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Issue 1066 coverCell Injury: Mechanisms, Responses, and Repair Volume 1066 published December 2005
Ann. N.Y. Acad. Sci. 1066: 136–151 (2005). doi: 10.1196/annals.1363.019
Copyright © 2005 by the New York Academy of Sciences
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Articles by FRIDLYAND, L. E.
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Articles by FRIDLYAND, L. E.
Articles by PHILIPSON, L. H.
Oxidative Reactive Species in Cell Injury: Mechanisms in Diabetes Mellitus and Therapeutic Approaches

LEONID E. FRIDLYAND AND LOUIS H. PHILIPSON

Department of Medicine, University of Chicago, MC-1027, Chicago, Illinois 60637, USA

Address for correspondence: Louis H. Philipson, Department of Medicine, MC-1027, The University of Chicago, 5841 S. Maryland Ave., Chicago, IL 60637. Voice: 773-702-9180; fax: 773-702-9194. l-philipson{at}uchicago.edu

Mammalian cells are continuously subject to insult from reactive species. Most of the pathogenic mechanisms that have been considered to date reflect overproduction of reactive oxygen species (ROS) or a peculiar failure in intracellular defenses against ROS. We have attempted to consider briefly the most important mechanisms of ROS production, defense, and reactive species-induced cell damage and approaches to therapy, focusing on the example of diabetes mellitus. An improved understanding of these mechanisms should facilitate development of antioxidant intervention strategies leading to reduction in diseases associated with oxidative stress.

Key Words: beta-cell • insulin resistance • mitochondria • diabetes mellitus




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