Inhibition of Desipramine 2-Hydroxylation by Quinidine and Quinine in Rapid and Slow Debrisoquine Hydroxylators
Polymorphic oxidation has been described for debrisoquine (Mahgoub et al. 1977) and for sparteine (Eichelbaum et al. 1979). Reduced ability to oxidize these compounds is inherited as an autosomal recessive trait (Price-Evans et al. 1980), and the prevalence of the slow hydroxylator phenotype varies between 3% and 9%, depending on the country (Eichelbaum 1982). Biochemical studies indicate that this polymorphism is caused by an inherited absence or functional deficiency of a particular cytochrome P-450 isozyme, called debrisoquine hydroxylase (Boobies et al. 1983). The oxidative metabolism of several other drugs has been shown to cosegregate with the debrisoquine/sparteine oxidation polymorphism (Jacqz et al. 1986).
KeywordsHuman Liver Microsome Poor Metabolizers Autosomal Recessive Trait Oxidation Polymorphism Polymorphic Oxidation
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