Polymorphic hydroxylation of Debrisoquine in man

Abstract

Debrisoquine and its primary metabolite, 4-hydroxydebrisoquine, were measured in the urine of 94 volunteers after a single oral dose of 10 mg debrisoquine. The ratio between excreted debrisoquine and its metabolite was bimorphically distributed in the study population. Family studies supported the view that alicyclic 4-hydroxylation of debrisoquine is controlled by a single autosomal gene and that a defect in this metabolic step is caused by a recessive allele.