Logistic regression analysis of the data revealed the null genotype of GSTM1 and the GG genotype of the GSTP1 (313A/G) gene were associated with an approximately twofold enhanced risk of developing CAD, whereas GSTT1(-) plays a defensive role against CAD development in north Indians.
Therefore, in this study we aimed to determine the role of oxidative DNA damage and some variations in glutathione S-transferase (GSTM1 and GSTT1) and DNA repair (hOGG1) genes in CAD risk.
Among the GST genetic variants examined, the GSTT1 null genotype was more prevalent in CAD participants with 3 stenosed vessels than in control participants (OR=1.64, P=.02).
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).
Our work concludes that GSTM1, GSTT1 and GSTP1 variants might contribute to the development of T2DM and GSTT1 variant alone is involved in the development of T2DM associated CAD complications in the South Indian population.
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.
Therefore, in this study, we focus on determining whether genetic variations in xenobiotic-metabolizing [glutathione-S-transferase theta 1 (GSTT1), glutathione-S-transferase mu 1 (GSTM1), cytochrome P450 IIEI (CYP2E1)] and DNA repair [X-ray cross-complementing group 1 (XRCC1)] genes might be associated with increased risk for CAD.
Because elevated RBC count correlate well with risk of coronary heart disease, it might be concluded that GSTM1 and GSTT1 null genotypes have protective role(s) for developing coronary heart disease.
The common variant in the GSTM1 and GSTT1 genes is related to markers of oxidative stress and inflammation in patients with coronary artery disease: a case-only study.
We assessed the potential glutathione S-transferase (GST) gene-gene (GSTM1(null)-GSTT1(null)) and gene-smoking interactions on the development of CAD in patients with Type 2 diabetes.
We assessed the potential glutathione S-transferase (GST) gene-gene (GSTM1(null)-GSTT1(null)) and gene-smoking interactions on the development of CAD in patients with Type 2 diabetes.
Patients who smoke having the null genotypes of GSTM1 (OR: 1.63 (1.10 - 2.63)) and GSTT1 (2.66 (1.50 - 4.72)) and both (3.20 (1.37 - 7.45)) were at a higher risk for developing coronary heart disease.
The results of this analysis of preclinical atherosclerosis extend reports from the ARIC study of an interaction between smoking and GSTT1-1 in relation to the risk of incident coronary heart disease and lower extremity arterial disease.