Abstract
Ischemia-reperfusion (IR) injury is a multifactorial process triggered when the liver or other organs are transiently subjected to reduced blood supply followed by reperfusion. It has been shown that reactive oxygen species (ROS) are generated during ischemia and reperfusion and may represent pivotal mediators of the ensuing pathological complications. In some cases, however, moderate production of ROS may exert protective effects, a phenomenon presumably related to ischemic preconditioning. This review will focus mainly on: a) describing the sources and the biochemical mechanisms of ROS generation during ischemia and reperfusion, b) discussing current developments in understanding the biochemical pathways by which ROS may induce toxic or protective effects, c) critically evaluating the results of previous attempts to counteract the toxic effects of ROS by using a variety of antioxidant and transition metalchelating agents, and d) if feasible, proposing potential new pharmaceutical agents aimed at ameliorating ROS-inducing deleterious effects during reperfusion. It is concluded that ROS are generated from different sources, at different periods during IR, and may act by a variety of not well understood biochemical mechanisms which ultimately lead to cell damage and tissue failure.
Keywords: Antioxidants, iron chelators, ischemia reperfusion, liver, oxidative stress, preconditioning, reactive oxygen species
Current Pharmaceutical Design
Title: Oxidative Stress in Hepatic Ischemia-Reperfusion Injury: The Role of Antioxidants and Iron Chelating Compounds
Volume: 12 Issue: 23
Author(s): D. Galaris, A. Barbouti and P. Korantzopoulos
Affiliation:
Keywords: Antioxidants, iron chelators, ischemia reperfusion, liver, oxidative stress, preconditioning, reactive oxygen species
Abstract: Ischemia-reperfusion (IR) injury is a multifactorial process triggered when the liver or other organs are transiently subjected to reduced blood supply followed by reperfusion. It has been shown that reactive oxygen species (ROS) are generated during ischemia and reperfusion and may represent pivotal mediators of the ensuing pathological complications. In some cases, however, moderate production of ROS may exert protective effects, a phenomenon presumably related to ischemic preconditioning. This review will focus mainly on: a) describing the sources and the biochemical mechanisms of ROS generation during ischemia and reperfusion, b) discussing current developments in understanding the biochemical pathways by which ROS may induce toxic or protective effects, c) critically evaluating the results of previous attempts to counteract the toxic effects of ROS by using a variety of antioxidant and transition metalchelating agents, and d) if feasible, proposing potential new pharmaceutical agents aimed at ameliorating ROS-inducing deleterious effects during reperfusion. It is concluded that ROS are generated from different sources, at different periods during IR, and may act by a variety of not well understood biochemical mechanisms which ultimately lead to cell damage and tissue failure.
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Cite this article as:
Galaris D., Barbouti A. and Korantzopoulos P., Oxidative Stress in Hepatic Ischemia-Reperfusion Injury: The Role of Antioxidants and Iron Chelating Compounds, Current Pharmaceutical Design 2006; 12 (23) . https://dx.doi.org/10.2174/138161206777947614
DOI https://dx.doi.org/10.2174/138161206777947614 |
Print ISSN 1381-6128 |
Publisher Name Bentham Science Publisher |
Online ISSN 1873-4286 |
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