RT Journal Article
T1 Melatonin Mitigates Mitochondrial Meltdown: Interactions with SIRT3.
A1 Reiter, Russel J
A1 Tan, Dun Xian
A1 Rosales-Corral, Sergio
A1 Galano, Annia
A1 Jou, Mei-Jie
A1 Acuna-Castroviejo, Dario
K1 antioxidant enzymes
K1 molecular pathways
K1 oxidative phosphorylation
K1 oxidative stress
K1 reactive oxygen species
K1 sirtuins
AB 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.
YR 2018
FD 2018-08-18
LK http://hdl.handle.net/10668/12857
UL http://hdl.handle.net/10668/12857
LA en
DS RISalud
RD Apr 7, 2025