OBJECT: Melatonin is a very effective antioxidant agent. This study was performed to investigate the effects of melatonin in experimental spinal cord injury (SCI). The authors also compared its effects with those of methylprednisolone, which also protects the spinal cord from secondary injury because of its antioxidant effect on membrane lipids. METHODS: Adult male albino rats were used for the study, and paraplegia was produced using a previously described weight-drop technique. Melatonin and methylprednisolone were given intraperitoneally by bolus injections of 100 mg/kg and 30 mg/kg, respectively, immediately after induction of trauma. The animals were killed, and 1-cm samples of injured spinal cord were obtained at 1, 24, and 48 hours postinjury. Lipid peroxidation was estimated by thiobarbituric acid test. Electron microscopic studies were performed to determine the effects of melatonin on neurons, axons, and subcellular organelles after experimental SCI. A grading system was used for quantitative evaluation. Following SCI, there was significant increase in lipid peroxidation. In melatonin- and methylprednisolone-treated groups, lipid peroxidation was found to decrease to the baseline (preinjury) levels. There was a significant difference between trauma-alone and treatment groups, but no statistical difference was found between the melatonin- and methylprednisolone-treated groups. Electron microscopic findings showed that SCI produced by the weight-drop technique resulted in profound tissue damage. CONCLUSIONS: Both melatonin and methylprednisolone have been shown to protect neuron, axon, myelin, and intracellular organelles including mitochondrion and nucleus. However, this study provides quantitative evidence that this protection of neurons and subcellular organelles of spinal cord after secondary injury is much more obvious in melatonin-treated rats than those treated with methylprednisolone. In view of these data, melatonin has been shown to be very effective in protecting the injured spinal cord from secondary injury.
OBJECT: Melatonin is a very effective antioxidant agent. This study was performed to investigate the effects of melatonin in experimental spinal cord injury (SCI). The authors also compared its effects with those of methylprednisolone, which also protects the spinal cord from secondary injury because of its antioxidant effect on membrane lipids. METHODS: Adult male albino rats were used for the study, and paraplegia was produced using a previously described weight-drop technique. Melatonin and methylprednisolone were given intraperitoneally by bolus injections of 100 mg/kg and 30 mg/kg, respectively, immediately after induction of trauma. The animals were killed, and 1-cm samples of injured spinal cord were obtained at 1, 24, and 48 hours postinjury. Lipid peroxidation was estimated by thiobarbituric acid test. Electron microscopic studies were performed to determine the effects of melatonin on neurons, axons, and subcellular organelles after experimental SCI. A grading system was used for quantitative evaluation. Following SCI, there was significant increase in lipid peroxidation. In melatonin- and methylprednisolone-treated groups, lipid peroxidation was found to decrease to the baseline (preinjury) levels. There was a significant difference between trauma-alone and treatment groups, but no statistical difference was found between the melatonin- and methylprednisolone-treated groups. Electron microscopic findings showed that SCI produced by the weight-drop technique resulted in profound tissue damage. CONCLUSIONS: Both melatonin and methylprednisolone have been shown to protect neuron, axon, myelin, and intracellular organelles including mitochondrion and nucleus. However, this study provides quantitative evidence that this protection of neurons and subcellular organelles of spinal cord after secondary injury is much more obvious in melatonin-treated rats than those treated with methylprednisolone. In view of these data, melatonin has been shown to be very effective in protecting the injured spinal cord from secondary injury.
Authors: Hakan Kayali; M Fatih Ozdag; Serdar Kahraman; Ahmet Aydin; Engin Gonul; Ahmet Sayal; Zeki Odabasi; Erdener Timurkaynak Journal: Neurosurg Rev Date: 2005-04-30 Impact factor: 3.042