Endothelial nitric oxide synthase G894T gene polymorphism in Chilean subjects with coronary artery disease and controls
Abstract
Background: Nitric oxide (NO) from the endothelium, produced by oxidation of l-arginine to l-citruline for the action at the endothelial nitric oxide synthase (eNOS), is considered an important atheroprotective factor. The Glu298Asp (G894T) polymorphic variant of the eNOS gene has been implicated in the development of coronary artery disease (CAD). We investigated the association between occurrence of CAD documented by angiography and the G894T polymorphism of the NOS3 gene in Chilean individuals. Methods: A total of 112 unrelated patients with diagnosis of CAD and 72 controls were included in this study. G894T gene polymorphism was analyzed by polymerase chain reaction (PCR) and restriction fragment length polymorphism (RFLP). Results: The frequency of TT homozygous genotype for G894T polymorphism was 7% in CAD patients and 1% in the control group. However, the genotype distribution and allele frequencies were not significantly different between CAD and control subjects (P > 0.05). Moreover, the odds ratio for CAD associated with the T variant failed to reach statistical significance (OR = 1.5; 95% CI: 0.87-2.59, P > 0.05). Conclusion: These findings suggest that the G894T polymorphism of the eNOS gene was not associated with CAD in Chilean individuals. © 2006 Elsevier B.V. All rights reserved.
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Título según WOS: | Endothelial nitric oxide synthase G894T gene polymorphism in Chilean subjects with coronary artery disease and controls |
Título según SCOPUS: | Endothelial nitric oxide synthase G894T gene polymorphism in Chilean subjects with coronary artery disease and controls |
Título de la Revista: | CLINICA CHIMICA ACTA |
Volumen: | 371 |
Número: | 01-feb |
Editorial: | ELSEVIER SCIENCE BV |
Fecha de publicación: | 2006 |
Página de inicio: | 102 |
Página final: | 106 |
Idioma: | English |
URL: | http://linkinghub.elsevier.com/retrieve/pii/S0009898106001471 |
DOI: |
10.1016/j.cca.2006.02.030 |
Notas: | ISI, SCOPUS |