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IntroductionOne of the most important processes of xenobiotic metabolism reaction is acetylation, which involves catalysis by acetyl CoA‐dependent arylamine N‐acetyltransferase (NAT) enzymes. In addition, acetylation is a common cellular process and is crucial in protein formation, drug biotransformation, regulation of deoxyribonucleic acid (DNA), and other genetic elements (Heal et al., , Zhao et al., ). In most instances of acetylating small molecules, the acetylated metabolites are made more water‐soluble than the parent compound, which is also rendered less toxic.Xenobiotic N‐acetylation is catalyzed by two cytoplasmic acetyltransferases, N‐acetyltransferase type I (encoded by NAT1) and N‐acetyltransferase type II (encoded by NAT2). Each of the two genes, NAT1 and NAT2, possess open reading frames (ORFs) of 870 base pairs (Blum et al., ). The two genes are 87% homologous and are located at 8p22, a chromosomal region commonly deleted in human cancers (Grant et al., , Starheim et al., ). The genes NAT1 and NAT2 are separated by the nonfunctional pseudogene NATP (AACP). Both NAT1 and NAT2 genes show pronounced allelic heterogeneity with each of them having multiple distinct alleles in humans (Matas et al., ).The association between acetylator status and the risk of various diseases has been extensively recorded and reviewed in detail (Evans et al., 1993). Altered
Annals of Human Genetics – Wiley
Published: Sep 1, 2017
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