Melatonin attenuates brain mitochondria DNA damage induced by potassium cyanide in vivo and in vitro

Yamamoto, Hiroaki; Mohanan, P.V.

doi:10.1016/s0300-483x(02)00244-5

Cited by 41 publications

(31 citation statements)

References 33 publications

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“…The results in this work show that after an oxidative stress mtDNA becomes hydrolyzed; they also establish that fragments of the hydrolyzed mtDNA are released from matrix mitochondria. These results are in agreement with Yamamoto and Moharan (2002) who have demonstrated that reactive oxygen species may cause mtDNA damage, in such a way that there is a depletion of this genome from mitochondria. By the same token it has been reported (Shafer et al, 1999) that in Saccharomyces cerevisiae the mtDNA can be released from mitochondria, depending on the carbon source, without RNA as intermediate.…”

Section: Resultssupporting

confidence: 95%

The permeability transition pore as a pathway for the release of mitochondrial DNA

et al. 2005

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Section: Resultssupporting

confidence: 95%

The permeability transition pore as a pathway for the release of mitochondrial DNA

et al. 2005

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“…Melatonin significantly reduced escape of the enzyme from the neurons and preserved their morphology (Yamamoto and Tang, 1998). These researchers also showed, both in vitro and in vivo, that the damage to rat mtDNA by cyanide is also abolished by melatonin co-treatment (Yamamoto and Mohanan, 2002). The authors assumed that the mitochondrial dysfunction caused by cyanide initiated essentially uncontrolled free radical generation leading to oxidative mutilation of the neighboring mtDNA.…”

Section: Mitochondrial Toxins: Protection By Melatoninmentioning

confidence: 95%

Melatonin combats molecular terrorism at the mitochondrial level

Reíter¹,

Paredes²,

Korkmaz³

et al. 2008

Interdisciplinary Toxicology

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The intracellular environmental is a hostile one. Free radicals and related oxygen and nitrogen-based oxidizing agents persistently pulverize and damage molecules in the vicinity of where they are formed. The mitochondria especially are subjected to frequent and abundant oxidative abuse. The carnage that is left in the wake of these oxygen and nitrogen-related reactants is referred to as oxidative damage or oxidative stress. When mitochondrial electron transport complex inhibitors are used, e.g., rotenone, 1-methyl-1-phenyl-1,2,3,6-tetrahydropyridine, 3-nitropropionic acid or cyanide, pandemonium breaks loose within mitochondria as electron leakage leads to the generation of massive amounts of free radicals and related toxicants. The resulting oxidative stress initiates a series of events that leads to cellular apoptosis. To alleviate mitochondrial destruction and the associated cellular implosion, the cell has at its disposal a variety of free radical scavengers and antioxidants. Among these are melatonin and its metabolites. While melatonin stimulates several antioxidative enzymes it, as well as its metabolites (cyclic 3-hydroxymelatonin, N1-acetyl-N2-formyl-5-methoxykynuramine and N1-acetyl-5-methoxykynuramine), likewise effectively neutralize free radicals. The resulting cascade of reactions greatly magnifies melatonin's efficacy in reducing oxidative stress and apoptosis even in the presence of mitochondrial electron transport inhibitors. The actions of melatonin at the mitochondrial level are a consequence of melatonin and/or any of its metabolites. Thus, the molecular terrorism meted out by reactive oxygen and nitrogen species is held in check by melatonin and its derivatives.

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“…Melatonin has been stimulates activities and mRNA levels of antioxidative enzymes including (SOD), (GPx), and catalase [48,49]. Thereby, these multiple actions of melatonin protect cells from ROS-mediated lipid peroxidation, protein destruction and nuclear DNA damage [50-54]. …”

Section: Intoductionmentioning

confidence: 99%

The role of melatonin as an antioxidant in the follicle

Tamura

Takasaki

Tanaka

et al. 2012

Journal of Ovarian Research

211

171

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Melatonin (N-acetyl-5-methoxytryptamine) is secreted during the dark hours at night by pineal gland, and it regulates a variety of important central and peripheral actions related to circadian rhythms and reproduction. It has been believed that melatonin regulates ovarian function by the regulation of gonadotropin release in the hypothalamus-pituitary gland axis via its specific receptors. In addition to the receptor mediated action, the discovery of melatonin as a direct free radical scavenger has greatly broadened the understanding of melatonin's mechanisms which benefit reproductive physiology. Higher concentrations of melatonin have been found in human preovulatory follicular fluid compared to serum, and there is growing evidence of the direct effects of melatonin on ovarian function especially oocyte maturation and embryo development. Many scientists have focused on the direct role of melatonin on oocyte maturation and embryo development as an anti-oxidant to reduce oxidative stress induced by reactive oxygen species, which are produced during ovulation process. The beneficial effects of melatonin administration on oocyte maturation and embryo development have been confirmed by in vitro and in vivo experiments in animals. This review also discusses the first application of melatonin to the clinical treatment of infertile women and confirms that melatonin administration reduces intrafollicular oxidative damage and increase fertilization rates. This review summarizes our recent works and new findings related to the reported beneficial effects of melatonin on reproductive physiology in its role as a reducer of oxidative stress, especially on oocyte maturation and embryo development.

show abstract

Melatonin attenuates brain mitochondria DNA damage induced by potassium cyanide in vivo and in vitro

Cited by 41 publications

References 33 publications

The permeability transition pore as a pathway for the release of mitochondrial DNA

The permeability transition pore as a pathway for the release of mitochondrial DNA

Melatonin combats molecular terrorism at the mitochondrial level

The role of melatonin as an antioxidant in the follicle

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