Colon mucosal cells can catalyze the activation of precarcinogens to mutagenic metabolites without the intermediacy of intestinal bacteria as shown in a mutagenesis assay system composed of Salmonella typhimurium strain TA100 and the 9000 × g supernatant fraction of rat colon mucosal cells. Pretreatment of rats with β-naphthoflavone increased the activation of 2-aminoanthracene 10- to. 20-fold and the activation of benzo(a)pyrene 4-fold. Pretreatment of rats with Aroclor 1254 doubled the activation of 2-aminoanthracene over control but had no effect on the activation of benzo(a)pyrene. The activation of 2-aminoanthracene and benzo(a)pyrene by liver was induced significantly by pretreatment with β-naphthoflavone and Aroclor 1254. Phenobarbital/hydrocortisone pretreatment did not increase the activation by the colon system of any precarcinogen tested but did increase the activation of 2-aminoanthracene, cyclophosphamide, and isophosphamide by the liver system. The activation of precarcinogens in the bacterial test system is directly correlated with the activities of the pretreated colon and liver preparations toward several drug and polycyclic hydrocarbon substrates assayed in vitro.


This investigation was supported by Grant CA-19105 awarded by the National Cancer Institute through the National Large Bowel Cancer Project.

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