ABSTRACT
Cardiovascular diseases (CVD) have become a major worldwide cause of morbidity and mortality (Teo et al. 2013). CVD are a result of genetic and environmental factors such as smoking, obesity, lack of exercise, overweight, high blood pressure, elevated blood cholesterol levels, Insulin Resistance (IR) and diabetes (Potvin et al. 2000, Lusis et al. 2008). The physiopathological mechanism implicates an infl ammatory process that might contribute to the endothelial dysfunction (Zhang 2008). Tumor Necrosis Factor-C (TNF-C), IL-6 the pro-coagulant Plasminogen Activator Inhibitor-1 (PAI) and macrophages contribute to CVD (Matsuzawa 2005). Oxidative stress has been proposed to be a potential pathogenic mechanism linking obesity and IR with the development of the CVD where an oxidative stress occurs in the vessel wall, resulting in a pathogenic feature of vascular atherosclerosis (Van Gaal et al. 2006). Increased oxidative stress is a primary cause of endothelial dysfunction by reducing Nitric Oxide (NO.) production, promoting infl ammation, and through its involvement in the activation of intracellular signal transduction pathways infl uencing ion channel activation, intercellular communication, and gene expression to, eventually, produce the cessation of cell division and premature senescence (Elnakish et al. 2013, Victor 2013).
