Oxidative stress gene polymorphisms may have an impact in the development of ischemic stroke.

Abstract

Antioxidants are responsible for detoxification of harmful effects of reactive oxygen species. Genetic factors may influence antioxidant activity as a result of polymorphisms on antioxidant enzymes. These polymorphisms can be risk in ischemic stroke (IS) risk. IS is a disorder with genetic and environmental factors contributing to overall risk. Although a few studies have been conducted, there have been no reports on catalase (CAT C262T), manganese superoxide dismutase (MnSOD Ala16Val) and glutathione peroxidase 1 (GPX1 Pro198Leu) gene polymorphisms and IS risk. We aimed to perform a case-control study to increase the awareness of the impact of oxidative stress (OS) gene polymorphism in the development of IS. A restriction fragment length polymorphism-polymerase chain reaction was used to determine genotypes. The interactions between genes and smoking and possible risk factors were evaluated. An approximately four-fold higher IS risk was found in patients with the Val allele compared to the Ala allele. Smoking was a risk factor in the development of IS for CAT TT and MnSOD Ala/Val genotypes; we found a 3.5- to 5.5-fold higher IS risk in CAT TT and MnSOD Ala/Val genotypes. Different logistic regression models were performed for possible risk factors (smoking, body mass index, low-density lipoprotein and diabetes mellitus). The IS risk increases statistically significant only with age by multiple logistic regression analysis. CAT gene polymorphisms in IS patients were not different from controls. It is unlikely that CAT and GPX1 single nucleotide polymorphisms are risk factors for IS. The results of the present study show that smoking may be a risk factor for IS risk in patients with MnSOD mutant genotypes.