Abstract

The pro-oxidant effects of hydroxyl radical (-OH, ferrous ammonium sulfate/Fe 2+) or nitric oxide (NO-, S-nitroso-N-acetylpenicillamine/SNAP) generating compounds were studied in rat brain homogenate preparations. Submicromolar concentrations of Fe 2+, but not SNAP (up to 100 μM), increased the formation of fluorescent products of malondialdehyde in cortical homogenates. In fact, iron-catalyzed brain lipid peroxidation was inhibited by SNAP (100 μM), but not by light-exposed SNAP or its degradation product penicillamine (100 μM). This study provides relevant evidence to suggest that submicromolar concentrations of Fe 2+ can potentiate lipid peroxidation in disrupted brain tissue. NO· released from SNAP did not stimulate, but rather inhibited brain lipid peroxidation. These results support the hypothesis that NO·, as opposed to ·OH radicals, is not a pro-oxidant but rather an antioxidant.

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