Department of Medical Biology, Faculty of Medicine, Ankara University, Ankara, Turkey.
DNA Cell Biol. 2012 Feb;31(2):211-8. doi: 10.1089/dna.2011.1252. Epub 2011 Aug 17.
Carcinogenic and toxic molecules produce DNA adducts that contribute to the development of atherosclerosis. Genetic polymorphisms of xenobiotic-detoxified enzymes, which control the level of DNA adducts, may affect both enzymatic activity and individual susceptibility to coronary artery disease (CAD). In this study we investigated the effects of genetic polymorphisms of the CYP1A1*2C, GSTT1, and GSTM1 enzymes on CAD risk in a Turkish population. Genotypes were determined for 132 CAD patients and 151 healthy controls by the polymerase chain reaction/restriction fragment length polymorphism method. There were no significant differences between patients and controls in terms of CYP1A1, GSTT1, and GSTM1 genotypes. Analysis of the possible interactions between the genotypes, after adjustment for the risk factors, demonstrated that individuals carrying CYP1A1 variant GSTT1 null genotypes had an 8.907-fold increased CAD risk compared to their wild status (p<0.05). We suggest that genetic polymorphisms of xenobiotic-metabolizing enzymes could play an important role in CAD. Therefore, CYP1A1 and GSTM1 polymorphisms should be considered as important parameters for the prediction of CAD.
致癌和有毒分子会产生 DNA 加合物，从而促进动脉粥样硬化的发展。控制 DNA 加合物水平的外源性毒物解毒酶的遗传多态性可能会影响酶活性和个体对冠心病（CAD）的易感性。在这项研究中，我们调查了 CYP1A1*2C、GSTT1 和 GSTM1 酶的遗传多态性对土耳其人群 CAD 风险的影响。通过聚合酶链反应/限制性片段长度多态性方法确定了 132 名 CAD 患者和 151 名健康对照者的基因型。在 CYP1A1、GSTT1 和 GSTM1 基因型方面，患者与对照组之间无显着差异。在调整了危险因素后，对基因型之间可能存在的相互作用进行分析表明，与野生状态相比，携带 CYP1A1 变异 GSTT1 无效基因型的个体 CAD 风险增加了 8.907 倍（p<0.05）。我们认为，外源性毒物代谢酶的遗传多态性可能在 CAD 中起重要作用。因此，CYP1A1 和 GSTM1 多态性应被视为预测 CAD 的重要参数。
