Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: DrugBank:EXPT03226 (vitamin E)
 17,558 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Biochemical studies were performed on blood and lung tissue of squirrel monkeys (Saimiri sciureus) following acute exposure to 0.75 ppm ozone (O3) for 4 h/d for 4 consecutive days. One group of animals was sacrificed at the end of the last exposure day and another group was sacrificed 4 d later after the last exposure. Evidence was sought for oxidation-induced changes known to occur in rodents when high levels of O3 are inhaled. A significant increase in red blood cell membrane fragility was observed, as well as significant decreases in red blood cell glutathione and erythrocyte acetylcholinesterase; however, the red blood cell enzymes, lactic acid dehydrogenase (LDH), and glucose-6-phosphate dehydrogenase (G6PDH) were not changed significantly. Lung tissue analysis showed that lipid peroxidation was markedly increased and tissue vitamin E levels were significantly decreased. The tissue enzymes G6PDH, glutathione reductase, and LDH significantly increased in activity. No significant changes were seen in either superoxide dismutase or malic acid dehydrogenase. The results of this experiment indicate that O3, or reaction products resulting from O3-tissue interaction in the lung, pass the air-blood barrier and are capable of producing biochemical changes in blood as well as in lung tissue.
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PMID:Biochemical response of squirrel monkeys to ozone. 10 43

Experiments were conducted to determine the effects of exercise on rat glutathione peroxidase system enzymes and lipid peroxidation among animals supplemented and unsupplemented with selenium (Se) and vitamin E (E). Liver, muscle and blood were taken before, immediately after and 24 hours after exercising to exhaustion by swimming. No effect of exercise was found on muscle or liver enzymes, although exercise resulted in depressed glutathione reductase (GR) and glucose-6-phosphate dehydrogenase (G6PD) activities in erythrocytes immediately after exercise. Dietary Se supplementation did result in increased hepatic muscle and erythrocyte glutathione peroxidase activity, and decreased hepatic GR, G6PD and "malic enzyme" activities. Thiobarbituric acid reactive substances, and indicator of lipid peroxidation, increased in liver and muscle subsequent to exercise. This increase was reduced in liver, but not eliminated, by dietary E supplementation. The increase was not affected by dietary E in muscle, nor by dietary Se in either tissue.
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PMID:Selenium, vitamin E and the response to swimming stress in the rat. 44 49

Statistically significant changes (P less than .05) were observed in erythrocytes (RBC) and sera of young adult human males following a single short-term exposure to 0.50 ppm ozone (O3) for 2 3/4 hours. The RBC membrane fragility, glucose-6-phosphate dehydrogenase (G-6-PDH) and lactate dehydrogenase (LDH) enzyme activities were increased, while RBC acetylcholinesterase (AcChase) activity and reduced glutathione (GSH) levels were decreased. The RBC glutathione reductase (GSSRase) activities were not significantly altered. Serum GSSRase activity, however, was significantly decreased while serum vitamin E, and lipid peroxidation levels were significantly increased. These alterations tend to disappear gradually, but were still detectable two weeks following exposure.
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PMID:Ozone and human blood. 110 71

Nutritional muscular dystrophy (NMD) in the chick results from a simultaneous deficiency of vitamin E and cystine. Muscle and liver of dystrophic and nondystrophic chicks were assayed for nonprotein sulfhydryl (NP-SH), reduced glutathione (GSH) and glutathione reductase. Red blood cells were assayed for NP-SH and GSH content. Glutathione peroxidase was determined in muscle, plasma and liver. Dystrophic muscle GSH was increased and at times was approximately double that of normal muscle, while liver GSH was lower in dystrophic than in normal chicks. During recovery from NMD, brought about by addition of either vitamin E or cystine to the dystrophogenic diet, muscle GSH declined and liver GSH increased to normal levels. Glutathione peroxidase was equivalent in both dystrophic and nondystrophic plasma and liver, but was significantly increased in dystrophic muscle. The mode of action of dietary cystine in preventing NMD in chicks remains unknown; it is not mediated through the role of amino acid as a component of the GSH needed for the action of glutathione peroxidase.
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PMID:Studies on the changes in reduced glutathione of chick tissues during onset and regression of nutritional muscular dystrophy. 124 44

