The earliest events in the development of the pathology are endothelial dysfunction and oxidative stress in the vascular cell wall, activation of inflammatory cells, and migration of vascular smooth muscle cells to the intima with the modification of the extracellular matrix, leading to the artery remodelling. Development of atherosclerosis is thought to be closely dependent upon increased oxidative stress, that is, an imbalance between reactive oxygen species (ROS) generation (chiefly superoxide an- ions, hydrogen peroxide, hydroxyl radicals) and natural cell antioxi- dant capacity in favour of the former (Frei, 1994).