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日本人单胺氧化酶基因多态性与吸烟行为

Monoamine oxidase polymorphisms and smoking behaviour in Japanese.

作者信息

Ito Hidemi, Hamajima Nobuyuki, Matsuo Keitaro, Okuma Katashi, Sato Sigeki, Ueda Ryuzo, Tajima Kazuo

机构信息

Division of Epidemiology and Prevention, Aichi Cancer Center Research Institute, 1-1 Kanokoden, Chikusa-ku, Nagoya Aichi 464-8681, Japan.

出版信息

Pharmacogenetics. 2003 Feb;13(2):73-9. doi: 10.1097/00008571-200302000-00003.

Abstract

Although nicotine dependence is one of the primary reasons why smokers cannot quit smoking, nicotine cannot explain all of the psychopharmacological effects of tobacco smoke. Accumulating evidence points to potent inhibition of monoamine oxidase (MAO) which metabolizes neurotransmitters relating to additive behaviour. We have therefore investigated the association between smoking behaviour and MAO ( variable number of tandem repeat in the promoter region and A644G) polymorphisms. The genotypes were examined in 504 Japanese outpatients (217 men and 287 women) who visited Aichi Cancer Centre Hospital. The age-adjusted odds ratios (aORs) were estimated by a logistic model. Among males, we did not find a significant association of the smoking habit with either of the polymorphisms. The median Fargastrom test for nicotine dependence (FTND) score among male current smokers was significantly higher with than without the 4-repeat allele (5.8 and 4.7, respectively). The aOR of FTND 6 versus FTND 6 was 2.72 (95% confidence interval 1.13-6.50) for males with the 4-repeat allele. Among females, the aOR of being current smokers compared to never smokers was 0.49 (0.26-0.93) for individuals with the 4-repeat allele. Our results indicate that the polymorphisms of influence the smoking habit for female, as well as the nicotine dependence and smoking initiation for male smokers. These findings among male smokers support the view that MAO affects a smokers' requirement for nicotine and may explain why some people are predisposed to tobacco addiction and why some individuals find it difficult to stop smoking.

摘要

尽管尼古丁依赖是吸烟者无法戒烟的主要原因之一,但尼古丁并不能解释烟草烟雾的所有心理药理学效应。越来越多的证据表明,烟草烟雾会强力抑制单胺氧化酶(MAO),该酶可代谢与成瘾行为相关的神经递质。因此,我们研究了吸烟行为与MAO(启动子区域串联重复序列可变数目及A644G)基因多态性之间的关联。对504名前往爱知县癌症中心医院就诊的日本门诊患者(217名男性和287名女性)的基因型进行了检测。通过逻辑模型估计年龄调整后的优势比(aORs)。在男性中,我们未发现吸烟习惯与任何一种基因多态性之间存在显著关联。男性当前吸烟者中,携带4重复等位基因者的尼古丁依赖Fargastrom测试(FTND)得分中位数显著高于未携带该等位基因者(分别为5.8和4.7)。携带4重复等位基因的男性中,FTND评分为6分者与评分为6分者的aOR为2.72(95%置信区间1.13 - 6.50)。在女性中,携带4重复等位基因的个体当前吸烟者与从不吸烟者相比的aOR为0.49(0.26 - 0.93)。我们的结果表明,该基因多态性影响女性的吸烟习惯,以及男性吸烟者的尼古丁依赖和开始吸烟情况。男性吸烟者中的这些发现支持了MAO影响吸烟者对尼古丁需求的观点,并且可以解释为什么有些人易患烟草成瘾以及为什么有些人难以戒烟。

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