Melatonin is uncommonly effective in reducing oxidative stress under a remarkably large number of circumstances. It achieves this action via a variety of means: direct detoxification of reactive oxygen and reactive nitrogen species and indirectly by stimulating antioxidant enzymes while suppressing the activity of pro-oxidant enzymes.
Melatonin is a versatile molecule, synthesized not only by the pineal gland, but also in small amounts by many other organs like retina, gastrointestinal tract, thymus, bone marrow, lymphocytes etc.
The experimental data obtained from both human and rodent studies suggest that melatonin may have utility in the treatment of several cardiovascular conditions. In particular, melatonin's use in reducing the severity of essential hypertension should be more widely considered. In rodent studies melatonin has been shown to be highly effective in limiting abnormal cardiac physiology and the loss of critical heart tissue resulting from ischemia/reperfusion injury.
This review summarizes the numerous reports that have documented the neuroprotective actions of melatonin in experimental models of ischemia/reperfusion injury (stroke).