MnSOD and GPx1 polymorphism relationship with coronary heart disease risk and severity
BACKGROUND: 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...
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author | Yosra Souiden Hela Mallouli Salah Meskhi Yassine Chaabouni Ahmed Rebai Foued Chéour Kacem Mahdouani |
author_facet | Yosra Souiden Hela Mallouli Salah Meskhi Yassine Chaabouni Ahmed Rebai Foued Chéour Kacem Mahdouani |
author_sort | Yosra Souiden |
collection | DOAJ |
description | BACKGROUND: 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 METHODS: 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 RESULTS: 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 CONCLUSIONS: 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 |
first_indexed | 2024-04-14T02:39:33Z |
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issn | 0716-9760 |
language | English |
last_indexed | 2024-04-14T02:39:33Z |
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series | Biological Research |
spelling | doaj.art-e568637b182646c89c5c58908f030d742022-12-22T02:17:12ZengBMCBiological Research0716-976049011210.1186/s40659-016-0083-6S0716-97602016000100022MnSOD and GPx1 polymorphism relationship with coronary heart disease risk and severityYosra Souiden0Hela Mallouli1Salah Meskhi2Yassine Chaabouni3Ahmed Rebai4Foued Chéour5Kacem Mahdouani6Hospital of Ibn Eljazzar of KairouanHospital of Ibn Eljazzar of KairouanHospital of Ibn Eljazzar of KairouanHospital of Ibn Eljazzar of KairouanCenter of Biotechnology of SfaxInstitute of Applied Biology of MedenineHospital of Ibn Eljazzar of KairouanBACKGROUND: 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 METHODS: 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 RESULTS: 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 CONCLUSIONS: 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 progressionhttp://www.scielo.cl/scielo.php?script=sci_arttext&pid=S0716-97602016000100022&lng=en&tlng=enGenetic polymorphismCoronary heart diseaseSOD activityGPx activityTotal antioxidant statusAtherosclerosis |
spellingShingle | Yosra Souiden Hela Mallouli Salah Meskhi Yassine Chaabouni Ahmed Rebai Foued Chéour Kacem Mahdouani MnSOD and GPx1 polymorphism relationship with coronary heart disease risk and severity Biological Research Genetic polymorphism Coronary heart disease SOD activity GPx activity Total antioxidant status Atherosclerosis |
title | MnSOD and GPx1 polymorphism relationship with coronary heart disease risk and severity |
title_full | MnSOD and GPx1 polymorphism relationship with coronary heart disease risk and severity |
title_fullStr | MnSOD and GPx1 polymorphism relationship with coronary heart disease risk and severity |
title_full_unstemmed | MnSOD and GPx1 polymorphism relationship with coronary heart disease risk and severity |
title_short | MnSOD and GPx1 polymorphism relationship with coronary heart disease risk and severity |
title_sort | mnsod and gpx1 polymorphism relationship with coronary heart disease risk and severity |
topic | Genetic polymorphism Coronary heart disease SOD activity GPx activity Total antioxidant status Atherosclerosis |
url | http://www.scielo.cl/scielo.php?script=sci_arttext&pid=S0716-97602016000100022&lng=en&tlng=en |
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