Six-week-old Sprague Dawley rats were fed the diets of 20% casein or soy protein. Two weeks after the feeding, hepatocellular chemical carcinogenesis was initiated by diethylnitrosamine(DEN), and promoted by the diet containing 0.01% 2-acetylamino-fluorene(AAF) and two-thirds partial hepatectomy(PH). The animals were sacrificed at 8 weeks after the DEN injection. The area of placetal glutathione S-trnasferase(GST-P) positive foci, the activities of several enzymes in cellualr antioxidant enzyme systems and glucose 6-phosphatase were determined to investigate the mechanism of the anticarcinogenic effect by the dietary proteins. In another set of experiments, the drinking water of rats fed casein was supplemented with 1.5% inositol hexaphosphate(InsP6) to elucidate whether it has the comparable anticancer action of soy protein. The area and number of GST-P positive foci in the soy protein group were significantly(p<0.05) lower than those inthe casein group. The livers of rats fed casein showed moderate fattydegeneration and larger hyperplastic nodules than those of rats fed soy protein. In another set of experiments, the area and number of GST-P positive foci in the rats fed casein supplemented with InsP6 were not significantly different from those in the rats fed casein or soy protein. The lipid peroxidation of rats fed different protein sources showed no significant difference. Glutathione S-transferase(GST) activities were increased significantly(p<0.05) by carcinogen treatment in all dietary groups. Glucose 6-phosphatase(G6Pase) activities were decreased by carcinogen treatment, and hence showed a reverse relationship(r=-0.695, p<0.01) to the GST-P positive foci. Therefore, the activities in the rats fed casein were lower than those in the rats fed soy protein. These results suggest that the soy protein seems to be more anti-carcinogenic than casein by decreasing the preneoplastic lesion and by increasing the membrane stability but inositol hexaphosphate, a component of soy protein, may not be protective against hepatocarcinogenesis.