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Melatonin Reduces Oxidant Damage and Promotes Mitochondrial Respiration

Melatonin has a number of properties as a consequence of which it could be beneficial to animals as they age. Of particular interest are its ubiquitous actions as a direct and indirect antioxidant and free radical scavenger. Besides directly detoxifying a variety of reactive oxygen and reactive nitr...

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Bibliographic Details
Published in:Annals of the New York Academy of Sciences 2002-04, Vol.959 (1), p.238-250
Main Authors: REITER, RUSSEL J., TAN, DUN XIAN, MANCHESTER, LUCIEN C., EL-SAWI, MAMDOUH R.
Format: Article
Language:English
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Summary:Melatonin has a number of properties as a consequence of which it could be beneficial to animals as they age. Of particular interest are its ubiquitous actions as a direct and indirect antioxidant and free radical scavenger. Besides directly detoxifying a variety of reactive oxygen and reactive nitrogen species, at least one product that is formed as a result of these interactions is also a potent free radical scavenger. Thus, the product that is formed when melatonin detoxifies hydrogen peroxide, that is, N1‐acetyl‐N2‐formyl‐5‐methoxykynuramine is an efficient scavenger, at least equivalent to melatonin itself. This antioxidant cascade increases the ability of melatonin to resist oxidative damage. Other actions of melatonin, such as stimulation of antioxidative enzymes also improves its status as an antioxidant. Finally, recent observations documenting melatonin's ability to stimulate electron transport and ATP production in the inner‐mitochondrial membrane also has relevance for melatonin as an agent that could alter processes of aging. These findings, coupled with diminished melatonin production in advanced age, has prompted scientists to consider melatonin in the context of aging. As of this writing there is no definitive evidence to prove that melatonin alters the rate of aging, although data relating to melatonin deferring some age‐related degenerative conditions is accumulating rapidly.
ISSN:0077-8923
1749-6632
DOI:10.1111/j.1749-6632.2002.tb02096.x