Association between Polymorphisms of Antioxidant Gene (Mnsod, CAT and Gpx1) and Risk of Coronary Artery Disease

Abstract

Objective. Reactive oxygen species (ROS) been cited as one of the major causes of atherosclerosis and coronary artery disease which are possible agents inducing DNA damage. Manganese superoxide dismutase (MnSOD), catalase (CAT), and glutathione peroxidase-1 (GPx1) have evolved to address primary defense against free radical mediated damage in mitochondria. The aim of this study was to delineate the association of MnSOD, CAT, and GPx1 polymorphisms and risk of CAD in Taiwan. Methods. We conducted a case-control study with 657 participants recruited at a medical center. All subjects were evaluated by noninvasive stress test and then quantitative coronary angiography to confirm the diagnosis of CAD. 447 CAD cases were defined as >50% stenosis of coronary artery and 210 controls were stenosed below 50%. Polymorphisms of MnSOD (Val16Ala), CAT (C-262T), and GPx1 (Pro198Leu) genes were determined by polymerase chain reaction methods. Multivariate logistic regression model was used to calculate the odds ratios (ORs) and 95% confidence intervals (CIs). Results. The MnSOD Val/Ala+Ala/Ala genotype was significantly associated with an increased risk of CAD compared to the Val/Val genotype (OR = 1.86, 95% CI = 1.15-3.01). This polymorphism was also associated with the severity of CAD of single and two vessel diseases. The corresponding ORs were 2.31 (95% CI = 1.32-4.03) and 1.92 (95% CI = 1.02-3.61), respectively. Among cigarette smokers, the harmful genetic effect of MnSOD Ala allele on CAD risk was much higher (OR = 2.23, 95% CI = 1.02-4.88). However, the interaction between MnSOD genotype and cigarette smoking on CAD risk was not significant. No significant association between CAT and GPx1 polymorphisms and CAD risk was observed. Conclusion. Our results suggest that MnSOD polymorphism is an independent risk factor for susceptibility to CAD in the Chinese population.

Associations between the phenotype and genotype of MnSOD and catalase in periodontal disease

“…In addition, the small sample size derived from low allelic frequency is a major limitation of this study. The less-frequent variant of the catalase gene in this study was similar to that in other Asian countries, such as Korea and China [62, 63]. Other factors, including dietary intake, the nutritional status, and dental care, that were not accurately measured in this study need to be further accounted for in future studies.…”

Endogenous SOD2 (Superoxide Dismutase) Regulates Platelet-Dependent Thrombin Generation and Thrombosis During Aging

“…33 This polymorphism is present at high frequency among certain ethnic groups, including 45% of people with African ancestry where it is associated with increased vascular complications in sickle cell disease. 34,35 This polymorphism and some others related to decreased SOD2 activity also have been linked to age-associated cardiovascular disease in several other ethnic groups 36–39 ; therefore, these findings could also be relevant to cardiovascular diseases in the general aging population. Hence, targeted therapies to increase platelet mitochondrial antioxidant capacity may have the potential to protect from aging-associated platelet activation, thrombosis, and their cardiovascular consequences.…”

A Preliminary Mini-Review on the Relations Between Lipofuscin, Aging and the Oxidative Stress Status - the Possible Implications of Gut Functionality

“…Some SNPs in antioxidant genes have been reported to impaired antioxidants in several diseases like obesity [41], inflammatory bowel disease [42], Hypertension 'silent killer' which is considered to be a risk factor for cardiovascular disease and kidney failure, coronary artery disease [43]- [45], Prostate Cancer [46] which older people are more likely to have it [47], the obstructive pulmonary disease [48]which could be considered a disease of accelerated aging [49], [50].…”