Benzo(a)pyrene metabolism in hepatic microsomes from female DA rats with a genetic sparteine oxidation deficiency.
The impact of the genetic hydroxylation deficiency described for several drugs such as sparteine, debrisoquine, and phenformin, has been studied with respect to benzo(a)pyrene (BP) metabolite formation. 14C-BP (80 microM) was incubated with liver microsomes from female DA rats deficient in sparteine oxidation; microsomes from female Sprague-Dawley rats served as controls. BP metabolites were separated by high pressure liquid chromatography (HPLC). No significant differences were detected in the overall formation rate of 9,10-,4,5-, and 7,8-dihydrodiol-BP, of 4 quinones, or of 9-OH- and 3-OH-BP. Thus, the study suggested no association between genetic hydroxylation polymorphism (debrisoquine/sparteine type) and the formation of at least 6 BP metabolites.
D000818:Animals; D001564:Benzo(a)pyrene / Q000378:metabolism*; D002851:Chromatography, High Pressure Liquid; D005260:Female; D008661:Metabolism, Inborn Errors / Q000378:metabolism*; D008862:Microsomes, Liver / Q000378:metabolism*; D010084:Oxidation-Reduction; D051381:Rats; D011919:Rats, Inbred Strains; D011922:Rats, Mutant Strains; D013034:Sparteine / Q000378:metabolism*; D013045:Species Specificity
D013034:Sparteine; D001564:Benzo(a)pyrene