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)

The effects of dietary vitamin B-2 and vitamin E on delta9-desaturation of stearoyl-CoA, catalase, glutathione peroxidase, superoxide dismutase and electron transport components in rat liver microsomes have been investigated. delta9-desaturase activities were decreased on diets deficient of vitamin B-2, E and supplemented with E. Among the peroxide-scavenging enzymes, only the catalase activity in microsomes correlates significantly with delta9-desaturase activity. In vitro addition of bovine catalase had no effect on microsomal delta9-desaturase activity on control diet. However, it enhanced the delta9-desaturation in microsomes on vitamin B-2-deficient diet which contained low catalase and high superoxide dismutase activities, compared to those in microsomes of control diet. It is suggested that the hydrogen peroxide-generating and -decomposing systems may play an important role on the delta9-desaturase activity in microsomes.
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PMID:Effects of dietary vitamin B-2 and vitamin E on the delta9-desaturase and catalase activities in the rat liver microsomes. 2 49

Disulfiram (Antabuse), a drug used in alcohol aversion therapy, has been demonstrated to protect various species against hyperbaric O2 toxicity. In contrast, we have found that disulfiram accelerates the onset of pulmonary edema and death of rats exposed to normobaric 95 to 97% O2. When rats were given 200 mg of disulfiram per kg b.wt., 100% of the rats died at 24 to 48 hr of O2 exposure whereas only 5% of the rats died when exposed to O2 without disulfiram. This effect was not seen with an equal dose of diethyldithiocarbamate, the reduced monomer of disulfiram. The toxic effect was not due to an inhibition of superoxide dismutase, nor did disulfiram significantly affect the level of glutathione or change the reduced to oxidized glutathione ratio in the lung. Concurrent administration of 200 mg per kg b.wt. of ascorbate, vitamin E or reduced glutathione or 100 mg/kg of catalase did not affect the toxic response.
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PMID:Enhancement by disulfiram (Antabuse) of toxic effects of 95 to 97% O2 on the rat lung. 21 76

Red blood cells (RBC) from normal and vitamin E-deficient rats were incubated in a hypertonic solution of reduced glutathione adjusted to pH 8. Methemoglobin formation occurred in intact RBC from both normal and vitamin E-deficient rats. Hemolysis was significantly greater in RBC from vitamin E-deficient rats. Experiments with catalase, superoxide dismutase, and methional showed that H(2)O(2) was the primary extracellular source of oxidant stress. Extracellular superoxide and hydroxyl radical were not involved in oxidant stress. Experiments with dimethyl sulfoxide showed that intracellular hydroxyl radical, generated from H(2)O(2), was the hemolytic agent. Neither methemoglobin formation nor lipid peroxidation involved hydroxyl radical. Indeed, lipid peroxidation and hemolysis in RBC from vitamin E-deficient rats were concurrent rather than consecutive events. Phase contrast microscopy showed that rigid, crenated RBC with a precipitate around the interior periphery formed during glutathione-induced oxidant stress. The precipitate dissolved slowly as the crenated RBC were converted to smooth ghosts. It appeared that protein precipitates involving mixed disulfide bonds were reduced and solubilized when extracellular glutathione penetrated the ruptured cell. Comparisons between normal RBC and vitamin E-deficient RBC suggest that vitamin E has little effect on the inward diffusion of extra-cellular H(2)O(2). Vitamin E apparently interacts with different oxidant species derived from intracellular H(2)O(2) in preventing lipid peroxidation and the sulfhydryl group oxidation leading to hemolysis.
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PMID:Role of vitamin E in glutathione-induced oxidant stress: methemoglobin, lipid peroxidation, and hemolysis. 33 49

The effects of various levels of selenium, alpha-tocopherol and sulfur on glutathione peroxidase (GSH-Px) activity in intestinal and liver tissues were determined in male rats fed corn-soybean or Torula yeast diets. Rats fed corn-soybean diets had greater GSH-Px activity in the small intestine, colon and liver tissues, catalase activity and selenium in the liver, and body weight gains than those fed Torula yeast diets. GSH-Px activity in the small intestine, colon, and liver tissues as well as concentration of selenium in the liver increased with increasing levels of selenium in Torula yeast diets but not with corn-soybean diets. Tocopherol supplementation had no significant effect on GSH-Px activity in rats fed Torula yeast or corn-soybean diets supplemented with selenium. Supplemental sulfur decreased GSH-Px activity in the small intestine tissues and increased activity in colon tissues.
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PMID:Glutathione peroxidase acitvity in intestinal and liver tissues of rats fed various levels of selenium, sulfur and alpha-tocopherol. 43 Feb 45

The effect of dietary selenium and vitamin E on the important cellular antioxidant defense systems was studied in rat erythrocytes. Weanling male Sprague-Dawley rats were fed a basal selenium and vitamin E deficient diet and supplemented with either none or 0.5 ppm selenium and either none or 45 ppm vitamin E for 35 or 40 days. Depletion of dietary selenium resulted in marked decrease of glutathione (GSH) peroxidase in the red cells, but the levels of GSH, catalase and superoxide dismutase were not significantly altered. The red cells of rats fed the basal diet deficient in both selenium and vitamin E had significantly lower levels of GSH and GSH peroxidase, but not of catalase and superoxide dismutase, than in those fed the basal diet and supplemented with either selenium, vitamin E or both. The results suggest that depletion of dietary selenium and vitamin may have a precipitate effect on lowering the levels of GSH and GSH peroxidase in rat erytyrocytes.
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PMID:Effect of dietary selenium and vitamin E on the antioxiant defense systems of rat erythrocytes. 46 73

