TitlePotential antiatherogenic mechanisms of ascorbate (vitamin C) and alpha-tocopherol (vitamin E).
Publication TypeJournal Article
Year of Publication2000
AuthorsCarr AC, Zhu BZ, Frei B
JournalCirc Res
Date Published2000 Sep 01
KeywordsAnimals, Antioxidants, Arteriosclerosis, Ascorbic Acid, Cell Adhesion, Cells, Cultured, Disease Models, Animal, E-Selectin, Endothelium, Vascular, Enzyme Activation, Humans, Leukocytes, Lipid Peroxidation, Lipoproteins, LDL, Nitric Oxide, Oxidation-Reduction, Protein Kinase C, Reactive Oxygen Species, Vasodilation, Vitamin E

The premise that oxidative stress, among several other factors, plays an important role in atherogenesis implies that the development and progression of atherosclerosis can be inhibited by antioxidants. In this minireview we discuss several mechanisms by which the antioxidants ascorbate (vitamin C) and alpha-tocopherol (vitamin E) may protect against atherosclerosis. These mechanisms include inhibition of LDL oxidation and inhibition of leukocyte adhesion to the endothelium and vascular endothelial dysfunction. Overall, ascorbate appears to be more effective than alpha-tocopherol in mitigating these pathophysiological processes, most likely as a result of its abilities to effectively scavenge a wide range of reactive oxygen and nitrogen species and to regenerate alpha-tocopherol, and possibly tetrahydrobiopterin, from its radical species. In contrast, alpha-tocopherol can act either as an antioxidant or a pro-oxidant to inhibit or facilitate, respectively, lipid peroxidation in LDL. However, this pro-oxidant activity of alpha-tocopherol is prevented by ascorbate acting as a coantioxidant. Therefore, an optimum vitamin C intake or body status may help protect against atherosclerosis and its clinical sequelae, whereas vitamin E may only be effective in combination with vitamin C.

Alternate JournalCirc. Res.
PubMed ID10969031
Grant ListAT-00066 / AT / NCCIH NIH HHS / United States
HL-56170 / HL / NHLBI NIH HHS / United States