How Melatonin Protects Cell Energy Centers from Damage
- Authors
- Dario Acuna-Castroviejo, Luis C. Lopez, Germaine Escames, Ana Lopez, Jose A. Garcia, Russel J. Reiter
- Journal
- Current Topics in Medical Chemistry
- Year
- 2011
- DOI
- 10.2174/156802611794863517
- Study Type
- clinical
- Peer Reviewed
- Yes
- Country
- Spain
- Health Condition
- Neurodegenerative diseases
- Body System
- nervous system
TL;DR
Melatonin is a natural substance that acts like a bodyguard for your mitochondria (the parts of cells that make energy), protecting them from damage caused by harmful molecules that build up when your body uses oxygen. Scientists think melatonin could help treat diseases involving broken mitochondria, like some nerve and muscle problems.
Key Finding
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Summary
Researchers conducted a comprehensive review of melatonin's protective effects on mitochondria, the cellular structures responsible for energy production. The study examined how mitochondria evolved through hydrogen-dependent symbiosis and how oxygen consumption creates harmful reactive oxygen species (ROS). Melatonin, a natural hormone with powerful antioxidant properties, helps protect mitochondria from oxidative and nitrosative damage. The research highlights melatonin's role in preventing mitochondrial dysfunction associated with neurodegenerative and neuromuscular diseases. By reducing cellular stress and inflammation, melatonin supports healthy mitochondrial function and may offer therapeutic benefits for conditions involving mitochondrial damage and energy metabolism disorders.
Abstract
Although two main hypotheses of mitochondrial origin have been proposed, i.e., the autogenous and the endosymbiotic, only the second is being seriously considered currently. The 'hydrogen hypothesis' invokes metabolic symbiosis as the driving force for a symbiotic association between an anaerobic, strictly hydrogen-dependent (the host) and an eubacterium (the symbiont) that was able to respire, but which generated molecular hydrogen as an end product of anaerobic metabolism. The resulting proto-eukaryotic cell would have acquired the essentials of eukaryotic energy metabolism, evolving not only aerobic respiration, but also the physiological cost of the oxygen consumption, i.e., generation of reactive oxygen species (ROS) and the associated oxidative damage. This is not the only price to pay for respiring oxygen: mitochondria possess nitric oxide (NO·) for regulatory purposes but, in some instances it may react with superoxide anion radical to produce the toxic reactive nitrogen species (RNS), i.e. peroxynitrite anion, and the subsequent nitrosative damage. New mitochondria contain their own genome with a modified genetic code that is highly conserved among mammals. The transcription of certain mitochondrial genes may depend on the redox potential of the mitochondrial membrane. Mitochondria are related to the life and death of cells. They are involved in energy production and conservation, having an uncoupling mechanism to produce heat instead of ATP, but they are also involved in programmed cell death. Increasing evidence suggest the participation of mitochondria in neurodegenerative and neuromuscular diseases involving alterations in both nuclear (nDNA) and mitochondrial (mtDNA) DNA. Melatonin is a known powerful antioxidant and anti-inflammatory and increasing experimental and clinical evidence shows its beneficial effects against oxidative/nitrosative stress status, including that involving mitochondrial dysfunction. This review summarizes the data and mechanisms of action of melatonin in relation to mitochondrial pathologies.