TY - JOUR
T1 - Association between Polymorphisms of Antioxidant Gene (MnSOD, CAT, and GPx1) and Risk of Coronary Artery Disease
AU - Yeh, Hseng Long
AU - Kuo, Li Tang
AU - Sung, Fung Chang
AU - Yeh, Chih Ching
N1 - Publisher Copyright:
© 2018 Hseng-Long Yeh et al.
PY - 2018/1/1
Y1 - 2018/1/1
N2 - 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.
AB - 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.
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U2 - 10.1155/2018/5086869
DO - 10.1155/2018/5086869
M3 - Article
AN - SCOPUS:85053406884
SN - 2314-6133
VL - 2018
JO - BioMed Research International
JF - BioMed Research International
M1 - 5086869
ER -