Lipid peroxidation and antioxidant defense systems in rat liver after chronic ethanol feeding

Authors

  • Tateo Kawase,

    1. Section of Liver Disease and Nutrition, and Alcohol Research and Treatment Center, Bronx Veterans Administration Medical Center, Bronx, New York 10468
    2. Mount Sinai School of Medicine, City University of New York, New York, New York 10029
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  • Shinzo Kato,

    1. Section of Liver Disease and Nutrition, and Alcohol Research and Treatment Center, Bronx Veterans Administration Medical Center, Bronx, New York 10468
    2. Mount Sinai School of Medicine, City University of New York, New York, New York 10029
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  • Charles S. Lieber M.D.

    Corresponding author
    1. Section of Liver Disease and Nutrition, and Alcohol Research and Treatment Center, Bronx Veterans Administration Medical Center, Bronx, New York 10468
    2. Mount Sinai School of Medicine, City University of New York, New York, New York 10029
    • Alcohol Research and Treatment Center, Bronx Veterans Administration Medical Center, 130 W. Kingsbridge Road, Bronx, New York 10468
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Abstract

The effects of chronic ethanol feeding on hepatic lipid peroxidation, ascorbic acid, glutathione and vitamin E levels were investigated in rats fed low or adequate amounts of dietary vitamin E. Hepatic lipid peroxidation was significantly increased after chronic ethanol feeding in rats receiving a low-vitamin E diet, indicating that dietary vitamin E is an important determinant of hepatic lipid peroxidation induced by chronic ethanol feeding. No significant change was observed in hepatic non-heme iron content, but hepatic content of ascorbic acid and glutathione was increased by ethanol feeding. Both low dietary vitamin E and ethanol feeding significantly reduced hepatic α-tocopherol content, and the lowest hepatic α-tocopherol was found in rats receiving a combination of low vitamin E and ethanol. Plasma α-tocopherol was elevated after ethanol feeding, probably because of the associated hyperlipemia. Both the ratio of plasma α-tocopherol/plasma lipid and the red blood cell α-tocopherol were reduced by ethanol feeding. Furthermore, ethanol feeding caused a marked increase of hepatic α-tocopheryl quinone, a metabolite of α-tocopherol by free radical reactions. Ethanol feeding caused little changes of α-tocopherol and α-tocopheryl quinone content in mitochondria, whereas a striking increase in α-tocopheryl quinone was observed in microsomes. These data suggest that ethanol feeding causes a marked alteration of vitamin E metabolism in the liver and that the combination of ethanol with a low-vitamin E intake results in a decrease of hepatic α-tocopherol content which renders the liver more susceptible to free radical attack.

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