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Melatonin Relieves the Neural Oxidative Burden that Contributes to Dementias
Department of Cellular and Structural Biology, University of Texas Health Science Center, San Antonio, Texas 78229-3900, USA
Address for correspondence: Russel J. Reiter, Ph.D., Department of Cellular and Structural Biology, University of Texas Health Science Center, 7703 Floyd Curl Drive, MC 7762, San Antonio, TX 78229-3900. Voice: 210-567-3859; fax: 210-567-3805. reiter{at}uthscsa.edu
This report summarizes some of the many publications that document the beneficial actions of melatonin within the central nervous system. Of particular interest are the multiple functions of melatonin and its metabolites as ubiquitously acting direct free radical scavengers and indirect antioxidants. The fact that melatonin and the metabolic progeny that are formed when it scavenges toxic reactants are all effective in neutralizing destructive molecules greatly increases the efficacy of melatonin as a protection against by-products of oxygen and nitrogen that normally mutilate essential molecules. Of the large number of situations in which oxidative stress may be the cause of disease processes or debilitating conditions, the current review examines melatonin's protection within the central nervous system, particularly in experimental ischemia/reperfusion (stroke) injury, Alzheimer's disease, and parkinsonism. In each of these conditions, melatonin has been found to provide significant neural protection against both the morphophysiological damage and the biobehavioral consequences of these infirmities. The report concludes with the suggestion that melatonin, alone or in combination with other antioxidants, be considered for routine usage to potentially combat some of the neural ravages of aging.
Key Words: melatonin • free radicals • oxidative stress • ischemia/reperfusion • Alzheimer's disease • Parkinson's disease This article has been cited by other articles:
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