Antioxidants and atherosclerosis: A current assessment

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Abstract
Numerous recently published studies demonstrate that, once altered by free radical oxidation, plasma lipoproteins undergo dramatic change, both in the manner in which they can interact with cells and in the ways in which they influence cell function. For example, with increasing degrees of oxidation, low‐density lipoprotein (LDL) will cease to be recognizable by the LDL receptor and ultimately can become a ligand for “scavenger” receptors on macrophages. Gene expression and production of certain cytokines and growth factors can be modified through the interaction of oxidized LDL with the cell sources of these potent cell regulators. These discoveries have stimulated the formulation of hypotheses of roles played in vivo by oxidized lipoproteins or their various oxidized lipid moieties in cellular regulation and in various disease processes. Among the more detailed of these hypotheses is a putative sequence in which LDL becomes oxidized and subsequently participates in the various facets of atherosclerotic lesion development, including monocyte recruitment, foam cell formation, vascular cell injury, and cellular proliferation. The evidence supporting this scenario makes a compelling story, one that is fed by reports that certain antioxidants favorably alter the course of vascular lesion development. However, other studies suggest that antioxidants do not inhibit lesion progression or that any alleviation is secondary to lipid lowering. This brief accounting examines some of the more recent studies dealing specifically with the effects of antioxidants on atherosclerosis.