Pacini Nicola, Borziani Fabio
Laboratorio Privato di Biochimica F. Pacini, via trabocchetto 10, 89126 Reggio Calabria, Italy.
Int J Mol Sci. 2016 Mar 7;17(3):341. doi: 10.3390/ijms17030341.
For several years, oncostatic and antiproliferative properties, as well as thoses of cell death induction through 5-methoxy-N-acetiltryptamine or melatonin treatment, have been known. Paradoxically, its remarkable scavenger, cytoprotective and anti-apoptotic characteristics in neurodegeneration models, such as Alzheimer's disease and Parkinson's disease are known too. Analogous results have been confirmed by a large literature to be associated to the use of many other bioactive molecules such as resveratrol, tocopherol derivatives or vitamin E and others. It is interesting to note that the two opposite situations, namely the neoplastic pathology and the neurodegeneration, are characterized by deep alterations of the metabolome, of mitochondrial function and of oxygen consumption, so that the oncostatic and cytoprotective action can find a potential rationalization because of the different metabolic and mitochondrial situations, and in the effect that these molecules exercise on the mitochondrial function. In this review we discuss historical and general aspects of melatonin, relations between cancers and the metabolome and between neurodegeneration and the metabolome, and the possible effects of melatonin and of other bioactive molecules on metabolic and mitochondrial dynamics. Finally, we suggest a common general mechanism as responsible for the oncostatic/cytoprotective effect of melatonin and of other molecules examined.
多年来，人们已经知晓5-甲氧基-N-乙酰色胺或褪黑素具有抑癌和抗增殖特性，以及诱导细胞死亡的特性。矛盾的是，在神经退行性疾病模型（如阿尔茨海默病和帕金森病）中，其显著的清除自由基、细胞保护和抗凋亡特性也为人所知。大量文献证实，使用许多其他生物活性分子（如白藜芦醇、生育酚衍生物或维生素E等）也会产生类似结果。值得注意的是，肿瘤病理学和神经退行性疾病这两种相反的情况，其特征在于代谢组、线粒体功能和氧消耗的深度改变，因此，由于代谢和线粒体状态的不同，以及这些分子对线粒体功能的影响，抑癌和细胞保护作用可能有潜在合理的解释。在本综述中，我们讨论了褪黑素的历史和一般方面、癌症与代谢组之间以及神经退行性疾病与代谢组之间的关系，以及褪黑素和其他生物活性分子对代谢和线粒体动力学的可能影响。最后，我们提出了一种共同的一般机制，作为褪黑素和其他所研究分子的抑癌/细胞保护作用的原因。
