lunes, 21 de enero de 2013

Más de melatonina/More melatonine

CMO en linea http://www.smo.edu.mx/

http://www.smo.edu.mx/


Melatonina y sus metabolitos: nuevos datos relacionados a su producción y las acciones de sus radicales libres
Melatonin and its metabolites: new findings regarding their production and their radical scavenging actions.
Reiter RJ, Tan DX, Terron MP, Flores LJ, Czarnocki Z.
Department of Cellular and Structural Biology, University of Texas Health Science Center at San Antonio, San Antonio 78229-3900, USA.reiter@uthscsa.edu
Acta Biochim Pol. 2007;54(1):1-9. Epub 2007 Mar 9.
Abstract
This review summarizes some of the recent findings concerning the long-held tenet that the enzyme, N-acetyltransferase, which is involved in the production of N-acetylserotonin, the immediate precursor of melatonin, may in fact not always control the quantity of melatonin generated. New evidence from several different laboratories indicates that hydroxyindole-O-methyltransferase, which O-methylates N-acetylserotonin to melatonin may be rate-limiting in some cases. Also, the review makes the point that melatonin's actions are uncommonly widespread in organs due to the fact that it works via membrane receptors, nuclear receptors/binding sites and receptor-independent mechanisms, i.e., the direct scavenging of free radicals. Finally, the review briefly summarizes the actions of melatonin and its metabolites in the detoxification of oxygen and nitrogen-based free radicals and related non-radical products. Via these multiple processes, melatonin is capable of influencing the metabolism of every cell in the organism.
http://www.actabp.pl/pdf/1_2007/1.pdf


CMO en linea http://www.smo.edu.mx/

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Revisión de melatonina y reproducción
Melatonin and reproduction revisited.
Reiter RJ, Tan DX, Manchester LC, Paredes SD, Mayo JC, Sainz RM.
Department of Cellular and Structural Biology, University of Texas Health Science Center, San Antonio, Texas, USA. reiter@uthscsa.edu
Biol Reprod. 2009 Sep;81(3):445-56. doi: 10.1095/biolreprod.108.075655. Epub 2009 May 13.
Abstract
This brief review summarizes new findings related to the reported beneficial effects of melatonin on reproductive physiology beyond its now well-known role in determining the sexual status in both long-day and short-day seasonally breeding mammals. Of particular note are those reproductive processes that have been shown to benefit from the ability of melatonin to function in the reduction of oxidative stress. In the few species that have been tested, brightly colored secondary sexual characteristics that serve as a sexual attractant reportedly are enhanced by melatonin administration. This is of potential importance inasmuch as the brightness of ornamental pigmentation is also associated with animals that are of the highest genetic quality. Free radical damage is commonplace during pregnancy and has negative effects on the mother, placenta, and fetus. Because of its ability to readily pass through the placenta, melatonin easily protects the fetus from oxidative damage, as well as the maternal tissues and placenta. Examples of conditions in which oxidative and nitrosative stress can be extensive during pregnancy include preeclampsia and damage resulting from anoxia or hypoxia that is followed by reflow of oxygenated blood into the tissue. Given the uncommonly low toxicity of melatonin, clinical trials are warranted to document the protection by melatonin against pathophysiological states of the reproductive system in which free radical damage is known to occur. Finally, the beneficial effects of melatonin in improving the outcomes of in vitro fertilization and embryo transfer should be further tested and exploited. The information in this article has applicability to human and veterinary medicine.
http://www.biolreprod.org/content/81/3/445.full.pdf


CMO en linea http://www.smo.edu.mx/

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La melatonina mitiga la disfunción mitocondrial


Melatonin mitigates mitochondrial malfunction.
León J, Acuña-Castroviejo D, Escames G, Tan DX, Reiter RJ.
Department of Cellular and Structural Biology, University of Texas Health Science Center, San Antonio, TX 78229-3900, USA.
J Pineal Res. 2005 Jan;38(1):1-9.
Abstract
Melatonin, or N-acetyl-5-methoxytryptamine, is a compound derived from tryptophan that is found in all organisms from unicells to vertebrates. This indoleamine may act as a protective agent in disease conditions such as Parkinson's, Alzheimer's, aging, sepsis and other disorders including ischemia/reperfusion. In addition, melatonin has been proposed as a drug for the treatment of cancer. These disorders have in common a dysfunction of the apoptotic program. Thus, while defects which reduce apoptotic processes can exaggerate cancer, neurodegenerative disorders and ischemic conditions are made worse by enhanced apoptosis. The mechanism by which melatonin controls cell death is not entirely known. Recently, mitochondria, which are implicated in the intrinsic pathway of apoptosis, have been identified as a target for melatonin actions. It is known that melatonin scavenges oxygen and nitrogen-based reactants generated in mitochondria. This limits the loss of the intramitochondrial glutathione and lowers mitochondrial protein damage, improving electron transport chain (ETC) activity and reducing mtDNA damage. Melatonin also increases the activity of the complex I and complex IV of the ETC, thereby improving mitochondrial respiration and increasing ATP synthesis under normal and stressful conditions. These effects reflect the ability of melatonin to reduce the harmful reduction in the mitochondrial membrane potential that may trigger mitochondrial transition pore (MTP) opening and the apoptotic cascade. In addition, a reported direct action of melatonin in the control of currents through the MTP opens a new perspective in the understanding of the regulation of apoptotic cell death by the indoleamine.
http://onlinelibrary.wiley.com/doi/10.1111/j.1600-079X.2004.00181.x/pdf



Atentamente
Anestesiología y Medicina del Dolor
www.anestesia-dolor.org



CMO en linea http://www.smo.edu.mx/

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