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Absence of EC-SOD does not promote atherogenesis in mice: have we lost yet another player?

A convincing body of cell culture, animal, and epidemiological studies have provided support and plausible biological mechanisms of a role for lipid oxidation in atherogenesis.1,2 Oxidized structures associated with lipoproteins, primarily LDL, have been shown to be abundant in atherosclerotic plaques.3 The observation that cultured macrophages take up oxidized LDL through a family of scavenger receptors, receptors that appear to be part of a more general “cleaning up” function of the immune system, provides a good explanation for the formation of foam cells in plaques. The generation of cytotoxic and immunogenic structures associated with oxidation of lipoprotein lipids offers an apparent cause of the inflammatory activity in the arterial intima that characterizes almost all stages of atherosclerosis.4 A large majority of experimental animal studies show that antioxidants inhibit the development of atherosclerosis.5 Epidemiological data suggest that a low intake of antioxidant vitamins is associated with an increased risk of developing cardiovascular disease.6 With all this knowledge at hand, it is …