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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Sociedad de Biología de Chile
2016
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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 |
work_keys_str_mv |
AT souidenyosra mnsodandgpx1polymorphismrelationshipwithcoronaryheartdiseaseriskandseverity AT malloulihela mnsodandgpx1polymorphismrelationshipwithcoronaryheartdiseaseriskandseverity AT meskhisalah mnsodandgpx1polymorphismrelationshipwithcoronaryheartdiseaseriskandseverity AT chaabouniyassine mnsodandgpx1polymorphismrelationshipwithcoronaryheartdiseaseriskandseverity AT rebaiahmed mnsodandgpx1polymorphismrelationshipwithcoronaryheartdiseaseriskandseverity AT cheourfoued mnsodandgpx1polymorphismrelationshipwithcoronaryheartdiseaseriskandseverity AT mahdouanikacem mnsodandgpx1polymorphismrelationshipwithcoronaryheartdiseaseriskandseverity |
_version_ |
1718441551999270912 |