Monitoring systemic oxidative stress in an animal model of amyotrophic lateral sclerosis |
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Authors: | Francisco Javier Miana-Mena Cristina González-Mingot Pilar Larrodé María Jesús Muñoz Sara Oliván Lorena Fuentes-Broto Enrique Martínez-Ballarín Russel J Reiter Rosario Osta Joaquín José García |
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Institution: | 1.Departamento Farmacología y Fisiología,Universidad de Zaragoza,Zaragoza,Spain;2.Neurology Service,Universitary Hospital Lozano Blesa of Zaragoza,Zaragoza,Spain;3.LAGENBIO,Universidad de Zaragoza,Zaragoza,Spain;4.Department of Cellular and Structural Biology,University of Texas Health Science Center,San Antonio,USA |
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Abstract: | A mutant form of the ubiquitous copper/zinc superoxide dismutase (SOD1) protein has been found in some patients with amyotrophic
lateral sclerosis (ALS). We monitored oxidative stress in an animal model of ALS, the SODG93A mouse, which develops a disease similar to ALS with an accelerated course. The aim of this work was to show that ALS damages
several organs and tissues, from an oxidative stress point of view. We measured lipid and protein oxidative damage in different
tissue homogenates of SODG93A mice. The biomarkers that we analyzed were malondialdehyde + 4-hydroxyalkenal (MDA + 4-HDA) and carbonyls, respectively.
The spinal cord and brain of SODG93A mice showed increased lipid peroxidation after 100 or 130 days compared to age-matched littermate controls. The CNS was most
affected, but lipid peroxidation was also detected in the skeletal muscle and liver on day 130. No changes were observed in
protein carbonylation in the homogenates. Our results are consistent with a multisystem etiology of ALS and suggest that oxidative
stress may play a primary role in ALS pathogenesis. Thus, oxidative stress represents a potential biomarker that might be
useful in developing new therapeutic strategies for ALS. |
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