ABSTRACT
Vitamin C is an essential nutrient for humans and its deficiency has long been known to cause scurvy (1). Less well understood is the role vitamin C plays in preventing cardiovascular disease (CVD), the leading cause of mortality in the United States for over 50 years (2). As an antioxidant, vitamin C may protect lipids, particularly low density lipoproteins (LDL), from oxidation. Oxidized LDL may contribute to the development of atherosclerotic lesions through several mechanisms (3,4). The recruitment of monocytes to the vascular intima is increased by oxidized LDL and monocytes can develop into macrophages. Oxidized LDL are more readily taken up by macrophages than nonoxidized LDL, a process in which macrophages can be converted to foam cells with later progression to fatty streaks and plaques. Oxidized LDL inhibit macrophage motility, preventing macrophages from leaving the intima and facilitating continued uptake of oxidized LDL. Oxidized LDL are also cytotoxic, leading to cell death, endothelial loss and denudation of the artery. Some antioxidants can neutralize oxygen-derived free radicals through hydrogen donation, preventing the chain reaction in which LDL are oxidized (4,5). Vitamin C is the only antioxidant that has been shown to prevent the initiation of the oxidation chain reaction in lipids (6), trapping free radicals in the aqueous phase before they can diffuse into lipids such as LDL.
