Melatonin protects against lipid peroxidation induced by δ- aminolevulinic acid in rat cerebellum, cortex and hippocampus

The in vitro and in vivo effect of melatonin on δ-aminolevulinic acid- induced lipid peroxidation in rat cerebellum, cortex and hipppocampus was determined. The concentration of malonaldehyde and 4-hydroxyalkenals was assayed as an index of induced membrane oxidative damage. The rise in malonaldehyde+4-hydroxyalkenals concentrations induced by δ-aminolevulinic acid in cerebellar homogenates was concentration-dependent (P<0.001) and also time-dependent in cerebellar, cortical and hippocampal homogenates (P<0.01). In vitro melatonin and vitamin E protected, in a concentration-dependent manner, against δ-aminolevulinic acid-induced lipid peroxidation in cortical, cerebellar and hippocampal homogenates. In in vivo experiments it was demonstrated that δ-aminolevulinic acid-induced lipid peroxidation (40 mg/kg) in cerebellum and hippocampus was reduced by acute melatonin (10 mg/kg) treatment (P<0.05). The results show that both in vitro and in vivo melatonin confers protection against δ-aminolevulinic acid-induced oxidative toxicity in brain regions. The findings suggest that melatonin may be useful in reducing neural damage in individuals suffering from acute intermittent porphyria.