期刊论文详细信息
Biological research: BR
MnSOD and GPx1 polymorphism relationship with coronary heart disease risk and severity
Ahmed Rebai1  Hela Mallouli2  Yassine Chaabouni2  Yosra Souiden3  Foued Ché3  Salah Meskhi3  our4 
[1] Department of Cardiovascular, Hospital of Ibn Eljazzar of Kairouan, Kairouan, Tunisia;Laboratory of Analysis, Treatment and Valorization of the pollutants of the environment and products, Faculty of Pharmacy, Monastir, Tunisia;Laboratory of Biochemistry and Molecular Biology, Hospital of Ibn Eljazzar of Kairouan, Kairouan, Tunisia;Laboratory of Molecular and Cellular Screening Processes, Center of Biotechnology of Sfax, Sfax, Tunisia
关键词: Genetic polymorphism;    Coronary heart disease;    SOD activity;    GPx activity;    Total antioxidant status;    Atherosclerosis;   
DOI  :  10.1186/s40659-016-0083-6
学科分类:生物科学(综合)
来源: BioMed Central
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【 摘 要 】

Disturbance of the equilibrium between reactive oxygen species (ROS) and anti-oxidants (AOX) has been implicated in various diseases, including atherosclerosis, the most common pathologic process underlying coronary heart disease (CHD). Thus, the defense systems against ROS are critical protecting blood vessel walls against oxidative damage. In this study, we investigate whether Ala16Val MnSOD and Pro198Leu GPx polymorphisms are associated with CHD susceptibility and/or severity. Both polymorphisms were genotyped in a sample of 203 controls and 164 patients. CHD risk and severity, antioxidant status (enzymatic and/or non enzymatic) and biochemical parameters were assessed and analysed by genotype. A significant association of MnSOD variant to CHD risk was revealed in males. Males harboring the Val/Val genotype were approximately at twofold increased risk of CHD compared to controls (Ala carriers vs Val/Val, adjusted OR 1.89; 95 % CI 1.18‒3.42, p = 0.03). Significant decreases in SOD activity and total antioxidant status (TAS) were observed in Val carriers and by CHD status. Whereas, no association of GPx variant genotype (Leu/Leu) and activity to cardiopathy events was discerned. CHD severity, as demonstrated by the number of vessel stenosis, was associated with significantly higher frequency of Val allele and LDL levels in CHD subjects. Our results showed a lack of association of Pro198Leu GPx polymorphism to CHD risk and severity. However, they suggest that Ala16Val MnSOD polymorphism and decreased antioxidant defences are likely contributed to CHD risk in Tunisian men. Furthermore, the Val encoding MnSOD allele and decreased SOD activity were significantly correlated with CHD stenosis progression.

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