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Oxidative Stress and Ischemia-Reperfusion Injury in Gastrointestinal Tract and Antioxidant, Protective Agents

Exacerbation of hypoxic injury after reoxygenation is a crucial mechanism mediating organ injury in transplantation, and in myocardial, hepatic, gastrointestinal, cerebral, renal, and other ischemic syndromes. The occlusion and reperfusion of the splanchnic artery is a useful animal model to elucida...

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Detalles Bibliográficos
Autores principales: Sasaki, Makoto, Joh, Takashi
Formato: Texto
Lenguaje:English
Publicado: the Society for Free Radical Research Japan 2007
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2291499/
https://www.ncbi.nlm.nih.gov/pubmed/18437208
http://dx.doi.org/10.3164/jcbn.40.1
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author Sasaki, Makoto
Joh, Takashi
author_facet Sasaki, Makoto
Joh, Takashi
author_sort Sasaki, Makoto
collection PubMed
description Exacerbation of hypoxic injury after reoxygenation is a crucial mechanism mediating organ injury in transplantation, and in myocardial, hepatic, gastrointestinal, cerebral, renal, and other ischemic syndromes. The occlusion and reperfusion of the splanchnic artery is a useful animal model to elucidate the mechanism of gastrointestinal injury induced by ischemia-reperfusion (I/R). Although xanthine oxidase is a major source of reactive oxygen species (ROS), which plays an important role in the I/R-induced intestinal injury, there are many other sources of intracellular ROS. Various treatment modalities have been successfully applied to attenuate the I/R injury in animal models. This review focuses on the role of oxidant stress in the mechanism of I/R injury and the use of antioxidant agents for its treatment.
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spelling pubmed-22914992008-04-24 Oxidative Stress and Ischemia-Reperfusion Injury in Gastrointestinal Tract and Antioxidant, Protective Agents Sasaki, Makoto Joh, Takashi J Clin Biochem Nutr Serial Review Exacerbation of hypoxic injury after reoxygenation is a crucial mechanism mediating organ injury in transplantation, and in myocardial, hepatic, gastrointestinal, cerebral, renal, and other ischemic syndromes. The occlusion and reperfusion of the splanchnic artery is a useful animal model to elucidate the mechanism of gastrointestinal injury induced by ischemia-reperfusion (I/R). Although xanthine oxidase is a major source of reactive oxygen species (ROS), which plays an important role in the I/R-induced intestinal injury, there are many other sources of intracellular ROS. Various treatment modalities have been successfully applied to attenuate the I/R injury in animal models. This review focuses on the role of oxidant stress in the mechanism of I/R injury and the use of antioxidant agents for its treatment. the Society for Free Radical Research Japan 2007-01 2006-12-27 /pmc/articles/PMC2291499/ /pubmed/18437208 http://dx.doi.org/10.3164/jcbn.40.1 Text en Copyright © 2006 JCBN This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Serial Review
Sasaki, Makoto
Joh, Takashi
Oxidative Stress and Ischemia-Reperfusion Injury in Gastrointestinal Tract and Antioxidant, Protective Agents
title Oxidative Stress and Ischemia-Reperfusion Injury in Gastrointestinal Tract and Antioxidant, Protective Agents
title_full Oxidative Stress and Ischemia-Reperfusion Injury in Gastrointestinal Tract and Antioxidant, Protective Agents
title_fullStr Oxidative Stress and Ischemia-Reperfusion Injury in Gastrointestinal Tract and Antioxidant, Protective Agents
title_full_unstemmed Oxidative Stress and Ischemia-Reperfusion Injury in Gastrointestinal Tract and Antioxidant, Protective Agents
title_short Oxidative Stress and Ischemia-Reperfusion Injury in Gastrointestinal Tract and Antioxidant, Protective Agents
title_sort oxidative stress and ischemia-reperfusion injury in gastrointestinal tract and antioxidant, protective agents
topic Serial Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2291499/
https://www.ncbi.nlm.nih.gov/pubmed/18437208
http://dx.doi.org/10.3164/jcbn.40.1
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