Biotechnology & Biotechnological Equipment
ISSN: 1310-2818 (Print) 1314-3530 (Online) Journal homepage: http://www.tandfonline.com/loi/tbeq20
The Role of Endothelial Nitric Oxide Synthase Gene Polymorphism in Clinically Classified Patients with Coronary Artery Disease D.U. Cakir & N. Mete To cite this article: D.U. Cakir & N. Mete (2010) The Role of Endothelial Nitric Oxide Synthase Gene Polymorphism in Clinically Classified Patients with Coronary Artery Disease, Biotechnology & Biotechnological Equipment, 24:4, 2117-2121, DOI: 10.2478/V10133-010-0083-6 To link to this article: https://doi.org/10.2478/V10133-010-0083-6
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Published online: 15 Apr 2014.
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Article
DOI: 10.2478/v10133-010-0083-6
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THE ROLE OF ENDOTHELIAL NITRIC OXIDE SYNTHASE GENE POLYMORPHISM IN CLINICALLY CLASSIFIED PATIENTS WITH CORONARY ARTERY DISEASE D.U. Cakir1, N. Mete2 OnsekizMart University, Faculty of Medicine, Department of Clinical Biochemistry, Canakkale, Turkey 2 Dicle University, Faculty of Medicine, Department of Biochemistry, Diyarbakir, Turkey Correspondence to: Dilek Ulker Cakir E-mail:
[email protected],
[email protected]
1
ABSTRACT
The aim of the study was to investigate the relationship of eNOS (4. intron 27bp) polymorphism in clinically classified patients with coronary artery disease (CAD) in Turkish population. PCR and restriction fragment length polymorphism analysis were used to detect the variant of the eNOS gene in 74 patients with CAD and 20 healthy controls. The CAD group was separated into 3 clinical groups depending on angiography criteria and clinical form designation: 1st Group Myocardial infarction (MI) (n:20); 2nd Group Unstable Angina Pectoris (UAP) (n:18); 3rd Group Stable Angina Pectoris (SAP) (n:36). When a and b allele frequencies in the CAD and control groups were compared, no statistically significant difference was found. No significant difference was observed in the 4. intron 27 bp variants of the eNOS gene when CAD patients were compared without distinguishing them clinically from the control group. When we assessed CAD patients classified according to their clinical form, no significant difference was determined in allele frequencies and genotype distribution in the subgroups except for subgroup SAP. When we compared SAP patients with the other subgroups and with the control group, it was found that there was a significant increase in the ab genotype and the a allele frequency, and a decrease in the bb genotype (p