Circadian variations in antioxidant defences and lipid peroxidation were investigated in 12 rat hearts perfused during light (i.e., at 08.00, n = 6) and dark cycle (i.e., at 19.00, n = 6). Higher levels of non proteic thiol compounds (P < 0.01), glutathione transferase activity (P < 0.05) and lipid peroxidation (P < 0.01) were detected in evening-excised hearts, associated with a lower (P < 0.05) selenium-dependent glutathione peroxidase activity; superoxide dismutase and glutathione reductase activities, as well as vitamin E content, were similar in the two groups. Moreover, a greater release of thiobarbituric acid reactive substances (P < 0.01) and proteins (P < 0.05) was detected in the myocardial effluent of another group of 5 evening-excised hearts perfused with Krebs-Henseleit buffer containing 30 microM cumene hydroperoxide, as compared to 5 light-cycle hearts. In conclusion, a higher oxidative stress seems to be operative in the rat heart during early stages of the dark phase, in spite of the increase level of non proteic thiol compounds (namely, glutathione). An imbalance of antioxidant defences, and/or higher radical generation and unsaturation degree of biomembranes lipids, may be hypothesized to favour myocardial oxidative stress at the beginning of the motor activity phase in rats.
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PMID:Circadian variations in antioxidant defences and lipid peroxidation in the rat heart. 145 91

We investigated the effect of desferrioxamine, an effective iron chelator, on animal survival and on plasma vitamin E levels after administration of paraquat doses close to the LD50. Male Sprague-Dawley rats received 20 mg paraquat/kg followed by 300 mg desferrioxamine/kg/d given ip over 2 d at 3 equal intervals. The results suggested that desferrioxamine prevented the paraquat-induced depletion of vitamin E, but did not improve the mortality due to paraquat. In ancillary in vitro experiments with a paraquat-based free radical system, where glutathione reductase and NADPH were used as sources of enzymic activity for the redox cycling of paraquat, desferrioxamine effectively prevented the formation of hydroxyl radicals, as determined by deoxyribose degradation.
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PMID:The administration of desferrioxamine to paraquat-intoxicated rats. 150 87

Clinical evidence suggests that deprenyl may slow progression of Parkinson's disease, although mechanisms underlying this putative neuroprotective action remain poorly understood. To address this issue, we studied deprenyl in 12 parkinsonian patients using a single-blind, placebo-controlled, crossover design. After 1 month, deprenyl (10 mg/d) decreased the optimal levodopa requirement by 24% (oral) and 16% (intravenous). Levodopa-induced dyskinesias were prolonged by 430%, and antiparkinsonian action by 44%. Mood improved by 47%. One month after withdrawing deprenyl, effects on dyskinesias and mood had yet to return to baseline. There was no change in activities of circulating glutathione peroxidase, glutathione reductase, glutathione transferase, superoxide dismutase, and catalase, nor in levels of lipid peroxide and vitamin E. Deprenyl also failed to modify CSF levels of total glutathione and activities of glutathione peroxidase or superoxide dismutase. These effects on levodopa pharmacodynamics and mood complicate the interpretation of available investigations of deprenyl's neuroprotective action and increase the risk of adverse effects of levodopa.
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PMID:Deprenyl effects on levodopa pharmacodynamics, mood, and free radical scavenging. 154 14

