Association Assessment of Paraoxonase 1 Gene Polymorphism with Coronary Artery Disease in Golestan, Iran

authors:

avatar Samaneh Abdolahpour 1 , avatar Azam Bakhshandeh 1 , avatar Touraj Farazmandfar 1 , avatar Mehdi Rayatnavaz 1 , avatar Majid Shahbazi 1 , *

Medical Cellular and Molecular Research Center, Golestan University of Medical Sciences, Gorgan, Iran

how to cite: Abdolahpour S , Bakhshandeh A , Farazmandfar T , Rayatnavaz M , Shahbazi M . Association Assessment of Paraoxonase 1 Gene Polymorphism with Coronary Artery Disease in Golestan, Iran. Int Cardiovasc Res J. 2017;11(4):e61212. 

Abstract

Background: Cardiovascular disease (CVD) is the most common cause of mortality
and morbidity worldwide. Coronary artery disease (CAD) is the leading cause of CVD.
In CAD, atherosclerotic plaques lead to coronary artery stenosis, hereby impairing
myocardial blood and oxygen supply. The oxidative changes in LDL at the vascular
wall play a critical role in the development of atherosclerotic lesions. The paraoxonase 1
(PON1) enzyme present in the HDL surface is capable of destroying oxidized LDL and,
therefore has an antiatherogenic activity.
Objectives: This study was conducted to investigate the association of two functional
polymorphisms in PON1 gene with CAD in northern Iran.
Materials and Methods: This study was a case-control study with the case-base sampling
method for the control group. Genomic DNA was extracted from the peripheral blood
collected from 305 patients with CAD and 302 healthy controls. Two polymorphisms of
PON1(L55M)T > A and PON1(Q192R)A > G, for all samples were genotyped by Single-
Specific Primer-PCR. GraphPad6 software was used for statistical analysis.
Results: Logistic regression analysis showed that age, gender, smoking status, and
diabetes mellitus were significantly associated with CAD disease (P < 0.001). There was
a significant association between genotype A/A of PON1(L55M)T > A polymorphism
and CAD disease (P = 0.011). The results indicated that allele A in this SNP was also
significantly associated with the CAD disease (P = 0.005). Analysis of dominant genetic
model in PON1 (L55M)T > A showed that one copy of A is sufficient for increased risk
(P = 0.016).
Conclusions: Our findings, at least in the population of Golestan province, indicated
that the PON1(L55M) polymorphism might be associated with atherosclerotic disease.

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References

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