Limitation of cigarette consumption by CYP2A6*4, *7 and *9 polymorphisms

Eur Respir J. 2006 Feb;27(2):289-92. doi: 10.1183/09031936.06.00056305.

Abstract

The whole gene deletion CYP2A6*4, the defect of the main nicotine oxidase, contributes to limiting lifelong and daily cigarette consumption. However, the effects on smoking habits of CYP2A6*7 and *9, two major functional polymorphisms common in Asian populations, have not been reported. The present study examined the relationship between polymorphisms *4, *7 and *9 with the smoking habits of 200 Japanese smokers who visited the Keio University Hospital (Tokyo, Japan). The allele frequencies of *1 (wild type), *4, *7 and *9 were 52, 17, 11 and 20%, respectively. When the three polymorphisms were considered simultaneously, the percentages of homozygous wild type, heterozygote, and homozygous mutants and compound heterozygotes were 26.0, 52.5 and 21.5%, respectively. Homozygous mutants and compound heterozygotes (n = 43) smoked fewer cigarettes daily than heterozygotes (n = 105) and homozygous wild-type individuals (n = 52). Smokers with *7/*7, *9/*9 or *7/*9 had lower daily cigarette consumption than smokers with *1/*1. In conclusion, polymorphisms *4, *7 and *9 of CYP2A6 were detected in approximately three out of four Japanese smokers, and their daily cigarette consumption was genetically modulated by these functional polymorphisms.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Aged
  • Alleles*
  • Aryl Hydrocarbon Hydroxylases / genetics*
  • Cytochrome P-450 CYP2A6
  • Female
  • Gene Frequency
  • Genotype
  • Humans
  • Japan / epidemiology
  • Male
  • Middle Aged
  • Mixed Function Oxygenases / genetics*
  • Polymorphism, Genetic
  • Smoking / epidemiology
  • Smoking / genetics*
  • Statistics, Nonparametric

Substances

  • Mixed Function Oxygenases
  • Aryl Hydrocarbon Hydroxylases
  • CYP2A6 protein, human
  • Cytochrome P-450 CYP2A6