Oxygen-induced retinopathy (OIR) was produced by subjecting newborn albino rats to a 60% oxygen atmosphere for 14 days before they were killed and retinal analysis was done. The extent of OIR was measured by estimating the severity of retinal vasoobliteration in ink-perfused flat-mounted retinas. This was done with the aid of a digitizing camera and an image-analysis system designed to create binary images of the retinal blood vessels. Retinal levels of several antioxidant molecules also were measured. Alpha-tocopherol and ascorbic acid were reduced in oxygen-exposed rats by 34% and 20%, respectively, compared with room air-raised control animals. Retinal glutathione reductase, S-transferase, and peroxidase showed no differences between oxygen-treated and -untreated rats. Attempts to increase the newborn rats' retinal ascorbic acid by administering daily subcutaneous injections (5 g/kg body weight) to the mother rats were unsuccessful. However, the level of retinal alpha-tocopherol of newborn rats could be altered by dietary manipulation of the mothers. The mothers were fed diets containing either 1 g alpha-tocopherol acetate/kg food or none, starting 21-25 days before the birth of their litters and lasting throughout the exposure period. This treatment resulted in three- to fourfold differences in the retinal alpha-tocopherol levels of the pups. The combination of dietary and oxygen treatments also resulted in significant differences in retinal glutathione peroxidase activity, with the vitamin E-deprived, oxygen-exposed group having highest levels. Newborn rats both supplemented with and deprived of alpha-tocopherol had less vasoobliteration than did those nursed by mothers fed rat chow.
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PMID:Oxygen-induced retinopathy in the rat. Vitamins C and E as potential therapies. 158 86

The effects of vitamin E and vitamin B2 on DNA damage and cellular reduction of chromium(VI) were investigated using Chinese hamster V-79 cells. Pretreatment with alpha-tocopherol succinate (vitamin E) resulted in a decrease of DNA single-strand breaks produced by Na2CrO4, while similar treatment with riboflavin (vitamin B2) enhanced levels of DNA breaks. In contrast, levels of DNA-protein crosslinks induced by Na2CrO4 were unaffected by these vitamins. Electron spin resonance (ESR) studies showed that incubation of cells with Na2CrO4 resulted in the formation of both chromium(V) and chromium(III) complexes, and cellular pretreatment with vitamin E reduced the level of the chromium(V) complex, whereas pretreatment with vitamin B2 enhanced the level of this intermediate. However, the levels of chromium(III) were unchanged by these vitamins. The uptake of chromate was not affected by vitamin E or vitamin B2, nor were the levels of glutathione or glutathione reductase activity, which are both capable of reducing chromate. ESR studies demonstrated that a chromium(V) species was formed by the reaction of Na2CrO4 with vitamin B2 and that vitamin B2 enhanced the formation of hydroxyl radicals during the reaction of Na2CrO4 and hydrogen peroxide. Treatment cells with Na2CrO4 resulted in a decrease of glutathione reductase activity, and pretreatment with vitamin E restored the enzyme activity suppressed by this metal. However, pretreatment with vitamin B2 enhanced the inhibition of this enzyme by Na2CrO4. Using a colony-forming assay, pretreatment with vitamin E dramatically decreased the cytotoxicity of Na2CrO4, while pretreatment with vitamin B2 was found to result in only a decrease of cell lethality of this metal.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of vitamins on chromium(VI)-induced damage. 193 52

To delineate the effect of dietary supplementation with vitamin E (Vit E) alone or in combination with riboflavin (Rib) or selenium (Se) or both, on biological oxidative damage in rat brain and lungs we exposed rats to hyperbaric oxygen (HBO) and measured the activities of glutathione reductase (GSSG-R), glutathione peroxidase (GSH-Px), superoxide dismutase (SOD) and glucose-6-phosphate dehydrogenase (G-6-PD) prior to or 48 h after exposure. Rats fed the dietary supplements, and a control group maintained on an unsupplemented diet, for 30 d, were each divided into 2 subgroups, of which 1 was exposed to 4.5 absolute atmospheres (ATA) of 100% oxygen for 30 min, hereafter referred to as "exposed". The remaining subgroups were left unexposed. Pre-exposure GSSG-R activity in brain was elevated in all experimentally fed groups (ranging from 23 to 84%) compared with the unexposed control, whereas GSH-Px, G-6-PD and SOD activities were unchanged. The lungs showed significant increases in pre-exposure GSSG-R, ranging from 15 to 28%, and GSH-Px, ranging from 13 to 23%, activities in all the groups fed the supplemental nutrients, except those on Vit E alone. Increases in G-6-PD activity were observed only in those fed supplements of Rib. In most cases exposure to oxygen caused an increase in GSSG-R, GSH-Px and G-6-PD activities. However the increases were higher in the supplemented groups.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of dietary factors on antioxidant enzymes in rats exposed to hyperbaric oxygen. 203 36


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