| Mitochondria in exercise-induced oxidative stress. | |
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MedLine Citation:
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PMID: 11223645 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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In recent years it has been suggested that reactive oxygen species (ROS) are involved in the damage to muscle and other tissues induced by acute exercise. Despite the small availability of direct evidence for ROS production during exercise, there is an abundance of literature providing indirect support that oxidative stress occurs during exercise. The electron transport associated with the mitochondrial respiratory chain is considered the major process leading to ROS production at rest and during exercise. It is widely assumed that during exercise the increased electron flow through the mitochondrial electron transport chain leads to an increased rate of ROS production. On the other hand, results obtained by in vitro experiments indicate that mitochondrial ROS production is lower in state 3 (ADP-stimulated) than in state 4 (basal) respiration. It is possible, however, that factors, such as temperature, that are modified in vivo during intense physical activity induce changes (uncoupling associated with loss of cytochrome oxidase activity) leading to increased ROS production. The mitochondrial respiratory chain could also be a potential source of ROS in tissues, such as liver, kidney and nonworking muscles, that during exercise undergo partial ischemia because of reduced blood supply. Sufficient oxygen is available to interact with the increasingly reduced respiratory chain and enhance the ROS generation. At the cessation of exercise, blood flow to hypoxic tissues resumes leading to their reoxygenation. This mimics the ischemia-reperfusion phenomenon, which is known to cause excessive production of free radicals. Apart from a theoretical rise in ROS, there is little evidence that exercise-induced oxidative stress is due to its increased mitochondrial generation. On the other hand, if mitochondrial production of ROS supplies a remarkable contribution to exercise-induced oxidative stress, mitochondria should be a primary target of oxidative damage. Unfortunately, there are controversial reports concerning the exercise effects on structural and functional characteristics of mitochondria. However, the isolation of mitochondrial fractions by differential centrifugation has shown that the amount of damaged mitochondria, recovered in the lightest fraction, is remarkably increased by long-lasting exercise. |
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Authors:
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S Di Meo; P Venditti |
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Publication Detail:
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Type: Journal Article; Review |
Journal Detail:
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Title: Biological signals and receptors Volume: 10 ISSN: 1422-4933 ISO Abbreviation: Biol Signals Recept Publication Date: 2001 Jan-Apr |
Date Detail:
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Created Date: 2001-03-06 Completed Date: 2001-05-03 Revised Date: 2004-11-17 |
Medline Journal Info:
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Nlm Unique ID: 9808792 Medline TA: Biol Signals Recept Country: Switzerland |
Other Details:
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Languages: eng Pagination: 125-40 Citation Subset: IM |
Copyright Information:
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Copyright 2001 S. Karger AG, Basel |
Affiliation:
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Dipartimento di Fisiologia Generale ed Ambientale, Università di Napoli Federico II, Napoli, Italia. dimeo@biol.dgbm.unina.it |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Animals Antioxidants Exercise / physiology* Free Radicals Humans Lipid Peroxidation Mitochondria / physiology* Oxidative Stress / physiology* Oxygen Consumption Physical Conditioning, Animal / physiology Reperfusion Injury |
| Chemical | |
Reg. No./Substance:
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0/Antioxidants; 0/Free Radicals |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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