Effect of melatonin on brain oxidative damage induced by traumatic brain injury in immature rats
Language English Country Czech Republic Media print
Document type Journal Article, Research Support, Non-U.S. Gov't
PubMed
15720160
PII: 709
Knihovny.cz E-resources
- MeSH
- Glutathione Peroxidase analysis MeSH
- Injections, Intraperitoneal MeSH
- Rats MeSH
- Thiobarbituric Acid Reactive Substances analysis MeSH
- Melatonin administration & dosage pharmacology MeSH
- Disease Models, Animal MeSH
- Brain drug effects metabolism MeSH
- Animals, Newborn MeSH
- Oxidative Stress MeSH
- Lipid Peroxidation MeSH
- Brain Injuries etiology metabolism MeSH
- Rats, Wistar MeSH
- Free Radical Scavengers administration & dosage pharmacology MeSH
- Superoxide Dismutase analysis MeSH
- Animals MeSH
- Check Tag
- Rats MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Names of Substances
- Glutathione Peroxidase MeSH
- Thiobarbituric Acid Reactive Substances MeSH
- Melatonin MeSH
- Free Radical Scavengers MeSH
- Superoxide Dismutase MeSH
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.