Atherosclerosis is the major case of morbidity and mortality in the world today, accounting for half of death in world. The origin of atherosclerosis is attributed to diets rich in fats, tobacco, alcohol consumption and lack of physical activity along with genetic factors like increased insulin resistance, decreased beta cell function, diabetes mellitus, obesity, and elevated levels of LDL, triglycerides, with reduced HDL Cholesterol.

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The events responsible for generation of atheroma include damage of endothelial cell and formation of macrophages engorged foam cells leading to endothelial injury and infiltration of circulating lipoproteins and monocytes, the subsequent chemotaxis and phenotypic changes transform macrophages into foam cells. Atherosclerosis is greatly enhanced in patients with familial Hypercholesterolemia who lack LDL receptors, which are the scavenging receptors present on macrophages and endothelial cells (Ramprasad, 1995).

The next phase involves foam cell migration into the sub endothelial region, which slowly develops there and when stressed can synthesis platelet derived growth factor, which is a powerful chemotactic agent and vasoconstrictor. The other autocrine and paracrine factors present in platelets and atheroma cells include endothelial growth factor interleukin-1, fibroblast growth factor and serotonin, which are mitogenic towards vascular monocytes.

Free radicals damage compounds of all biochemical classes and they have been implicated in causation of several diseases such as liver cirrhosis, atherosclerosis, cancer etc. In in-vivo and health there is a balance between free radical generation and activity of preventive antioxidants like catalase, superoxide dismutase, glutathione peroxidase, ascorbic acid, vitamin E etc. (Jose and Kuttan,1995).

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