Influence of dietary lipotrope and lipid content on aflatoxin B1, N-2-fluorenylacetamide, and 1,2-dimethylhydrazine carcinogenesis in rats.

A marginally lipotrope-deficient diet, high in fat, enhances hepatocarcinogenesis by aflatoxin B, , diethyland dibutyl-ni trosamine, or N-2-fluorenylacetamide and colon carcinogene sis by 1,2-dimethylhydrazine in rats, when compared to a nutritionally complete diet that differs in several components from the deficient diet. Supplementation of the deficient diet with lipotropes and amino acids decreases diethylnitrosamine hepatocarcinogenesis, and, contrary to expectation, addition of the higher, more saturated fat content of the deficient diet to the complete diet also decreases tumor induction. This report presents evidence that lipotrope or amino acid supplementation of lipotrope-deficient diets prevented their enhancement of N2-fluorenylacetamide hepatocarcinogenesis but not of aflatoxin B1 hepatocarcinogenesis. Addition of fat to the complete diet had no eftect on tumor induction by N-2-fbuorenylacetamide and decreased tumor induction by aflatoxin B, . We concluded that specific interactions between hepatocarcinogenesis, die tary lipotropes, and lipid vary with the carcinogen. The effect of the marginally deficient diet on 1,2-dimethyl hydrazine colon carcinogenesis appeared to be the result of its lipid content. Lipotrope or amino acid supplementation of the deficient diet did not prevent its enhancement of 1,2-dimeth ybhydrazine colon carcinogenesis. Substitution of the fat con tent of the deficient diet into the complete diet increased cumulative probability of death with tumor but has less effect on tumor incidence and no effect on tumor number.