The association between GSTT1, M1, and P1 polymorphisms with coronary artery disease in Western Iran

• DOI: 10.1007/s11010-011-0817-2
• Publication Date: 2011-04-15T06:03:16Z
• Authors: Hamid Nomani; Hadi Mozafari; Shahrokh Mohamadz...; Zohreh Rahimi; Asad Vaisi Raygani; Mehr Ali Rahimi; Asghar Fadaei Haghi; Ali Asghar Keshavarz
• Keywords: Male; 0303 health sciences; Polymorphism, Genetic; Genotype; Blood Pressure; Coronary Artery Disease; Iran; Middle Aged; Lipids; Statistics, Nonparametric; 3. Good health; 03 medical and health sciences; Glutathione S-Transferase pi; Case-Control Studies; Humans; Female; Genetic Association Studies; Polymorphism, Restriction Fragment Length; Aged; Glutathione Transferase

DNA damage which occurred by the effect of oxidant and mutant agents has an essential role in the development of atherosclerosis. To investigate the possible association between GSTs polymorphism with coronary artery disease (CAD), we investigated the frequency of GSTT1, M1, and P1 genotypes in patients with CAD compared to controls. The genotypes of GSTT1, M1, and P1 were determined in 209 angiographically documented CAD patients and 108 normal coronary artery cases (as controls) by Multiplex Polymerase Chain Reaction and PCR-RFLP. In CAD patients, the frequency of GSTT1-null genotype was significantly (P = 0.025) lower than that in control. The presence of this genotype was associated with 2.2-fold increased risk of CAD. However, the frequency of GSTM1 and GSTP1 genotypes were not significantly different comparing both groups (P = 0.405 and P = 0.521, respectively). Moreover, non smokers patients had a lower frequency of GSTM1-null genotype (29.2%) compared to non smoker controls (43.5%, P = 0.043). Also, the frequency of both GSTT1-null and GSTM1-null genotypes in patients (3.8%) was significantly lower compared to controls with the same genotypes (10.2%, P = 0.014). Our results indicated that a reduction in the frequency of GSTT1-null and GSTM1-null genotypes that observed in our study might be involved in the pathogenesis of CAD in our population.