9
views
0
recommends
+1 Recommend
0 collections
    0
    shares
      • Record: found
      • Abstract: found
      • Article: not found

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

      Neuroscience
      Aminolevulinic Acid, antagonists & inhibitors, pharmacology, Animals, Antioxidants, Cerebellum, drug effects, metabolism, Cerebral Cortex, Hippocampus, Indicators and Reagents, Lipid Peroxidation, Male, Malondialdehyde, Melatonin, Neuroprotective Agents, Rats, Rats, Sprague-Dawley, Vitamin E

      Read this article at

      ScienceOpenPubMed
      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          The in vitro and in vivo effect of melatonin on delta-aminolevulinic acid-induced lipid peroxidation in rat cerebellum, cortex and hippocampus 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 delta-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 delta-aminolevulinic acid-induced lipid peroxidation in cortical, cerebellar and hippocampal homogenates. In in vivo experiments it was demonstrated that delta-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 delta-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.

          Related collections

          Author and article information

          Comments

          Comment on this article