The purpose of this study was to investigate the effect of vitamin E and selenium on the antioxidative defense mechanism in the liver of streptozotocin(STZ)-induced diabetic rats. Sprague-Dawley male rats(120$pm$10gm) were randomly assigned to one control and five STZ-diabetic groups. Diabetic groups were classified to STZ-0E (vitamin E free diet), STZ-40E(40mg vitamin E/kg of diet), STZ-400E(400mg vitamin E/kg of diet), STZ-S(0.5ppm Se/kg of diet) and STZ-400ES(400mg vitamin E and 0.5ppm Se/kg of diet) according to the level of vitamin E and selenium supplementation. Diabetes was experimentally induced by intravenous adminstration of 55mg/kg of STZ in citrate buffer(pH 4.3) after 4-weeks feedng of six experimental diets. Animals were sacrificed at the 4th day of diabetic states. Activities of the serum glutamic oxaloacetate transaminase(GOT) and the glutaminc pyruvate transaminase(GPT) in STZ-0E, STZ-40E and STZ-S rats were higher than those of control. Liver xanthine oxidase activities were similar to serum GOT and GPT. Liver superoxide dismutase(SOD) activities were higher in STZ-0E and STZ-40E groups by 33%, 22%, respectively than that of control. Glutathione S-transferase(GST) activities of liver were similar to GSH-Px activities. The contents of vitamin E in liver tissue were significantly lower STZ-0E, STZ-40E and STZ-S groups by 50%, 36%, 45% than that of control. Reduced glutathione(GSH) contents of liver were lower STZ-0E, STZ-40E, STZ-400E, STZ-S and STZ-400ES groups by 57%, 51%, 19%, 18%, 12% than that of control. Lipid peroxide values (LPO) in liver were higher 5.6, 2.3 and 2.3 times in STZ-0E, STZ-40E and STZ-S group than that of control. The present results indicate that STZ-induced diabetic rats are more sensitive to oxidative stress, leading to the acceleration of lipid peroxidation process, which can be more accelerated by feeding the low level of dietary vitamin E. In the coincident supplementation of high dietary vitamin E and selenium antioxidative enzymes activities and physiolosical antioxidants were increased more than those of the separate supplementation of vitamin E or selenium. Therefore, dietary vitamin E and selenium reduced peroxidative damage of tissue, promoting antioxidative defense mechanism against lipid peroxidation by diabetes.