Abstract
Melatonin exhibits extraordinary diversity in terms of its functions and distribution. When discovered, it was thought to be uniquely of pineal gland origin. Subsequently, melatonin synthesis was identified in a variety of organs and recently it was shown to be produced in the mitochondria. Since mitochondria exist in every cell, with a few exceptions, it means that every vertebrate, invertebrate, and plant cell produces melatonin. The mitochondrial synthesis of melatonin is not photoperiod-dependent, but it may be inducible under conditions of stress. Mitochondria-produced melatonin is not released into the systemic circulation, but rather is used primarily in its cell of origin. Melatonin’s functions in the mitochondria are highly diverse, not unlike those of sirtuin 3 (SIRT3). SIRT3 is an NAD+-dependent deacetylase which regulates, among many functions, the redox state of the mitochondria. Recent data proves that melatonin and SIRT3 post-translationally collaborate in regulating free radical generation and removal from mitochondria. Since melatonin and SIRT3 have cohabitated in the mitochondria for many eons, we predict that these molecules interact in many other ways to control mitochondrial physiology. It is predicted that these mutual functions will be intensely investigated in the next decade and importantly, we assume that the findings will have significant applications for preventing/delaying some age-related diseases and aging itself.
Highlights
Genetic diversity often exceeds that which is predicted based on the number of genes that have been sequenced [1,2]
As mentioned above, melatonin given to animals via any route reduces reactive oxygen species damage to cells implying that the indole gets to the source of the bulk of the free radicals, i.e., the mitochondria
Data showing that melatoninby reduces free radical generation/damage in mitochondria alongwith melatoninThe treatment was accompanied enhanced ovarian granulosa cell sirtuin 3 (SIRT3) activity along with the findings of several groups which indicate that this organelle rapidly takes up and the translocation of FOXO3a to the nucleus where it bound to the promoters of SOD2 and catalase synthesizes melatonin is of great interest; the specific mechanisms by which the indole (CAT) [211]
Summary
Genetic diversity often exceeds that which is predicted based on the number of genes that have been sequenced [1,2]. BestThe best-known members of the sirtuin family that function as metabolic sensors include. SIRT1, which known members of the sirtuin family that function as metabolic sensors include SIRT1, which is is primarily located the nucleus cellsand andSIRT3. Three (SIRT3, SIRT4 and SIRT5) are located, not exclusively, in the mitochondria, attesting to their potential involvement in their regulation of metabolism and especially of respiratory changes and oxidative phosphorylation [31,32,33]. Since SIRT3 is known to modulate the redox state of the mitochondria, as does melatonin, we surmised these actions may be interrelated. Those relationships are discussed in this report
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