Association between Polymorphisms of Antioxidant Gene (MnSOD, CAT, and GPx1) and Risk of Coronary Artery Disease

Hseng Long Yeh, Li Tang Kuo, Fung Chang Sung, Chih Ching Yeh

Research output: Contribution to journalArticle

4 Citations (Scopus)

Abstract

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.

Original languageEnglish
Article number5086869
JournalBioMed Research International
Volume2018
DOIs
Publication statusPublished - Jan 1 2018

Fingerprint

Polymorphism
Catalase
Superoxide Dismutase
Coronary Artery Disease
Computer aided design
Antioxidants
Genes
Confidence Intervals
Odds Ratio
Genotype
Logistic Models
Tobacco Products
Coronary Stenosis
glutathione peroxidase GPX1
Coronary Angiography
Taiwan
Exercise Test
Mitochondria
Angiography
DNA Damage

ASJC Scopus subject areas

  • Biochemistry, Genetics and Molecular Biology(all)
  • Immunology and Microbiology(all)

Cite this

Association between Polymorphisms of Antioxidant Gene (MnSOD, CAT, and GPx1) and Risk of Coronary Artery Disease. / Yeh, Hseng Long; Kuo, Li Tang; Sung, Fung Chang; Yeh, Chih Ching.

In: BioMed Research International, Vol. 2018, 5086869, 01.01.2018.

Research output: Contribution to journalArticle

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abstract = "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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