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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Autores principales: Souiden,Yosra, Mallouli,Hela, Meskhi,Salah, Chaabouni,Yassine, Rebai,Ahmed, Chéour,Foued, Mahdouani,Kacem
Lenguaje:English
Publicado: Sociedad de Biología de Chile 2016
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Acceso en línea:http://www.scielo.cl/scielo.php?script=sci_arttext&pid=S0716-97602016000100022
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spelling oai:scielo:S0716-976020160001000222016-12-01MnSOD and GPx1 polymorphism relationship with coronary heart disease risk and severitySouiden,YosraMallouli,HelaMeskhi,SalahChaabouni,YassineRebai,AhmedChéour,FouedMahdouani,Kacem Genetic polymorphism Coronary heart disease SOD activity GPx activity Total antioxidant status Atherosclerosis 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 progressioninfo:eu-repo/semantics/openAccessSociedad de Biología de ChileBiological Research v.49 20162016-01-01text/htmlhttp://www.scielo.cl/scielo.php?script=sci_arttext&pid=S0716-97602016000100022en10.1186/s40659-016-0083-6
institution Scielo Chile
collection Scielo Chile
language English
topic Genetic polymorphism
Coronary heart disease
SOD activity
GPx activity
Total antioxidant status
Atherosclerosis
spellingShingle Genetic polymorphism
Coronary heart disease
SOD activity
GPx activity
Total antioxidant status
Atherosclerosis
Souiden,Yosra
Mallouli,Hela
Meskhi,Salah
Chaabouni,Yassine
Rebai,Ahmed
Chéour,Foued
Mahdouani,Kacem
MnSOD and GPx1 polymorphism relationship with coronary heart disease risk and severity
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
author Souiden,Yosra
Mallouli,Hela
Meskhi,Salah
Chaabouni,Yassine
Rebai,Ahmed
Chéour,Foued
Mahdouani,Kacem
author_facet Souiden,Yosra
Mallouli,Hela
Meskhi,Salah
Chaabouni,Yassine
Rebai,Ahmed
Chéour,Foued
Mahdouani,Kacem
author_sort Souiden,Yosra
title 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_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_sort mnsod and gpx1 polymorphism relationship with coronary heart disease risk and severity
publisher Sociedad de Biología de Chile
publishDate 2016
url http://www.scielo.cl/scielo.php?script=sci_arttext&pid=S0716-97602016000100022
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