Effect of Melatonin on Brain Oxidative Damage Induced by Traumatic Brain Injury in Immature Rats

D. OZDEMIR¹, N. UYSAL², S. GONENC², O. ACIKGOZ², A. SONMEZ², A. TOPCU², N. OZDEMIR³, M. DUMAN¹, I. SEMIN², H. OZKAN<sup>1

1</sup>Department of Pediatrics, ²Department of Physiology, School of Medicine, Dokuz Eylul University, Inciralti and ³Ataturk Training and Research Hospital, Department of Neurosurgery, Izmir, Turkey

Received September 30, 2004
Accepted January 13, 2005
On-line available February 16, 2005


Summary
Progressive compromise of antioxidant defenses and free radical-mediated lipid peroxidation, which is one of the major mechanisms of secondary traumatic brain injury (TBI), has also been reported in pediatric head trauma. In the present study, we aimed to demonstrate the effect of melatonin, which is a potent free radical scavenger, on brain oxidative damage in 7-day-old rat pups subjected to contusion injury. Whereas TBI significantly increased thiobarbituric acid reactive substances (TBARS) levels, there was no compensatory increase in the antioxidant enzymes such as superoxide dismutase (SOD) and glutathione peroxidase (GPx) 24 hours after TBI in 7-day-old rats. Melatonin administered as a single dose of 5 mg/kg prevented the increase in TBARS levels in both non-traumatized and traumatized brain hemispheres. In conclusion, melatonin protects against oxidative damage induced by TBI in the immature brain.


Key words
Traumatic brain injury (TBI) • Immature rat • Lipid peroxidation • Superoxide dismutase (SOD) • Glutathione peroxidase (GPx) • Melatonin