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)

Serum vitamin A, vitamin E, vitamin B12, folate and leucocyte vitamin C were measured in 45 patients between the ages of one month and 2 1/2 years who were receiving total parenteral nutrition. After allowing for variations in intake the following recommendations are made: Vitamin A (central vein) 2,500 i.u./day (peripheral vein) 1,000 - 1,500 i.u./day. Vitamin E (peripheral vein) 0.8 mg/kg/day, Vitamin B12 (central vein) 0.8 - 1 microgram/day, Folate (central vein) 10 - 80 microgram/day, Vitamin C (central vein) 25 mg/day.
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PMID:[Supply of vitamin A, E, C, B 12 and folates during total parenteral nutrition in pediatrics]. 10 63

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

Increasing concentrations of malonaldehyde and beta-propiolactone were increasingly mutagenic with 7 mutants of Salmonella typhimurium, 5 of which mutated bya frameshift mechanism and 2 of which mutated through base-pair substitution. The antioxidants vitamin C, vitamin E, selenium and butylated hydroxytoluene (BHT) at 3 logarithmic concentrations markedly reduced mutagenesis in those strains which mutated by frameshift mechanism.
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PMID:Antioxidants reduce the mutagenic effect of malonaldehyde and beta-propiolactone. Part IX. Antioxidants and cancer. 37 30

Two groups of weanling male Hartley guinea pigs maintained on vitamin E deficient diet were supplemented with 0.4 I.U./100 g body weight/day of vitamin E and either 2 (Group A) or 10 (Group B) mg/100 g body weight/day of vitamin C for 5 weeks. As compared to Group A, the degree of erythrocyte hemolysis and liver TBAR level of Group B were significantly increased while plasma vitamin E and erythrocyte GSH levels were significantly decreased. In another experiment, two groups of guinea pigs were given 0.8 I.U./100 g body weight/day of vitamin E and 2 (Group C) or 30 mg/100 g body weight/day (Group D) of vitamin C. Levels of plasma vitamin E and erythrocyte GSH of Group D were significantly lower than those of Group C: however, erythrocyte hemolysis and liver TBAR were not affected by the level of vitamin C supplementation. The results suggest that the high levels of vitamin C supplementation lowered tissue antioxidant potential of animal when vitamin E was marginally adequate, and the hemolytic and peroxidizing effect of high level of vitamin C may be counteracted by increasing the level of vitamin E.
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PMID:Effects of high level of vitamin C on tissue antioxidant status of guinea pigs. 44 55

Abnormal platelet aggregation was found in eight (44%) of 18 patients with beta-thalassaemia major and transfusional iron overload. The aggregation defect bore no correlation with the degree of hepatic fibrosis, liver function tests, whether or not splenectomy had been performed, the degree of iron overload, haematocrit, platelet count, serum vitamin E level, or leucocyte ascorbate concentration. Only three of the 18 patients showed prolonged bleeding times as well as abnormal platelet aggregation, and only one of these suffered clinically significant haemorrhage. The results show that a proportion of patients with beta-thalassaemia major have abnormal platelet function. It is possible, however, that the in vitro abnormality might be due partly to artefacts induced by manipulations required to remove the abnormal thalassaemic red cells, and this may explain the much lower incidence of significant haemorrhage.
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PMID:Platelet function in beta-thalassaemia major. 46 99

Five-week old, male, Japanese quail (Coturnix coturnix japonica) were given ad libitum access to glucose- soybean meal-10% fat diets containing 0, 0.25, 0.5, or 1% cholesterol, with or without the addition of a vitamin supplement (vitamin C--1 g/kg of diet, vitamin E--30 I.U./kg of diet and choline chloride--5.5 g/kg of diet). After 12 weeks, 9 quail from the 24 quail fed each diet were killed and the total cholesterol concentration of serum, liver, kidney, and aorta was determined. Cholesterol concentrations of these organs increased with increasing levels of dietary cholesterol. The vitamin supplementation enhanced the increase in the cholesterol concentration of serum and kidney, lessened the elevation of the liver cholesterol concentration and had no effect on the aorta cholesterol concentration. The remaining quail were fed the same diets, for a subsequent 12 week period, except that cholesterol was deleted. At the termination of the experiment, the total cholesterol concentration of serum, liver, and kidney returned to control level for all treatments in which organ cholesterol concentrations had been increased previously. Aortic cholesterol concentration decreased during the second 12 week period (0.5 and 1% cholesterol diets fed for the first 12 weeks), however, the aortic cholesterol concentration remained higher than those of the control at 24 weeks. No significant effect of vitamin supplementation on organ cholesterol concentration was noted at 24 weeks although serum cholesterol concentration was significantly lower for the vitamin- fed groups at all levels of dietary cholesterol. Aortic ahteromata were observed at both 12 and 24 weeks in all groups fed 0.5 and 1% cholesterol.
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PMID:Cholesteremia in Japanese quail: response to a mixture of vitamins C and E and choline chloride. 53 18

