| Literature DB >> 27108742 |
Irene Paterniti1, Marika Cordaro1, Emanuela Esposito1, Salvatore Cuzzocrea1,2.
Abstract
INTRODUCTION: This review briefly summarizes some of the large amount of data documenting the ability of melatonin to limit molecular and organ tissue damage in neural ischemia-reperfusion injury (stroke), where free radicals are generally considered as being responsible for much of the resulting tissue destruction. AREA COVERED: Melatonin actions that have been identified include its ability to directly neutralize a number of toxic reactants and stimulate antioxidative enzymes. Furthermore, several of its metabolites such as N(1)-acetyl-N(2)-formyl-5- methoxykynuramine (AFMK) and N(1)-acetyl-5-methoxykynuramine (AMF), are themselves scavengers suggesting that there is a cascade of reactions that greatly increase the efficacy of melatonin. Expert Commentary: However, the mechanisms by which melatonin is protective in such widely diverse areas of the cell and different organs are likely not yet all identified.Entities:
Keywords: Melatonin; antioxidant; free radicals; ischemia-reperfusion injury; oxidative stress
Mesh:
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Year: 2016 PMID: 27108742 DOI: 10.1080/14737175.2016.1182020
Source DB: PubMed Journal: Expert Rev Neurother ISSN: 1473-7175 Impact factor: 4.618