Melatonin, hydroxyl radical-mediated oxidative damage, and aging: A hypothesis
Article first published online: 30 JAN 2007
Journal of Pineal Research
Volume 14, Issue 4, pages 151–168, May 1993
How to Cite
Poeggeler, B., Reiter, R. J., Tan, D.-X., Chen, L.-D. and Manchester, L. C. (1993), Melatonin, hydroxyl radical-mediated oxidative damage, and aging: A hypothesis. Journal of Pineal Research, 14: 151–168. doi: 10.1111/j.1600-079X.1993.tb00498.x
- Issue published online: 30 JAN 2007
- Article first published online: 30 JAN 2007
- Received December 15, 1992; accepted March 1, 1993.
- hydroxyl radical;
Abstract: Melatonin is a very potent and efficient endogenous radical scavenger. The pineal indolamine reacts with the highly toxic hydroxyl radical and provides on-site protection against oxidative damage to biomolecules within every cellular compartment. Melatonin acts as a primary non-enzymatic antioxidative defense against the devastating actions of the extremely reactive hydroxyl radical. Melatonin and structurally related tryptophan metabolites are evolutionary conservative molecules principally involved in the prevention of oxidative stress in organisms as different as algae and rats. The rate of aging and the time of onset of age-related diseases in rodents can be retarded by the administration of melatonin or treatments that preserve the endogenous rhythm of melatonin formation. The release of excitatory amino acids such as glutamate enhances endogenous hydroxyl radical formation. The activation of central excitatory amino acid receptors suppress melatonin synthesis and is therefore accompanied by a reduced detoxification rate of hydroxyl radicals. Aged animals and humans are melatonin-deficient and more sensitive to oxidative stress. Experiments investigating the effects of endogenous excitatory amino acid antagonists and stimulants of melatonin biosynthesis such as magnesium may finally lead to novel therapeutic approaches for the prevention of degeneration and dysdifferentiation associated with diseases related to premature aging.