Abstract

Atherosclerosis is a major source of mortality, being the underlying cause for most cases of cardiovascular diseases such as ischemic heart disease and cerebrovascular disease. Reactive oxygen species (ROS) can regulate several cellular processes, having a key role in the homeostasis of the vascular wall. There is compelling evidence pointing to ROS as important factors for the development of atherosclerosis. Many of the proatherogenic actions of ROS occur through the generation of oxidized LDL. Also, ROS can contribute to the development of endothelial dysfunction through the consumption of nitric oxide and generation of peroxynitrite. Endothelial dysfunction constitutes an early feature of atherogenesis, preceding the alterations that later perpetuate the lesion formation. Atherogenesis includes several processes, such as accumulation and oxidation of LDL in the subendothelial space, expression of adhesion molecules and chemoattractant mediators, adhesion of monocytes, generation of foam cells, production of inflammatory mediators and proliferation of certain cell types. Since most of these processes can be modulated by ROS, supplementation with antioxidants is expected to exert some degree of protection against atherosclerosis. Several lines of evidence support a role of antioxidant supplementation in attenuating some of the processes involved in atherogenesis. However, clinical trials have failed to consistently prove a protective effect. The potential role of antioxidant supplementation against atherosclerosis development or progression remains an open question.