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.
The effect of green tea drinking on the hepatocellular chemical cacinogenesis have been studied. Placental glutathione S-transferase(GST-P) positive foci area in a liver tissue, contents of thiobarbituric acid reactive substances(TBARS), total cytochrome P450 and glucose 6-phospphatase(G6P) activity in hepatic microsomes were investigated. Weaning Sprague-Dawley male rats were fed AIN-76A diet with deionized water or green tea infusion, Rats of CTR and CTR+ groups were provided deionized water while GTI and GTI+ groups were provided green tea instead of deionized water for the entire experimental period of 13weeks. Rats of GTP and GTP + groups had deionized water for the first 6 weeks and switched to green tea for the last 7weeks of the experimental period. CTR+, GTI +, and GTP + groups were carcinogen treated groups, Diethylnitrosamine(DEN) was injected as a single dose of 200 mg/kg body weight intraperitoneally after 4 weeks of feeding. 2-Acetyla-minofluorene(AAF) was used as a carcinogen proliferater and suppled in the diets of carcinogen treated rats as 0.02% content for the last 6weeks starting from 2weeks after DEN injection. Rats were sacrificed after 13week weeks of feeding. The area and number of GST-P positive foci detected in carcinogen treated rats were decreased by green tea ingestion but when timing and duration of green tea ingestion was delayed after promotion period as in GTP + group, GST-P positive foci were not decreased as much as in GTI+ group. TBARS contents of carcinogen treated rats decreased by 13weeks of green tea ingestion but GTP groups did not show statiscally significant differences. G6P activities tended to decrease by carcinogen treatment but changes were not statiscally significant by green tea ingestion. Total cytochrome P450 contents were increased by carcinogen treatment. Thirteen weeks of green tea ingestion (GTI) also increased to total cytochrome P450 contents while 7weeks of green tea ingestion(GTP) did show any effects. These results suggest that green tea has suppressive effects on hepatocellular chemical carcinogenesis probably through the activities of antioxidant compounds.