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

N. Minematsu, H. Nakamura, M. Furuuchi, T. Nakajima, S. Takahashi, H. Tateno, A. Ishizaka

Research output: Contribution to journalArticlepeer-review

37 Citations (Scopus)


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. Copyright

Original languageEnglish
Pages (from-to)289-292
Number of pages4
JournalEuropean Respiratory Journal
Issue number2
Publication statusPublished - 2006 Feb


  • CYP2A6
  • Genetic polymorphism
  • Nicotine
  • Smoking habit

ASJC Scopus subject areas

  • Pulmonary and Respiratory Medicine


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