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Joint Bone Spine
Volume 74, n° 4
pages 324-329 (juillet 2007)
Doi : 10.1016/j.jbspin.2007.02.002
Received : 9 May 2006 ;  accepted : 1 February 2007
Reactive oxygen species and superoxide dismutases: Role in joint diseases

Valéry Afonso, Romuald Champy, Dragoslav Mitrovic, Pascal Collin, Abderrahim Lomri
INSERM U606, IFR-139, Paris 7 University, Lariboisière Teaching Hospital, 2 rue Ambroise Paré, 75475 Paris Cedex 10, France 

Corresponding author. Tel.: +33 149 956 328; fax: +33 149 958 452.

Reactive oxygen species (ROS) are produced in many normal and abnormal processes in humans, including atheroma, asthma, joint diseases, aging, and cancer. The superoxide anion O2 - is the main ROS. Increased ROS production leads to tissue damage associated with inflammation. Superoxide dismutases (SODs) convert superoxide to hydrogen peroxide, which is then removed by glutathione peroxidase or catalase. Thus, SODs prevent the formation of highly aggressive ROS, such as peroxynitrite or the hydroxyl radical. Experimental models involving SOD knockout or overexpression are beginning to shed light on the pathophysiological role of SOD in humans. Although the antiinflammatory effects of exogenous native SOD (orgotein) are modest, synthetic SOD mimetics hold considerable promise for modulating the inflammatory response. In this review, we discuss new knowledge about the role of the superoxide anion and its derivates as mediators of inflammation and the role of SODs and SOD mimetics as antioxidant treatments in joint diseases such as rheumatoid arthritis, osteoarthritis, and crystal-induced arthropathies.

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Keywords : Reactive oxygen species, Superoxide anion, Superoxide dismutase, SOD mimetics, Arthritis, Rheumatoid arthritis, Crystal-induced arthropathies

© 2007  Elsevier Masson SAS. All Rights Reserved.