Ascorbate-dependent formation of hydroxyl radicals in the presence of iron chelates.
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1993-10-01
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The autoxidation of L-ascorbate on incubation in saline phosphate buffer (pH 7.4) is accompanied by hydroxyl radical (.OH) generation. The metal chelator EDTA showed significant inhibition of ascorbate autoxidation and ascorbate-dependent .OH release. On the other hand, Fe2+ (EDTA) greatly augmented both ascorbate autoxidation and ascorbate-dependent .OH production. The biological iron chelating compounds such as ATP, ADP, citrate and pyrophosphate suppressed both ascorbate autoxidation and ascorbate-mediated .OH production, thereby indicating that these compounds suppress the activating effect of iron. Ascorbate autoxidation and ascorbate-dependent .OH formation, stimulated by Fe2+ (EDTA) were significantly inhibited by .OH scavengers, namely mannitol, thiourea and sodium formate, as well as by catalase and to a lesser extent by bovine serum albumin, superoxide dismutase (native and heat denatured) and heat denatured catalase.
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Prabhu HR, Krishnamurthy S. Ascorbate-dependent formation of hydroxyl radicals in the presence of iron chelates. Indian Journal of Biochemistry & Biophysics. 1993 Oct; 30(5): 289-92