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Am J Physiol Renal Physiol 292: F1673-F1680, 2007. First published March 6, 2007; doi:10.1152/ajprenal.00356.2006
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Role of peroxynitrite on cytoskeleton alterations and apoptosis in renal ischemia-reperfusion

Jose Luis Viñas,1 Gina Hotter ,1,* Felip Pi,1 Luis Palacios,2 and Anna Sola1,*

1Department of Experimental Pathology, Instituto de Investigaciones Biomédicas, Institut d'Investigacions Biomediques de Barcelona of the Council for Scientific Research, Institut d'Investigacions Biomediques August Pi i Sunyer, and 2Department of Physiology, University of Barcelona, Barcelona, Spain

Submitted 14 September 2006 ; accepted in final form 26 February 2007

During renal ischemia-reperfusion (I/R) injury, apoptosis has been reported as a very important contributor to final kidney damage. The determinant role of cytoskeleton derangement in the development of apoptosis has been previously reported, but a clear description of the different mechanisms involved in this process has not been yet provided. The aim of our study was to know the role of peroxynitrite as an inductor of cytoskeleton derangement and apoptosis during renal I/R. Based on a rat kidney I/R model, using experiments in which both the actin cytoskeleton and peroxynitrite generation were pharmacologically manipulated, results indicate that the peroxynitrite produced during the I/R-derived oxidative stress state is able to provoke cytoskeleton derangement and apoptosis development. Thus control of peroxynitrite generation during I/R could be an effective tool for the improvement of cytoskeleton damage and reduction of apoptosis incidence in renal I/R injury.

kidney; nitric oxide; cell death; cytoskeleton derangement


Address for reprint requests and other correspondence: J. L. Viñas, Depart. of Experimental Pathology, IIBB-CSIC-IDIBAPS, C/ Roselló, 161, 7a planta, 08036 Barcelona, Spain (e-mail: jvmbam{at}iibb.csic.es)






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