Glutathione S-transferase M1 and T1 genotypes and myocardial infarction Tulin Cora • Mehmet Tokac • Hasan Acar • Ahmet Soylu • Ziya Inan Received: 15 November 2011 / Accepted: 17 December 2012 / Published online: 30 December 2012 Ó Springer Science+Business Media Dordrecht 2012 Abstract Myocardial infarction (MI), which is the most important manifestation of coronary artery disease, is the leading cause of morbidity and mortality in the world. Glu- tathione S transferases (GSTs) are enzymes responsible for the metabolism of numerous xenobiotics and are known to be polymorphic in humans. We investigated the association between the GSTM1 and GSTT1 gene polymorphisms and MI. The study consists of 296 healthy controls and 324 consecutive patients who had undergone coronary angiog- raphy for suspicion of coronary artery disease and with a past history of myocardial infarction. DNA was extracted from whole blood of patient and control. GSTM1 and GSTT1 gene polymorphisms were examined using multiplex PCR. We found that the null GSTM1 was associated with protective effect on MI, although this increase was not significant for GSTM1 (p \ 0.054). However, GSTT1 genotype was asso- ciated with an increase in the risk of developing MI. In addition to after adjusting other all coronary risk factors, the interactive effect of GSTT1 null genotype remained statis- tically significant (p \ 0.001) for MI disease but GSTM1 null genotype was not statistically significant. Patients, who smoke having the null genotypes of GSTM1, were at a higher risk for developing MI (p \ 0.001, OR = 0.41, 95 % CI = 0.240–0.207). There was an effect of interaction of GSTM1 null genotype and smoking on MI development between patient and control groups (p \ 0.001). Our results showed that individuals with the null genotypes for GSTM1 had protective effect, while GSTT1 was at a higher risk for MI disease. In addition, there was additional effects of smoking when smoking and non-smoking groups were compared. Keywords Glutathione S-transferase Á Genotype Á Polymorphism Á Myocardial Infarction Introduction Myocardial infarction (MI), which is the most important manifestation of coronary artery disease is characterized by atherosclerotic plaque disruption and coronary thrombosis. Although mechanisms in vascular disease remain unclear, tobacco smoke is a major cause of cardiovascular diseases [1]. Oxidative stress and inflammation are emerging unify- ing patho-physiological mechanisms leading to cardiovas- cular disease [2]. The role of DNA oxidative stress in the pathogenesis of atherosclerosis and its association with increased production of reactive oxygen species has been well known [3]. Mutagenic activity of cigarette smoke chemicals can cause DNA adducts in target tissues and the oxidative modification and progression of atherosclerotic lesions [4, 5]. The binding of chemicals to DNA is mod- ulated by detoxification enzymes [6]. Various cellular detoxification systems including glutathione S transferases (GSTs) exist that protect against toxic substances. GSTs have an essential role in protection of DNA from genotoxic damage by inhibiting the formation of DNA adducts [7]. These enzyme groups play an important role in protecting tissue from oxidative and other damages. GSTs are classi- fied into eight separate classes, including GSTA (alpha), GSTM (mu), GSTK (kapa), GSTO (omega), GSTP (pi), T. Cora (&) Á H. Acar Á Z. Inan Department of Medical Genetics, Medical Faculty of Selcuk University, Konya, Turkey e-mail: tulincora@gmail.com M. Tokac Á A. Soylu Department of Cardiology, Meram Medical Faculty of Selcuk University, Konya, Turkey 123 Mol Biol Rep (2013) 40:3263–3267 DOI 10.1007/s11033-012-2401-6