Epidemiologic studies have demonstrated an association betweenincreased intake of antioxidant vitamins such as vitamin E andvitamin C and reduced morbidity and mortality from coronaryartery disease. This association has been explained on the basisof the "oxidative-modification hypothesis" of atherosclerosis,which proposes that atherogenesis is initiated by oxidationof the lipids in low-density lipoprotein (LDL), also termedlipid peroxidation. As a corollary to this hypothesis, antioxidantsthat inhibit lipid peroxidation in LDL should limit atherosclerosisand its clinical manifestations, such as myocardial infarctionand stroke. In this review, we will evaluate the current literatureinvolving antioxidants and vascular . . . [Full Text of this Article]
Human Studies Linking Antioxidants with a Reduction in Cardiovascular Events
The Oxidative-Modification Hypothesis of Atherosclerosis
Relation between Resistance of LDL Particles to Oxidation and Atherosclerosis in Animals
Resistance of LDL to Oxidation in Humans
Inhibition of LDL Oxidation and Reduction in Coronary Events
Problems in Linking Increased Resistance of LDL to Oxidation with Inhibition of Atherosclerosis
Vascular Effects of Antioxidants Related to the Resistance of LDL to Oxidation
Reduced Cytotoxicity
Endothelium-Derived Nitric Oxide
Vascular Effects of Antioxidants Not Strictly Related to the Protection of LDL from Oxidation
Preservation of Endothelium-Derived Nitric Oxide Action
Inhibition of Leukocyte Adhesion
Reduction of Cellular Oxidative Injury
Inhibition of Platelet Activation and Smooth-Muscle Proliferation
Summary
Source Information
From the Evans Memorial Department of Medicine (M.N.D., B.F., J.A.V., J.F.K.) and the Whitaker Cardiovascular Institute (B.F., J.A.V., J.F.K.), Boston University School of Medicine, Boston.
Address reprint requests to Dr. Keaney at the Whitaker Cardiovascular Institute, Boston University School of Medicine, 80 E. Concord St., Rm. W507, Boston, MA 02118.
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