Abstract
Background and Objective: Reactive oxygen species (ROS) been cited as one of the major causes of atherosclerosis and coronary artery disease (CAD) 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 genetic polymorphisms and risk of CAD in Taiwan. Methods: We conducted a case-control study with 657 participants who received quantitative coronary angiography to assess CAD at a medical center. Individuals with at least one coronary artery diameter stenosis = 50% were defined as cases (n = 447) and the others as controls (n = 210). Polymorphisms of MnSOD (Ala-9Val), CAT (C-262T), and GPX1 (Pro198Leu) genes were determined by PCR-RFLP methods. Multivariate logistic regression model was used to calculate the odds ratios (ORs) and 95% confidence intervals ...
Highlights
Cardiovascular disease (CVD) is the leading cause of mortality worldwide
After controlling for covariates, the CAD risk was statistically significantly increased by Manganese superoxide dismutase (MnSOD) Val/Ala+Ala/Ala genotype (OR = 1.86, 95%confidence intervals (CIs) = 1.153.01), compared to MnSOD Val/Val genotype
The glutathione peroxidase-1 (GPx1) polymorphism was not associated with CAD risk
Summary
Cardiovascular disease (CVD) is the leading cause of mortality worldwide. Through large-scale epidemiologic studies, several conventional risk factors for CVDs have been identified for instance, cigarette smoking, hypertension, hyperlipidemia, diabetes mellitus, and obesity [3]. An intensified intervention strategy, treating multiple risk factors to target, brings about a 20 percent reduction in cardiovascular events in high risk individuals [4]. Some discovered that these well-known risk factors merely account for 50-80% of CVDs [5, 6] and still around 15-20% of myocardial infarction occurred in individuals lacking any of the traditional risks [5]. Further studies to investigate novel CVDs risk markers and thereby early recognizing preclinical disease are essential
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
