2.1 OXIDATIVE STRESS The term oxidative stress is often used to imply a condition in which cells are exposed to excessive levels of molecular oxygen or derivatives oxygen chemicals called reactive oxygen species; (Kojda et al., 1999). This occurs when oxygen molecules are reduced to various subunits such as water, producing superoxide anion radical, 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 in blood vessels are superoxides. Superoxides are formed from the remains of reduced oxygen which is catalyzed by two enzymes which are NADPH oxidase and xanthine oxidase (Taniyama et al., 2003). Superoxides are able to act on different cells but can produce ROS by reacting with other substances, for example superoxides can react with nitric oxide to produce peroxynitrite which is potentially deleterious for ROS (Helmut, 1997). This occurs through the use of the enzyme superoxide dismutase, through the use of this enzyme a production of stable ROS such as hydrogen peroxide (H2O2) is formed which is then broken down into water (H2O) and oxygen (O2), this occurs in all types of vascular cells (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 muscle cells both endothelial and vascular smooth membranes are oxidase-bound, 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… half of the article… migration and proliferation of smooth muscle cells involved in inflammatory lesions. These help to further thicken the artery by slow dilation, this is called “remodelling”. Monocyte-derived macrophages and specific T lymphocyte subtypes are primarily associated with the inflammatory response (Russell, 1997). Normal permeability of the endothelium is mediated by nitric oxide. Therefore an imbalance in this would lead to an increase in endothelial permeability and therefore to the formation of atherosclerotic lesions. At the beginning the fatty streaks consist of monocytes made up of lipids and macrophages together with T lymphocytes and this combines with smooth muscle cells in later stages. This leads to the formation of foam cells that are stimulated by macrophage-stimulating factors, tumor necrosis factors, and oxidized low-density lipoproteins (Russell, 1997).