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.