Nutritional Interrelationships among Vitamin E, Selenium, Antioxidants and Ethyl Alcohol in the Rat

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Abstract
Giving 20% alcohol as the sole drinking fluid delayed the onset of liver necrosis in rats fed a basal diet deficient in vitamin E and selenium. Addition of ethanol in vitro had no effect on the decline in respiration suffered by liver slices prepared from vitamin E- and Se-deficient rats. Determination of hepatic triglycerides in rats given alcohol for 5 to 6 weeks revealed that animals fed the basal vitamin E- and Se-deficient diet tended to have less fat in their livers than animals fed the same diet supplemented with either 500 ppm vitamin E or 0.3 ppm Se as Na2SeO3, or both. Certain fat-soluble antioxidants tended to diminish the hepatolipogenic action of ethanol, whereas vitamin E or Se did not. Examination of the time course of the development of alcoholic fatty liver showed that animals fed either the basal necrogenic diet or the basal diet supplemented with vitamin E and Se underwent a similar pathogenesis of alcoholic fatty liver for about 4 weeks. After this time, however, the vitamin E- and Se-deficient animals lost much of their liver fat, whereas the vitamin E- and Se-supplemented animals did not. The sparing action of alcohol on vitamin E- and Se-deficient animals appears inconsistent with a lipoperoxidative mechanism for chronic ethanol hepatotoxicity. The fact that vitamin E and Se tended to enhance the development of alcoholic fatty liver, whereas certain fat-soluble antioxidants did not, seems inconsistent with an antioxidant role for these two nutrients.