Abstract

Abstract H 2 O 2 , a product of the aerobic autoxidation of 6-hydroxydopamine, is also consumed as a reactant, contributing progressively more to the oxidation as the concentration of O 2 becomes limiting H 2 O 2 is a less effective oxidant than O 2 , since the anaerobic peroxidatic oxidation of 6-hydrodopamine is slower than the aerobic oxidation by three orders of magnitude. The anaerobic peroxidation was inhibited by the hydroxyl scavengers mannitol (13–40%), glucose (41–62%) and benzoate (15–100%), implying a catalytic role for . OH. -9e strongly inhibitory action of desferrioxamine (76–91%), regardless of which other scavengers were present, suggests a specific role for iron in the reaction, despite the use of Chelex 100-treated buffers. Further addition of diethylenetriaminepentaacetate (DTPA), benzoate or formate to the desferrioxamine-treated reactions resulted in complete inhibition. In contrast, the presence of DTPA alone, accelerated the reaction by 160%. This acceleration is in part due to stimulation by DTPA of production of . OH (by Fenton-type reactions), since it was partially prevented by the hydroxyl scavengers benzoate (32% inhibition) and glucose (41%). Thus, DTPA inhibits the participation of metals other than iron, but potentiates the catalytic role of iron, in the reduction of hydrogen peroxide. The semidehydromannitol radical can reduce the DTPA-Fe 3+ chelate directly, since mannitol further accelerated the DTPA-stimulated peroxidation (by 55%). Superoxide dismutase also accelerated the reaction (by 57–84%). This activation was seen regardless of which other scavengers were present. These effects are explained in terms of potentiating or moderating interactions among the reactive intermediates which propagate the overall reaction.

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