Combined vitamin E deficiency and ethanol pretreatment: liver glutathione and enzyme changes.
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.
D000410:Alanine Transaminase / Q000378:metabolism; D000426:Alcohol Dehydrogenase / Q000378:metabolism; D000444:Aldehyde Dehydrogenase / Q000378:metabolism; D000818:Animals; D000431:Ethanol / Q000633:toxicity*; D005969:Glutamate Dehydrogenase / Q000378:metabolism; D005978:Glutathione / Q000378:metabolism*; D008099:Liver / Q000187:drug effects* / Q000378:metabolism; D008297:Male; D051381:Rats; D014811:Vitamin E Deficiency / Q000378:metabolism*
D000431:Ethanol; D000426:Alcohol Dehydrogenase; D000444:Aldehyde Dehydrogenase; D005969:Glutamate Dehydrogenase; D000410:Alanine Transaminase; D005978:Glutathione