Polymorphically acetylated aminoglutethimide in humans.
The urinary excretion during 24 h of aminoglutethimide (AG) its major metabolite (N-acetylAG) and two minor metabolites (N-formylAG and nitroG) were measured in 10 volunteers given AG who had been typed for acetylator phenotype using sulphadimidine. The slow acetylators of sulphadimidine excreted more AG (mean 28% of the administered dose) than did the fast acetylators (12%), but the latter excreted more of the dose as N-acetylAG (8.8%) than did the former (3.9%). NitroG and N-formylAG were minor urinary metabolites of AG in humans. The former was more abundant in the urine of slow acetylators (0.10% of the dose) than in that of fast acetylators (0.047%), whereas the respective proportions of doses excreted as the N-formyl derivative (0.475 and 0.465%) were not significantly different for the two acetylator phenotypes. These results show that AG is among those drugs that are polymorphically acetylated in humans.
D000107:Acetylation; D000328:Adult; D000616:Aminoglutethimide / Q000031:analogs & derivatives / Q000378:metabolism* / Q000652:urine; D006801:Humans; D010641:Phenotype; D011110:Polymorphism, Genetic; D013418:Sulfamethazine / Q000378:metabolism
D000616:Aminoglutethimide; C036163:N-acetylaminoglutethimide; C036164:nitroglutethimide; D013418:Sulfamethazine; C036165:N-formylaminoglutethimide