OBJECTIVES: Glutathione S-transferase (GST) plays a key role in the detoxification of xenobiotic atherogens generated by smoking. We investigated whether functional GST gene polymorphism might be associated with acute myocardial infarction (AMI) and smoking. No such investigation has previously been conducted among North Indians. METHODS: 230 patients with AMI and 300 healthy controls of North Indian ethnicity were enrolled in the study. GSTM1/T1/P1 gene polymorphisms were examined using restriction fragment length polymorphism. RESULTS: When GST polymorphism was analyzed in patients with AMI, GSTM1 null genotype frequencies were 0.24 and 0.21 among cases with coronary artery disease and controls, respectively. The respective GSTT1 null genotype frequencies were 0.10 and 0.20 (p = 0.001). GSTP1 variant Val/Val allele frequencies were 0.02 and 0.07 with p = 0.03. After risk factor adjustment, only GSTP1Val/Val was found to be protective against disease. Considering the effect of GST (T1, M1, and P1) gene polymorphism on smoking, subjects were further divided into smokers and nonsmokers. However, GSTT1 null as well as GSTP Val/Val genotypes were protective only in nonsmokers (p = 0.01 and p = 0.04). CONCLUSIONS: A significant protective effect of GSTT1 null and GSTP1 Val genotype against disease was observed in patients with AMI although protection was limited to nonsmokers.
OBJECTIVES:Glutathione S-transferase (GST) plays a key role in the detoxification of xenobiotic atherogens generated by smoking. We investigated whether functional GST gene polymorphism might be associated with acute myocardial infarction (AMI) and smoking. No such investigation has previously been conducted among North Indians. METHODS: 230 patients with AMI and 300 healthy controls of North Indian ethnicity were enrolled in the study. GSTM1/T1/P1 gene polymorphisms were examined using restriction fragment length polymorphism. RESULTS: When GST polymorphism was analyzed in patients with AMI, GSTM1 null genotype frequencies were 0.24 and 0.21 among cases with coronary artery disease and controls, respectively. The respective GSTT1 null genotype frequencies were 0.10 and 0.20 (p = 0.001). GSTP1 variant Val/Val allele frequencies were 0.02 and 0.07 with p = 0.03. After risk factor adjustment, only GSTP1Val/Val was found to be protective against disease. Considering the effect of GST (T1, M1, and P1) gene polymorphism on smoking, subjects were further divided into smokers and nonsmokers. However, GSTT1 null as well as GSTP Val/Val genotypes were protective only in nonsmokers (p = 0.01 and p = 0.04). CONCLUSIONS: A significant protective effect of GSTT1 null and GSTP1 Val genotype against disease was observed in patients with AMI although protection was limited to nonsmokers.