Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0042875 (vitamin E deficiency)
 916 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The vitamin E deficiency was studied for its effect on the activity of enzymes participating in metabolism of xenobiotics. Experiments with 54 rats have demonstrated that the maintenance of animals on the vitamin-E-deficient diet within 13-14 weeks decreases the activity of microsomal monooxygenases (demethylase and hydroxylase), NADH- and NADPH-reductases, aryl- and aliesterases in the liver and lungs, which is a result of disturbance of hydrophobic and polar interactions in microsomal membranes. Vitamin E deficiency makes the extent of solubilization of these enzymes higher under the influence of deoxycholate and trypsin and intensifies inactivation of these enzymes under the effect of urea. In the lungs and in the liver of the vitamin E deficient rats the content of reduced glutathione decreases as well as the activity of glutathione reductase, glutathione-S-transferase, aldehyde dehydrogenase, while the activity of gamma-glutamyltransferase increases; glutathione disulphide is accumulated.
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PMID:[The effect of vitamin E deficiency on enzyme activity and the status of the membrane fraction of rat liver microsomes]. 258 40

After 7 weeks on a vitamin E deficient diet plasma and liver content of vitamin E were reduced by 60-70%. This treatment, a two week chronic ethanol intake or their combination all caused a significantly higher level of liver glutathione as compared to untreated rats. The chronic ethanol treatment also increased the activity of both alcohol dehydrogenase and aldehyde dehydrogenase and this effect was potentiated by vitamin E deficiency. The activity of the mitochondrial enzyme glutamate dehydrogenase was reduced both by vitamin E deficiency and by ethanol treatment. The activity of the cytosolic alanine aminotransferase was, on the other hand, markedly elevated by vitamin E deficiency, but this effect was completely abolished by ethanol treatment. Several similarities between the effects of chronic ethanol intake and vitamin E deficiency indicates that a poor vitamin E status may potentiate some of the ethanol-induced derangements in the liver.
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PMID:Combined vitamin E deficiency and ethanol pretreatment: liver glutathione and enzyme changes. 378 47

Malondialdehyde (MDA) production and cytosolic aldehyde dehydrogenase (ALDH) response were examined in rat liver tissues after feeding different levels of dietary vitamin E and/or selenium and polyunsaturated fat for 12-38 wk. MDA production was significantly increased by vitamin E deficiency or by high levels of polyunsaturated fat intake, but not by selenium deficiency. The activity of cytosolic ALDH increased upon increased production of MDA after 12-16 wk of feeding the lipid peroxidation-inducing diets. However, ALDH activity was suppressed after 38 wk of feeding the vitamin E-deficient diet. The results indicate that the hepatic cytosolic ALDH may be involved in the metabolism of MDA during a relatively short-term increase in in vivo lipid peroxidation, but that ALDH activity becomes suppressed after more severe in vivo lipid peroxidation has been produced. Hepatic and plasma alpha-tocopherol levels and lipid peroxidation products were measured for the various dietary groups.
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PMID:The influence of vitamin E and selenium on lipid peroxidation and aldehyde dehydrogenase activity in rat liver and tissue. 801 65