indicating that vitamin E, a well-known antioxidant, had acted as a pro-oxidant at low levels of 2.5 μM and had increased the oxidative stress. Menadione, a well known oxidant also increased riboflavin production and secretion at 1.0, 2.5 and 5.0 μM level. This is the first report were vitamin E and menadione effects support the concept that overproduction of riboflavin is a stress induced phenomenon. These findings are not only of scientific interest but also useful for improving the industrial production of riboflavin.     

Effect of aminoguanidine on oxidative modification of proteins in experimental diabetes mellitus in rats

It was shown that administration of aminoguanidine is accompanied by a decrease of the content of nitric oxide stable metabolites, as well as protein carbonyl groups in leukocytes and blood plasma in diabetic and control animals. Aminoguanidine is proposed to be used for pharmacological correction of NO biosynthesis. Aminoguanidine, being the selective iNOS inhibitor, antioxidant and the factor eliminating post-translational protein nitrozylation and oxidative modification, weaken the toxic effects of NO and positively modulates the pathological state caused by NO hyperproduction.     

The effects of vitamin C supplementation on oxidative stress and antioxidant content in the brains of chronically exercised rats

The purpose of this study was to ascertain whether vitamin C supplementation during chronic exercise training alters rat brain antioxidant content. Female Wistar albino rats were exercised on a treadmill for 30 min/day for 6.5 weeks and were administered daily intraperitoneal injections of vitamin C (20 mg/kg). After the training period, chronically exercised rats showed no significant changes in total brain thiobarbituric acid reactive substances (TBARS) levels. In contrast, rats supplemented with vitamin C during the training period showed significantly elevated brain TBARS levels. If such results were extrapolated to man, where vitamin supplementation is a common practice, this would indicate that vitamin C supplementation may not protect brain tissue against exercise-induced oxidative damage, in such circumstances, this water-soluble antioxidant behaves as a pro-oxidant. (Mol Cell Biochem xxx: 135–138, 2005)     

Simvastatin and vitamin E effects on cardiac and hepatic oxidative stress in rats fed on high fat diet

High fat diet (HFD) is a common cause of metabolic syndrome and type 2 diabetes mellitus. Published data showed that HFD and subsequent dyslipidemia are major triggers for oxidative stress. Forty-eight male Sprague–Dawley rats, weighing 170–200 g, were divided into six groups: control, control with vitamin E (100 mg/kg/day, i.p.), control with simvastatin (SIM) (10 mg/kg of body weight/day), HFD, HFD with vitamin E, and HFD with SIM. Standard and high cholesterol diets were given for 15 weeks and SIM and vitamin E were added in the last 4 weeks. In all rats, serum vitamin E, total cholesterol (TC), triglycerides (TG), low (LDL) and high (HDL) density lipoproteins, alanine (ALT) and aspartate (AST) transaminases, alkaline phosphatase (ALP), and gamma glutamyl transpeptidase (GGT) as well as cardiac and hepatic thiobarbituric acid-reactive substances (TBARS) and antioxidants (reduced glutathione (GSH), superoxide dismutase (SOD), and catalase (CAT)) were measured. Also, electrocardiogram (ECG) was recorded. HFD significantly increased QTc interval, heart rate (HR), serum TC, TG, LDL, ALT, AST, ALP, GGT, liver TG, and cardiac and hepatic TBARS but decreased antioxidants and HDL, while SIM decreased HR, liver TG, serum TC, TG, and LDL and increased HDL in HFD rats. Vitamin E had no effect. Moreover, SIM and vitamin E decreased QTc interval, serum ALT, AST, ALP, GGT, and cardiac and hepatic TBARS and increased antioxidants in HFD rats. Histopathological observations confirm the biochemical parameters. SIM and vitamin E slow progression of hypercholesterolemia-induced oxidative stress in liver and heart and improve their functions.     

Dietary supplementation of vitamin A, C and E prevents p-dimethylaminoazobenzene induced hepatic DNA damage in rats

The preventive effect of antioxidant vitamins A, C, E and their analogues against DNA damage induced by a hepatocarcinogen p-dimethylaminoazobenzene (DAB) was assessed by comet assay. For genotoxicity (DNA damage) study, male albino rats were divided into 11 groups, consisting of four rats each. Group I served as control. Group II to VII received 1, 10, 100, 200, 300 and 400 mg per kg body wt of DAB respectively; group VIII to XI received 500 mg/kg body wt of DAB. They were sacrificed by cervical decapitation 3, 6, 12 and 24 h after treatment; livers were excised immediately and subjected to comet assay to measure DNA damage. To study the effect of vitamins, experiments were conducted on a group of 275 rats divided into 3 sets of 25 rats each. First set served as control; second set received 0.06% DAB and third set received 0.06% DAB, along with analogues of vitamins A, C and E. Rats fed with 0.06% DAB were provided water ad libitum for a period of 4 months, followed by a normal (basal) diet for further 2 months. Vitamins A (10,000-50,000 IU), C (75-1000 mg) and E (50-500 mg) and their analogues were given (per kg body wt) to the third set of rats by gavage route once in a week for a period of 6 months. The DAB induced DNA damage only at the highest tested dose of 500 mg/kg body wt. Administration of high doses of vitamin A acid, L-ascorbic acid and vit. E succinate individually prevented the DNA damage. However, administration of a mixture of these vitamins at low doses prevented the DAB-induced DNA damage, which may be due to their synergistic effect. The results indicate that there is a significant advantage in mixed vitamins therapy at low dose over the treatment with individual vitamins.     

Effects of vitamin C on muscle glycogen and oxidative events in experimental diabetes

Streptozotocin (STZ) is an agent used in creating experimental diabetes. Varying findings have been reported about the striated muscle glycogen levels in diabetes. In this study, it was planned to observe interaction of vitamin C (AA), of which deficiency has been shown in diabetics, with soleus muscle glycogen levels and oxidative events on STZ-diabetic subjects. Material and Method: In the study, 38 male adult Wistar Albino rats with weights 200 ± 20 g were used by separating them into four groups: Control, Vitamin C, Diabetes, Diabetes + Vitamin C. Body weights and fasting blood glucose were measured at the beginning and end of the experiment. AA, TBARS, GSH, NOx and glycogen levels of soleus muscles, and AA level of blood were measured. The results were compared using Anova variance and Mann-Whitney U tests. Results showed that AA levels in blood increased with vitamin C administration; AA, GSH and NOx levels in the muscle were low and MDA and glycogen levels were high in diabetics; and that vitamin C in the given dosage partially corrected these values. These results indicate that higher dosage than daily 20 mg/kg Vitamin C is required for being effective on metabolic and oxidizing events in diabetic rats.