Abstract
The ability of melatonin to modify H2O2-induced lipid peroxidation in brain homogenates was determined. The concentrations of brain malonaldehyde (MDA) and 4-hydroxyalkenals (4-HDA) were assayed as an index of induced membrane oxidative damage. Homogenates from five different regions of the brain (cerebral cortex, cerebellum, hippocampus, hypothalamus, and corpus striatum) derived from two different strains of rats, Sprague-Dawley and Wistar, were incubated with either H2O2 (5 mM) alone or H2O2 together with melatonin at increasing concentrations ranging from 0.1 to 4 mM. The basal level of lipid peroxidation was strain-dependent and about 100% higher in homogenates from the brain of Wistar rats than those measured in Sprague-Dawley rats. MDA + 4-HDA levels increased after H2O2 treatment in homogenates obtained from each region of the brain in both rat strains but the sensitivity of the homogenates from Sprague-Dawley rats was greater than that for the homogenates from Wistar rats (increases after H2O2 from 45 to 165% compared 20 to 40% for Sprague-Dawley and Wistar rats, respectively). Melatonin co-treatment reduced H2O2-induced lipid peroxidation in brain homogenates in a concentration-dependent manner; the degree of protection against lipid peroxidation was similar in all brain regions.
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