Abstract
Melatonin, along with its metabolites, have long been known to significantly reduce the oxidative stress burden of aging cells or cells exposed to toxins. Oxidative damage is a result of free radicals produced in cells, especially in mitochondria. When measured, melatonin, a potent antioxidant, was found to be in higher concentrations in mitochondria than in other organelles or subcellular locations. Recent evidence indicates that mitochondrial membranes possess transporters that aid in the rapid uptake of melatonin by these organelles against a gradient. Moreover, we predicted several years ago that, because of their origin from melatonin-producing bacteria, mitochondria likely also synthesize melatonin. Data accumulated within the last year supports this prediction. A high content of melatonin in mitochondria would be fortuitous, since these organelles produce an abundance of free radicals. Thus, melatonin is optimally positioned to scavenge the radicals and reduce the degree of oxidative damage. In light of the “free radical theory of aging”, including all of its iterations, high melatonin levels in mitochondria would be expected to protect against age-related organismal decline. Also, there are many age-associated diseases that have, as a contributing factor, free radical damage. These multiple diseases may likely be deferred in their onset or progression if mitochondrial levels of melatonin can be maintained into advanced age.
Highlights
A surplus of chemically-reduced oxygen derivatives, often referred to as reactive oxygen species (ROS), some of which are free radicals, commonly leads to an augmented level of molecular damage identified as oxidative stress [1]
While there are many molecules that potentially function as free radical scavengers, in the current survey, we only summarize the actions and mechanisms of melatonin and its metabolites in terms of their ability to forestall the cellular damage associated with an excess of ROS
Based on the literature surveyed in this review, it might be assumed that the routine long term use of supplemental antioxidants would aid in deferring aging and in delaying the onset or progression of age-associated diseases
Summary
A surplus of chemically-reduced oxygen derivatives, often referred to as reactive oxygen species (ROS), some of which are free radicals (with an unpaired valence electron), commonly leads to an augmented level of molecular damage identified as oxidative stress [1]. The generation of ROS, including free radicals, is inevitable and continuous in aerobic organisms [3] Since their creation cannot be totally smothered, the alternative is to neutralize them before they vandalize a neighboring critical molecule. Once formed, free radicals can cause a chain reaction of events that leads to massive molecular annihilation of healthy structures This occurs when the first free radical formed extracts an electron from an otherwise normal molecule in its vicinity, causing it to become a destabilized free radical; in turn, it captures an electron from another molecule to sabotage it. Even when very large amounts of an antioxidant are given, the signaling pathways that utilize ROS seem to be left functionally intact
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