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

¹ Division of Pulmonary Medicine, Dept of Medicine, Keio University, Tokyo, and ² Dept of Medicine, Tokyo Electric Power Company Hospital, Tokyo, Japan.

CORRESPONDENCE: H. Nakamura, Dept of Medicine, Tokyo Electric Power Company Hospital, 9-2 Shinanomachi, Shinjuku-ku, Tokyo 160-0016, Japan. Fax: 81 343566419. E-mail: hnakamura{at}cpnet.med.keio.ac.jp

Keywords: CYP2A6, genetic polymorphism, nicotine, smoking habit

Received: May 12, 2005
Accepted October 24, 2005

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.

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