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Although little direct evidence for a causative role of \u2018oxidized LDL\u2019 in atherogenesis exists, several studies show that,\n                    <jats:italic>in vitro<\/jats:italic>\n                    , oxidized LDL exhibits potentially proatherogenic activities and lipoproteins isolated from atherosclerotic lesions are oxidized. As a consequence, the molecular mechanisms of LDL oxidation and the actions of \u03b1\u2010tocopherol (\u03b1\u2010TOH, vitamin E), the major lipid\u2010soluble lipoprotein anti\u2010oxidant, have been studied in detail. Based on the known antioxidant action of \u03b1\u2010TOH and epidemiological evidence, vitamin E is generally considered to be beneficial in coronary artery disease. However, intervention studies overall show a null effect of vitamin E on atherosclerosis. This confounding outcome can be rationalized by the recently discovered diverse role for \u03b1\u2010TOH in lipoprotein oxidation; that is, \u03b1\u2010TOH displays neutral, anti\u2010, or, indeed, prooxidant activity under various conditions. This review describes the latter, novel action of \u03b1\u2010TOH, termed tocopherol\u2010mediated peroxidation, and discusses the benefits of vitamin E supplementation alone or together with other antioxidants that work in concert with \u03b1\u2010TOH in ameliorating lipoprotein lipid peroxidation in the artery wall and, hence, atherosclerosis.\u2014Upston, J. M., Terentis, A. C., Stocker, R. 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