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Melatonin and mitochondrial function.

机译：褪黑激素和线粒体功能。

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摘要

Melatonin is a natural occurring compound with well-known antioxidant properties. In the last decade a new effect of melatonin on mitochondrial homeostasis has been discovered and, although the exact molecular mechanism for this effect remains unknown, it may explain, at least in part, the protective properties found for the indoleamine in degenerative conditions such as aging as well as Parkinson's disease, Alzheimer's disease, epilepsy, sepsis and other injuries such as ischemia-reperfusion. A common feature in these diseases is the existence of mitochondrial damage due to oxidative stress, which may lead to a decrease in the activities of mitochondrial complexes and ATP production, and, as a consequence, a further increase in free radical generation. A vicious cycle thus results under these conditions of oxidative stress with the final consequence being cell death by necrosis or apoptosis. Melatonin is able of directly scavenging a variety of toxic oxygen and nitrogen-based reactants, stimulates antioxidative enzymes, increases the efficiency of the electron transport chain thereby limiting electron leakage and free radical generation, and promotes ATP synthesis. Via these actions, melatonin preserves the integrity of the mitochondria and helps to maintain cell functions and survival.
机译：褪黑激素是一种天然化合物，具有众所周知的抗氧化性能。在过去的十年中，发现了褪黑激素对线粒体体内稳态的新作用，尽管该作用的确切分子机理尚不清楚，但它至少可以部分解释在退化性条件下（例如衰老）对吲哚胺的保护作用以及帕金森氏病，阿尔茨海默氏病，癫痫，败血症和其他损伤，例如缺血再灌注。这些疾病的共同特征是由于氧化应激而导致线粒体损伤，这可能导致线粒体复合物活性降低和ATP产生，结果，自由基产生进一步增加。因此，在这些氧化应激条件下导致恶性循环，最终结果是坏死或凋亡导致细胞死亡。褪黑素能够直接清除各种有毒的氧和氮基反应物，刺激抗氧化酶，提高电子传输链的效率，从而限制电子泄漏和自由基的产生，并促进ATP的合成。通过这些作用，褪黑激素可以保持线粒体的完整性，并有助于维持细胞功能和存活。

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