ABSTRACT
I. OXIDATIVE STRESS AND ATHEROSCLEROSIS Atherosclerosis is the leading cause of morbidity and mortality among people with a Western world lifestyle. The early atherosclerotic lesion is characterized by foam cells derived from cholesterol-loaded macrophages (1,2). Most of the accumulated cholesterol in foam cells originates from plasma low-density lipoprotein (LDL), which is internalized into the cells by the LDL receptor. However, native LDL does not induce cellular cholesterol accumulation, because the LDL receptor activity is down-regulated by the cellular cholesterol content (3,4). LDL has to undergo some modifications, such as aggregation or oxidation, to be taken up by macrophages at an enhanced rate by the macrophage scavenger receptors pathway, which is not subjected to down-regulation by increased cellular cholesterol (5-7). The underlying mechanisms leading to the formation of atherosclerotic lesion are complicated and represent the outcome of multiple interactive processes. Several mechanisms for atherogenesis have evolved, all based on the fact that plasma LDL lipids give rise to the development of the atherosclerotic lesion (8,9).
