Streptonigrin-induced deoxyribose degradation: inhibition by superoxide dismutase, hydroxyl radical scavengers and iron chelators.
The aminoquinone antitumour antibiotic streptonigrin stimulates deoxyribose degradation in cell-free systems. This degradation is dependent both on reduction of the drug to a semiquinone and on traces of molecular oxygen in the reaction. Inhibition by a variety of hydroxyl radical scavengers and by catalase implicates a radical species with properties similar to the hydroxyl radical. Iron salts appear to play some part in radical formation as DETAPAC and desferrioxamine partly inhibit. Deoxyribose degradation under conditions of low oxygen concentration is strongly inhibited by superoxide dismutase.
D002374:Catalase / Q000494:pharmacology; D002614:Chelating Agents / Q000494:pharmacology*; D003855:Deoxyribose / Q000378:metabolism*; D006878:Hydroxides; D017665:Hydroxyl Radical; D007501:Iron / Q000378:metabolism*; D013308:Streptonigrin / Q000494:pharmacology*; D013482:Superoxide Dismutase / Q000494:pharmacology*; D014969:Xanthine Oxidase / Q000494:pharmacology
D002614:Chelating Agents; D006878:Hydroxides; D013308:Streptonigrin; D017665:Hydroxyl Radical; D003855:Deoxyribose; D007501:Iron; D002374:Catalase; D013482:Superoxide Dismutase; D014969:Xanthine Oxidase