Nicotine metabolism defect reduces smoking

被引：318

作者：

Pianezza, ML ^{[1
]}

Sellers, EM ^{[1
]}

Tyndale, RF ^{[1
]}

机构：

[1] Univ Toronto, Addict Res Fdn Ontario, Ctr Res Womens Hlth, Dept Pharmacol Med & Psychiat, Toronto, ON M5S 1A8, Canada

来源：

NATURE | 1998年 / 393卷 / 6687期

关键词：

D O I：

10.1038/31623

中图分类号：

O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];

学科分类号：

07 ; 0710 ; 09 ;

摘要：

Nicotine is the primary compound in tobacco that establishes and maintains tobacco dependence1. Most of this nicotine is metabolized to cotinine by the genetically variable enzyme CYP2A6. Here we show that individuals lacking full functional CYP2A6, who therefore have impaired nicotine metabolism, are significantly protected against becoming tobacco-dependent smokers. In addition, smokers whose nicotine metabolism is thus impaired smoke significantly fewer cigarettes than those with normal nicotine metabolism.

引用

页码：750 / 750

页数：1

共 10 条

[1]

BENOWITZ NL, 1994, J PHARMACOL EXP THER, V268, P296

[2] HUMAN CYTOCHROME P450IIA3 - CDNA SEQUENCE, ROLE OF THE ENZYME IN THE METABOLIC-ACTIVATION OF PROMUTAGENS, COMPARISON TO NITROSAMINE ACTIVATION BY HUMAN CYTOCHROME P450IIE1 [J].