Detection of a mutagen during dietary fat associated colon carcinogenesis in rats treated with 1,2 dimethylhydrazine

Fecal samples collected from rats fed diets supplemented with differing types of fat show mutagenic activity during, 1, 2-dimethylhydrazine-induced colon carcinogenesis. Employing the detector strain, Bacillus subtilis TKJ6321, detection of mutagen in the feces of DMH-treated animals correlated well with hepatic postmicrosomal enzyme activity. Although tumor development varied with the type of dietary lipid, the fecal mutagen levels and the ability of liver functions to form mutagen from DMH were markedly similar among animals fed different lipids and receiving DMH injections. It is concluded that DMH is converted to a mutagen, detectable in the feces, and that this carcinogen induces an elevated level of postmicrosomal enzyme in the liver of treated animals. Lipid type does not appear to be related to the metabolism of the carcinogen, but more likely related to promotion of tumor development after the initial genetic alteration in the mucosal cells of the colon.