Rogers A E
Cancer Res. 1975 Sep;35(9):2469-74.
Earlier studies demonstrated enhanced chemical carcinogenesis in the liver, colon, and probably esophagus of male rats that were fed a lipotrope-deficient, high-fat diet. In further experiments, designed to examine the range of the dietary effect on chemical carcinogenesis, rats were fed either the marginally lipotrope-deficient, high-fat diet or an adequate control diet, and treated wit- N-2-fluorenylacet-amide, 3,3 diphenyl-3-diemthylcarbamoyl-1-propyne, N-methyl-N-nitroso-N'-nitroguanidine, N-[4-(5-nitro-2-furyl)-2-thiazolyl]formamide, aflatoxin G1, or ethionine. N-2-Fluorenylacetamide indiced hepatocarcinomas more rapidly and in higher incidence in deficient rats than in control rats. 3,3-Diphenyl-3-dimethylcarbamoyl-1-propyne induced a higher incidence of hepatocarcinomas but not gastric tumors in deficient rats. Aflatoxin B1, included as a positive control, was significantly more hepatocarcinogenic in deficient rats. Gastric tumor induction by N-methyl-N-nitroso-N'-nitroguanidine and induction of tumors of the urinary bladder by N-[4-(5-nitro-2-furyl)-2thiazylyl]formamide were not influenced by diet. Aflatoxin G1 and ethionine were toxic to deficient rats, and carcinogenic doses could not be administered.