title: Virus-inactivating effect of D-isoascorbic acid.
abstract: The effect of D-isoascorbic acid, an epimer of L-ascorbic acid, on viruses was investigated using a wide variety of bacterial viruses (phages) as model systems. D-isoascorbic acid exerted an inactivating effect on all phages examined. The reaction mechanism of virus inactivation by D-isoascorbic acid was investigated using phage J1 as a model system. Bubbling oxygen through the reaction mixture and the addition of H2O2 or transition metal ions into the reaction mixture enhanced the phage inactivation by D-isoascorbic acid. In contrast, nitrogen bubbling and the addition of reducing agents, chelating agents or radical scavengers prevented phage inactivation. Experiments using specific radical scavengers, superoxide dismutase or catalase showed that OH. could be mainly responsible for phage inactivation by D-isoascorbic acid. These findings are similar to those obtained with L-ascorbic acid, and indicate that phage-inactivating activity is independent of the stereoisomerism with inversion of the hydroxyl group at carbon 5 of ascorbic acids.
mesh_terms: D001205:Ascorbic Acid / Q000494:pharmacology*; D001435:Bacteriophages / Q000187:drug effects*; D002374:Catalase / Q000494:pharmacology; D004492:Edetic Acid / Q000494:pharmacology; D005609:Free Radicals; D006878:Hydroxides / Q000494:pharmacology; D017665:Hydroxyl Radical; D008670:Metals / Q000494:pharmacology; D010084:Oxidation-Reduction; D010100:Oxygen / Q000494:pharmacology; D013482:Superoxide Dismutase / Q000494:pharmacology
chemical_list: D005609:Free Radicals; D006878:Hydroxides; D008670:Metals; C005056:isoascorbic acid; D017665:Hydroxyl Radical; D004492:Edetic Acid; D002374:Catalase; D013482:Superoxide Dismutase; D001205:Ascorbic Acid; D010100:Oxygen