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Título : Melatonin in mitochondrial dysfunction and related disorders
Autor : Srinivasan, Venkataramanujan 
Spence, David Warren 
Pandi Perumal, Seithikurippu R. 
Brown, Gregory M. 
Cardinali, Daniel Pedro 
Fecha de publicación : 2011
Editorial : Hindawi
Cita : Srinivasan, V., et al. Melatonin in mitochondrial dysfunction and related disorders [en línea]. International Journal of Alzheimer's Disease. 2011. doi:10.4061/2011/326320. Disponible en:
Resumen : Abstract: Mitochondrial dysfunction is considered one of the major causative factors in the aging process, ischemia/reperfusion (I/R), septic shock, and neurodegenerative disorders like Parkinson’s disease (PD), Alzheimer’s disease (AD), and Huntington’s disease (HD). Increased free radical generation, enhanced mitochondrial inducible nitric oxide (NO) synthase activity, enhancedNOproduction, decreased respiratory complex activity, impaired electron transport system, and opening of mitochondrial permeability transition pore all have been suggested as factors responsible for impaired mitochondrial function. Melatonin, the major hormone of the pineal gland, also acts as an antioxidant and as a regulator of mitochondrial bioenergetic function. Both in vitro and in vivo, melatonin was effective for preventing oxidative stress/nitrosative stress-induced mitochondrial dysfunction seen in experimental models of PD, AD, and HD. In addition, melatonin is known to retard aging and to inhibit the lethal effects of septic shock or I/R lesions by maintaining respiratory complex activities, electron transport chain, and ATP production in mitochondria. Melatonin is selectively taken up by mitochondrial membranes, a function not shared by other antioxidants. Melatonin has thus emerged as a major potential therapeutic tool for treating neurodegenerative disorders such as PD or AD, and for preventing the lethal effects of septic shock or I/R.
ISSN : 2090-8024 (Print)
2090-0252 (Online)
Disciplina: MEDICINA
DOI: 10.4061/2011/326320
Derechos: Acceso Abierto
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