, Volume 91, Issue 3, pp 349-352
Date: 24 Nov 2012

Endothelial nitric oxide synthase polymorphism G298T in association with oxidative DNA damage in coronary atherosclerosis

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Introduction

Heart disease has become a major public health problem in many developing countries and is the most important cause of mortality in India. There is an epidemiological transition of this degenerative disease with increase in prevalence of cardiovascular risk factors (Sukanta et al.2009). Coronary artery disease (CAD) is the most common form of heart disease (Sukanta et al.2009).

There is evidence that physiological and functional alterations in endothelial cells may play a pivotal role in progression of atherosclerotic lesions (De 2000). Nitric oxide (NO) is an important free radical mostly produced by endothelial cells. It plays an important role in vascular relaxation, and displays vasoprotective effects by scavenging superoxide radicals (Loscalzo and Welch 1995) and suppressing platelet aggregation, leucocyte adhesion and smooth muscle cell proliferation and signalling (Radomski et al.1887).

Generally NO is synthesized by endothelial nitric oxide synthase (eNOS) in vasculat

[Kumar R. G., Spurthi M. K., Kumar K. G., Sahu S. K. and Rani S. H. 2012 Endothelial nitric oxide synthase polymorphism G298T in association with oxidative DNA damage in coronary atherosclerosis. J. Genet. 91, xx–xx]