Oxidative stress by free radicals or reactive oxygen species (ROS) is often associated with aging and the development of numerous chronic diseases, including cancer, multiple sclerosis, Parkinson’s disease, autoimmune disease, and senile dementia (Ali et al. 2008; Caillet et al. 2011). Furthermore, stress, physical damage, viral infection, and cytotoxic or carcinogenic compounds resulting from chemical or biological aggression may cause the peroxidation of cell membrane lipids and the liberation of toxic substances, such as free radicals (Aruoma 1998). Indeed, oxidative stress, a major contributor to cardiovascular diseases (CVDs), is associated with lipid peroxidation in arterial macrophages and in lipoproteins. Oxidized low-density lipoprotein (Ox-LDL) has been shown to be atherogenic (Anoosh, Mojtab, and Fatemeh 2010). The simultaneous production of nitric oxide (•NO) and superoxide anions O2
i−( ) by vascular cells may explain peroxynitrite (ONOO−) formation within the vascular wall. Peroxynitrite-modied LDL binds to scavenger receptors, leading to accumulation of the cholesteryl esters involved in the production of atherosclerotic lesions (Thomas, Davies, and Stocker 1998).