The influences of dietary supplements of vitamin E on hepatocellular chemical carcinogenesis have been studied, Placental glutathione S-transferase(GST-P) positive foci area, antioxidant enzymes(superoxide dismutase(SOD), catalase, glutathione reductase, glutathione peroxidase, glutathione S-transferase(GST)), glucose 6-phosphatase(G6Pase) activities, and lipid peroxidation of mecrosomes(thiobarbituric acid reactive substances(TBARS) contents) were investigated. For is purpose , we used the murine chemical hepatocardinogenic procedure induced by modified Ito model, which consists of 200mg/kg body weight diethylinitrosamine (DEN) injection, 0.01% 2-acethlaminoflurene(2-AAF) feeding for 6 weeks, and partial hepatectomy on week 3. Weanling Sprague-Dawley male rats were fed pulverized Purina rat chow with 15, 000IU/kg diet vitamin E from initiation or promotion stages. We found that vitamin E supplement decreased the area of GST-P positive foci. Catalase, glutathione peroxidase, glutathione reductase. GST activities, and TBARS contents were decreased. On the other hand G6Pase activities were increased by vitamin E supplement. It seemed that vitamin E supplements helped endogenous defense systems against carcinogenesis by decreasing TBARS contents, $H_2O$$_2$ and organic peroxides. So, vitamin E seemed to protect cell from free radical damage in carcinogenesis. Anticarcinogenic effects of vitamin E were more effective at intiation that at promotion stage. These results suggest that vitamin E has suppressive effects on hepatocellular chemical carcinogenesis, probably through antioxidant effects against TBARS contents $H_2O$$_2$ and orgainc peroxides.