Metabolism of dimethylnitrosamine to mutagenic intermediates by kidney microsomal enzymes and correlation with reported host susceptibility to kidney tumors.
Purified kidney microsomal enzymes from C3H/HeJ and Ha/1CR 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.
D000818:Animals; D004128:Dimethylnitrosamine / Q000378:metabolism*; D066298:In Vitro Techniques; D007668:Kidney / Q000378:metabolism*; D007680:Kidney Neoplasms / Q000139:chemically induced*; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D008809:Mice, Inbred C3H; D008813:Mice, Inbred ICR; D008861:Microsomes / Q000201:enzymology / Q000378:metabolism; D009153:Mutagens / Q000378:metabolism*; D009374:Neoplasms, Experimental / Q000139:chemically induced; D009602:Nitrosamines / Q000378:metabolism*; D013045:Species Specificity
D009153:Mutagens; D009602:Nitrosamines; D004128:Dimethylnitrosamine