The protective role of melatonin in experimental hypoxic brain damage.

BACKGROUND

It is known that oxygen-derived free radicals play an important role in the pathogenesis of brain injury. Melatonin is a powerful scavenger of the oxygen free radicals. In this study, the protective effect of melatonin against the damage inflicted by reactive oxygen species during brain hypoxia was investigated in newborn rats using biochemical parameters.

METHODS

For biochemical analyses, the levels of lipid peroxidation product (malondialdehyde ([MDA]), levels of reduced glutathione (GSH) and the activities of superoxide dismutase (SOD) and catalase (CAT) were estimated.

RESULTS

After the third day of brain hypoxia, the brain levels of MDA increased. Pretreatment of animals with melatonin abolished the rise in MDA induced by hypoxia. GSH concentration did not increase by pretreatment with melatonin. Additionally, the activities of two antioxidative enzymes (SOD and CAT) decreased after the experimental period with melatonin only preventing the change of CAT. The activity of SOD was not influenced by melatonin administration as expected.

CONCLUSION

In this experimental study, exogenously administered melatonin effectively protected against brain injury by oxidative stress. This protective effect of melatonin may be due to its direct scavenger activity and activation of CAT. Thus, melatonin may potentially be useful in the treatment of neurodegenerative conditions that may involve free radical production, such as perinatal hypoxia.