It is now recognized that oxidation of low-density lipoprotein (LDL) is a key event in the development of atherosclerosis (1). In vivo, oxidation is believed to occur primarily in the arterial wall. In early atherosclerotic lesions oxidation may be initiated by enzymes, including myeloperoxidase and 15-lipoxygenase, or by reactive nitrogen species, while in more advanced lesions transition metals including copper play a role (2). Oxidized LDL has a number of atherogenic properties (3). It is taken up via the macrophage scavenger receptor and promotes the formation of foam cells. It is chemotatic for circulating monocytes and inhibits the migration of tissue macrophages out of the arterial wall. In addition, oxidized LDL promotes platelet aggregation, is directly toxic to cells in the arterial wall, promotes the synthesis of a range of cytokines and growth factors, and inhibits nitric oxide mediated arterial dilation.