The roles of the GPX1 Pro198Leu and OGG1 Ser326Cys variants in coronary artery disease / GPX1 geni Pro198Leu ve OGG1 geni Ser326Cys varyantlarının koroner arter hastalığındaki rolleri

Abstract

Abstract Objective: Coronary artery disease (CAD) is caused by plaque formation on inner walls of coronary arteries. Glutathione peroxidase-1 (GPX1), prevents oxidative damage by detoxifying hydrogen and lipid peroxides. GPX1 Pro198Leu polymorphism results in oxidant/antioxidant imbalance. 8-oxoguanine DNA glycosylase-1 (OGG1) is the key enzyme in DNA repair pathway. OGG1 Ser326Cys polymorphism leads to 8-oxoG accumulation and may play a role in cardiovascular diseases. Thus, our study aims to investigate GPX1 Pro198Leu and OGG1 Ser326Cys polymorphisms in CAD patients and the possible relationship of genotypes with serum lipids and CAD severity. Methods: A total of 169 CAD patients and 173 angiographically documented healthy controls were included in our study. The lesion severity in CAD patients was determined by Gensini scoring system. The genomic DNA was isolated from peripheral blood. Real-time polymerase chain reaction (RT-PCR) was used to genotype GPX1 Pro- 198Leu and OGG1 Ser326Cys polymorphisms. Results: Systolic and diastolic blood pressure, pulse, glucose, total- and LDL-cholesterol, triglycerides and waist circumference values were statistically significant between CAD patients and controls (p<0.05). No significant differences were observed in GPX1 Pro198Leu and OGG1 Ser- 326Cys genotype frequencies between CAD patients and controls (p=0.675, p=0.593; respectively). There was no significant differences between genotype frequencies of two SNPs and Gensini scores (p=0.317, p=0.911; respectively). Conclusion: Since no significant relation was observed in GPX1 Pro198Leu and OGG1 Ser326Cys genotype frequencies between CAD patients and controls, and no significant effect was determined between the two SNPs and Gensini scores, it was suggested that GPX1 Pro198Leu and OGG1 Ser- 326Cys polymorphisms do not seem to have an effect on CAD pathogenesis and lesion severity. This result may be due to the limited number of the sample size in the study group.