Concentrations of a peroxidation product (malondialdehyde), fluorescent chromophores, lipofuscin-like fluorescent products, superoxide dismutase, catalase, glutathione peroxidase, and vitamin E in the maternal blood and the cord blood were determined and the results obtained were related to the estimation of lipid peroxidation and protective mechanism against uncontrolled oxidative processes in late pregnancy. Serum levels of fluorescent products were higher in the maternal blood than in the cord blood, indicating less frequent lipid peroxidation in the fetus than in the mother. In support of this assumption, the three protective enzymes and vitamin E were present in relatively lower concentrations in the cord blood. Sudden exposure of the newborn infant to a normobaric atmosphere after beginning breathing seems, therefore, to cause oxidation of red blood cell membrane, denaturation of the membrane, inducing hemoglobin breakdown, and consequently hemolysis.
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PMID:Lipid peroxidation in maternal and cord blood and protective mechanism against activated-oxygen toxicity in the blood. 48 29

To investigate the possibility that human polymorphonuclear leukocytes (PMN) elaborate sufficient amounts of hydrogen peroxide (H2O2) and other radicals of reduced oxygen to be autotoxic and retard directed cell movement and phagocytosis, the rate of ingestion of opsonized lipopolysaccharide-paraffin oil particles and movement through Nuclepore filters were studied. Ingestion rates were increased under anaerobic conditions and in normal aerobic conditions in the presence of extracellular catalase but not superoxide dismutase (SOD) or scavengers of singlet oxygen or hydroxyl radicals. Conversely, ingestion rates were decreased when cells were exposed to H2O2 or a superoxide anion (O2-)-H2O2 generating system of xanthine-xanthine oxidase. Catalase, but not SOD, prevented the effect and also enhanced the directed movement of PMN in normal aerobic conditions. PMN from volunteers administered 1600 U/day of the membrane lipid antioxidant alpha-tocopherol were hyperphagocytic but killed Staphylococcus aureus 502A less effectively than controls, suggesting that less H2O2 was available to damage PMN or kill bacteria. H2O2-dependent stimulation of the hexose monophosphate shunt, H2O2 release from phaogytizing PMN, and fluoresceinated concanavalin A cap formation promoted by H2O2 damage to microtubules were all diminished, but the release of O2- from phagocytizing PMN was not diminished in the vitamin E group. These results support the hypothesis that directed movement and phagocytosis by PMN are attenuated by autooxidative damage to the cell membrane by endogenously derived H2O2 and that the administration in vivo of vitamin E may prevent this damage by scavenging H2O2.
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PMID:Autooxidation as a basis for altered function by polymorphonuclear leukocytes. 87 28

The effects of dietary vitamin E on the important cellular antioxidant defense systems were studied in rat blood. One-month-old male Sprague-Dawley rats were fed a basal vitamin E-deficient diet and supplemented with either none or 45 ppm vitamin E for 4 months. The activity of glutathione (GSH) peroxidase was decreased significantly (p less than 0.05) in the red blood cells and plasma of vitamin E-deficient rats. The level of GSH in the red cells of vitamin E-deficient rats was also significantly decreased. No detectable GSH was found in the plasma of both groups of animals. The activities of catalase and superoxide dismutase were not significantly altered by the status of dietary vitamin E. Similar results were obtained when 2-month-old male rats were fed the respective diets for 3 months. The results suggest that the decreased levels of GSH and GSH peroxidase in the red cells of animals fed a vitamine E-deficient diet may in part contribute to their increased susceptibility to hemolytic agents.
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PMID:Dietary vitamin E and levels of reduced glutathione, glutathione peroxidase, catalase and superoxide dismutase in rat blood. 91 61

The activities of superoxide dismutase, glutathione peroxidase, catalase and xanthine oxidase were simultaneously studied in vitamin-E deficient and -supplemented rat liver and also measured the lipid peroxide content in liver. The lipid peroxide content of vitamin E-deficient rat liver, estimated by thiobarbituric acid, increased as compared with that of vitamin E-supplemented rat liver. No marked changes of activities of superoxide dismutase, glutathione peroxidase and catalase were observed, but the activity of xanthine oxidase which is strong superoxide generator increased in vitamin E-deficient rat liver. These results suggest that vitamin E prevents the accumulation of lipid peroxide, but not controls the level of peroxide scavenging system such as superoxide dismutase, glutathione peroxidase and catalase.
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PMID:Effect of vitamin E deficiency on the level of superoxide dismutase, glutathione peroxidase, catalase and lipid peroxide in rat liver. 103 31

Male Sprague-Dawley rats maintained for a period of 6 or 12 weeks on a basal vitamin E-dificient diet consisting of 70% sucrose, 20% vitamin-free casein, 4% tocopherol stripped lard, 4% salt mixture, and 2% tocopherol-free vitamin fortification mixture were used to compare two sets of commonly used salt mixtures (salt mixtures USP XIV versus Briggs' salt mixture) and two sets of vitamin fortification mixtures (NBC vitamin fortification mixture versus that of Weglicki). Among the rats maintained on the deficient diets for 6 weeks, only those that received the combination of salt mixture USP XIV and vitamin fortification mixture of Weglicki showed a significantly lower level of hepatic catalase activity compared to the corresponding control animals. While there were no significant changes in microsomal cytochromes at this time period, after 12 weeks on the deficient diet, a significant depression in these cytochromes was noted in all experimental groups except the one on salt mixture USP XIV and NBC vitamin fortification mixture. A similar decrease in hepatic catalase was observed in deficient animals at 12 weeks. Since the most striking differences in these diets are in their content of iron and menaquinone, it appears that these two dietary constituents may interact in modulating the effect of vitamin E on hepatic hemeproteins.
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PMID:Effects of different vitamin E-deficient basal diets on hepatic catalase and microsomal cytochromes P-450 and b5 in rats. 118 Feb 43


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