NAcetyltransferase NAT

NAT was first identified as the enzyme responsible for inactivation of the antitubercular drug isoniazid (45). NAT also plays an important role in carcinogen metabolism. The N-acetylation metabolizing pathway is a major route for the conjugative metabolism of many drugs and chemicals (46). Functional polymorphisms in the NAT gene were initially associated with differences in the susceptibility to occupational and smoking-related bladder cancer (47). Based on the substrate, individuals can be phenotyped as either "fast" or "slow" acetylators. Individuals with the slow phenotype are homozygotes for the slow allele, whereas subjects with the fast phenotype are either heterozygotes or homozygotes for the fast allele. The frequency of slow acetylator varies worldwide, ranging from 5% to 10% in Asia and reaching 90% frequency in certain European populations (13). Two functionally relevant human NAT genes, NATI and NAT2, have been identified that are highly polymorphic and are encoded at multi-allelic loci. The relationship between these polymorphisms and the resulting phenotypes is well established (48).

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