The effect of dietary vitamin C on vitamin E status and function was studied with weanling male Hartley guinea pigs. Thirty guinea pigs fed a basal diet free of vitamins E and C were divided into two groups; only one group received 2 mg/100 g body weight/day of vitamin C. Each group was further divided into three subgroups and received 0, 0.2, and 0.4 IU/100 g body weight/day of vitamin E. After 5 weeks the animals were killed. Degree of erythrocyte hemolysis induced by dialuric acid, level of plasma vitamin E and extent of liver lipid peroxidation were determined. Liver mitochondria were isolated and in vitro oxygen uptake was measured. The rate of swelling of mitochondria in two media was also determined. The results showed that the adequate dietary vitamin C supplementation did not affect the extent of erythrocyte hemolysis induced by dialuric acid, but increased the plasma vitamin E level and lowered liver lipid peroxidation. It also maintained the normal respiration and swelling rates of liver mitochondria when vitamin E was inadequate.
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PMID:Effect of dietary vitamin E and vitamin C on respiration and swelling of guinea pig liver mitochondria. 70 3

Leukocyte peroxidase deficiency has been demonstrated in a confirmed case of neuronal ceroid-lipofuscinosis with guaiacol, o-dianisidine, and p-phenylenediamine used as hydrogen donors in the peroxidase assay system. Nitroblue tetrazolium (NBT) reduction values in the leukocytes of the patient were also found to be significantly higher than those of normal controls, indicating the impaired hydrogen peroxide catabolism. When the patient was given a daily dose of vitamin E (400 I.U.), vitamin C (1 gm), and methionine (1 gm.) along with a weekly intramuscular injection of vitamin B12, the leukocyte peroxidase values of the patient returned to normal levels in about 7 weeks. NBT reductions values also decreased to normal levels. The regenerated enzyme in the patient's leukocytes was shown to have similar chromatographic and electrophoretic properties as the leukocyte peroxidase of normal controls. After about 28 weeks of therapy, the peroxidase levels in the leukocytes of the patient returned to original low levels, with concomitant increase in the NBT reduction values. The effect of vitamin therapy on normal control subjects was, at least in some cases, an increase of leukocyte peroxidase. A significant increase in the peroxidase levels of the patient's leukocytes during vitamin therapy remains unexplained, and the possibility of peroxidase deficiency being a secondary manifestation rather than the primary defect in Batten's disease cannot be ruled out.
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PMID:Studies in neuronal ceroid-lipofuscinosis: leukocyte peroxidase deficiency in a patient with neuronal ceroid-lipofuscinosis (Jansky-Bielschowsky type). 84 78

Rats fed a vitamin E-deficient diet containing 10% "stripped" corn oil had reduced growth rate and elevated platelet count by 12 weeks of age, and a normocytic anemia with elevated reticulocytes by 16 weeks of age. After 5 months, rats became emaciated and developed kyphoscoliosis. Some rats developed skin ulcers and tremors, and mortality was high. Neuromuscular lesions included a chronic necrotizing myopathy and localized axonal dystrophy. There was also a selective activation of lysosomes in the central nervous system microcirculation. Liver ascorbic acid of deficient rats was the same as in those receiving vitamin E. Urinary excretion of p-hydroxyphenylpyruvate after a tyrosine load was also the same in deficient and control rats. It was concluded that neither vitamin C synthesis or utilization was affected the E-deficient rats.
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PMID:Effects of a prolonged vitamin E deficiency in the rat. 87 63

Mechanisms of the inhibitory effect of vitamin E on the process of lipid peroxidation (LPO) in biological membranes are studied. Both alpha-tocopherol and its derivatives (a-tocopherylacetate, o- and p-tocopherylquinones possess no radical scavenging activity) inhibit non-enzymatic (Fe2+ + ascorbate)-induced LPO and prevent LPO-dependent inhibition of Ca2+ transport in sarcoplasmic reticulum membranes from skeletal muscles. The protective effect of alpha-tocopherylacetate, tocopherilquinones and partially of alpha-tocopherol is due to a stabilizing effect of these compounds on sarcoplasmic reticulum membranes, registered by a decrease of fluidity of membrane lipid bilayer (probed by nitroxile radical TEMPO) and by a decrease of its passive permeability for Ca2+. Under the enzymatic NADPH-dependent LPO induction in rat liver microsomal fraction a strong inhibitory effect of tocopherylquinones is similar to the effect of other electron acceptors (methylnaphtoquinone, TEMPO) and is due to their ability to compete with LPO reaction for reducing equivalents in NADPH-dependent electron carriers wich results in the formation of hydroxy-derivatives having pronounced radical scavenging activity.
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PMID:[Mechanisms of stabilizing effect of vitamin E against lipid peroxidation in biological membranes]. 91 44


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