Does melatonin protect or treat brain damage from traumatic oxidative stress?

• Published in: Experimental brain research 2005-06, Vol.163 (3), p.406-410
• Main Authors: KERMAN, Memduh, CIRAK, Bayram, OZGUNER, M. Fehmi, DAGTEKIN, Ahmet, SUTCU, Recep, ALTUNTAS, Irfan, DELIBAS, Namik
• Format: Article
• Language: English
• Subjects: Animals; Antioxidants; Antioxidants - metabolism; Biological and medical sciences; Brain - enzymology; Brain - pathology; Brain damage; Brain Injuries - metabolism; Brain Injuries - pathology; Brain research; Catalase - metabolism; Enzymes; Free Radical Scavengers - metabolism; Free radicals; Fundamental and applied biological sciences. Psychology; Glutathione Peroxidase - metabolism; Head injuries; Lipid peroxidation; Lipid Peroxidation - physiology; Lipids; Male; Medical sciences; Medicine; Melatonin; Melatonin - metabolism; Motor control and motor pathways. Reflexes. Control centers of vegetative functions. Vestibular system and equilibration; Nervous system; Neurology; Neurosurgery; Oxidative stress; Oxidative Stress - physiology; Rabbits; Superoxide Dismutase - metabolism; Trauma; Traumatic brain injury; Vascular diseases and vascular malformations of the nervous system; Vertebrates: nervous system and sense organs
• ISSN: 0014-4819; 1432-1106
• DOI: 10.1007/s00221-005-2338-2

A variety of experimental studies have demonstrated the neuroprotective effects of melatonin, based on its antioxidant activity. In a prospective randomized study, the effects of melatonin were investigated in experimental head trauma-induced oxidative stress in rabbits. The experimental study was performed on 30 rabbits. The animals were divided into three groups. Group I (sham procedure): a right parietal craniotomy was performed on each animal, and the dura mater was left intact. Group II: experimental brain trauma (EBT) was performed on each animal using a 1 cm inner diameter x 10 cm long glass tube, through which a 20 g weight (0.5 cm diameter) was dropped onto the brain at the craniotomy site, causing a contusional head trauma. Group III: the same EBT model was performed, but 2.5 mg/kg melatonin was injected intraperitoneally four times (total dose 10 mg/kg); these injections were performed 20 min before the operation, during the trauma, 1 h later and 2 h later. The rabbits were sacrificed after the EBT at 24 h after the brain trauma. The activities of the three principal antioxidant enzymes-catalase (CAT), superoxide dismutase (SOD), and glutathione peroxidase (GSH-Px)-were determined, and the levels of malondialdehyde (MDA), a product of lipid peroxidation, and glutathione (GSH) were measured in brain homogenates. MDA levels were found to be higher in the EBT group than in the EBT+melatonin group or the sham procedure group. The SOD activity was found to be higher in the EBT group than in the sham procedure group. Enzymatic parameters (except for SOD) were significantly higher in melatonin-treated animals than in EBT animals. GSH levels in melatonin-treated animals were decreased compared with EBT animals. In conclusion, the data indicate that melatonin protects against free radical-mediated oxidative changes in brain tissue by boosting antioxidant enzymes, and in particular lowering lipid peroxidation in rabbits with EBT.