Metabolism of Dimethylnitrosamine to Mutagenic Intermediates by Kidney Microsomal Enzymes and Correlation With Reported Host Susceptibility to Kidney Tumors

Summary

Purified kidney microsomal enzymes from C3H/HeJ and Ha/ICR mice exhibited an unusually high capacity to generate mutagenic metabolites from dimethylnitrosamine (DMNA) when compared with similar enzyme preparations from BALB/cJ and RF/J mice. These results suggested that the DMNA-activating enzymes involved in mutagen formation were either present at higher levels or were more active in the kidneys of C3H/HeJ and Ha/ICR mice than in those of the other two strains. This strain difference correlated with the established susceptibility of these four strains to the neoplastic activity of DMNA.