2.1 OXIDATIVE STRESSThe term oxidative stress is often used to imply a condition in which cells are exposed to excessive levels of molecular oxygen or chemical derivatives of oxygen called reactive oxygen species. ; (Kojda et al., 1999). This occurs when oxygen molecules are reduced to various subunits such as water, producing superoxide anion radicals, hydrogen peroxide, and hydrogen radicals (Geller, DA et al. 1993). On the other hand, ROS have different effects on individual blood vessels and also play a very important role on the physiological and pathological aspects of the vessels. The main ROS present in blood vessels are superoxides. Superoxides are formed from the remains of reduced oxygen which are catalyzed by two enzymes which are NADPH oxidase and xanthine oxidase (Taniyama et al., 2003). Superoxides are capable of acting on different cells, but they can produce ROS by reacting with other substances, for example superoxides can react with nitric oxide to produce peroxynitrite which is potentially harmful to ROS (Helmut, 1997). This occurs through the use of the enzyme superoxide dismutase, through the use of this enzyme a stable ROS production is formed, such as hydrogen peroxide (H2O2), which is then broken down into water (H2O ) and oxygen (O2). vascular cell types (Taniyama et al., 2003)Figure 1: Formation of free radicals in biological systems (Vet med, 2014)2.2 ROLE OF REACTIVE OXYGEN SPECIESThe main source of reactive oxygen species in Endothelial and vascular smooth muscle cells are membrane-bound oxidases, which use NADH and NADPH as substrates (Kojda et al., 1999). Impaired endothelium-dependent vasorelaxation: ROS play a very important role in endothelium dysfunction and ...... middle of article ...... migration and proliferation of smooth muscle cells involved in inflammatory lesions. These help to further thicken the artery through slow dilation, this is called “remodeling”. Monocyte-derived macrophages and specific T cell subtypes are primarily associated with the inflammatory response (Russell, 1997). Normal endothelial permeability is mediated by nitric oxide. Thus, an imbalance would cause an increase in endothelial permeability and thus lead to the formation of atherosclerotic lesions. Initially, fatty streaks consist of monocytes made of lipids and macrophages as well as T lymphocytes, which then combine with smooth muscle cells. This leads to foam cell formation which is stimulated by macrophage-stimulating factors, tumor necrosis factors and oxidized low-density lipoproteins (Russell, 1997).