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Variable Effects of a Lipotrope-deficient, High-Fat Diet on Chemical Carcinogenesis in Rats¹

Department of Nutrition and Food Science, Massachusetts Institute of Technology, Cambridge, Massachusetts 02139

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 with N-2-fluorenylacetamide, 3,3 diphenyl-3-dimethylcarbamoyl-1-propyne, N-methyl-N-nitroso-N'-nitroguanidine, N-[4-(5-nitro-2-furyl)-2-thiazolyl]formamide, aflatoxin G₁, or ethionine. N-2-Fluorenylacetamide induced 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)-2-thiazylyl]formamide were not influenced by diet. Aflatoxin G₁ and ethionine were toxic to deficient rats, and carcinogenic doses could not be administered.

¹ Supported in part by USPHS Contract NO1 CP 33238 from the National Cancer Institute.

Received 3/10/75. Accepted 5/22/75.