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American Journal of Clinical Nutrition, Vol 54, 1125S-1128S, Copyright © 1991 by The American Society for Clinical Nutrition, Inc

REVIEW ARTICLES

Ascorbic acid and oxidative inactivation of proteins

ER Stadtman
Laboratory of Biochemistry, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD 20892.

A number of active oxygen species are likely implicated in the etiology or manifestation of several pathological conditions, including aging, arthritis, carcinogenesis, atherosclerosis, and muscular dystrophy. Ascorbate plays a key role in protecting cells against oxidative damage. Paradoxically, in the presence of Fe3+ or Cu2+, ascorbate can promote the generation of the same reactive oxygen species (.OH, O2-, H2O2, and ferryl ion) it is known to destroy. This prooxidant activity derives from the ability of ascorbate to reduce Fe3+ or Cu2+ to Fe2+ or Cu+, respectively, and to reduce O2 to O2-. and H2O2. Damage to nucleic acid and proteins results from the binding of either Fe2+ or Cu+ to metal binding sites on these macromolecules followed by reaction of the metal complexes with H2O2; this leads to the production of active oxygen species that attack functional groups at or near the metal binding sites.


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I. Toth, J. T. Rogers, J. A. McPhee, S. M. Elliott, S. L. Abramson, and K. R. Bridges
Ascorbic Acid Enhances Iron-induced Ferritin Translation in Human Leukemia and Hepatoma Cells
J. Biol. Chem., February 10, 1995; 270(6): 2846 - 2852.
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Copyright © 1991 by The American Society for Nutrition