title: Ascorbic acid and oxidative inactivation of proteins.
abstract: 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.
authors.affiliation: Laboratory of Biochemistry, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD 20892.
authors.forename: E R
authors.initials: ER
authors.lastname: Stadtman
mesh_terms: D000975:Antioxidants / Q000494:pharmacology; D001205:Ascorbic Acid / Q000494:pharmacology*; D002384:Catalysis; D006801:Humans; D007477:Ions; D008670:Metals / Q000378:metabolism; D010084:Oxidation-Reduction; D011506:Proteins / Q000378:metabolism
chemical_list: D000975:Antioxidants; D007477:Ions; D008670:Metals; D011506:Proteins; D001205:Ascorbic Acid