Monitoring systemic oxidative stress in an animal model of amyotrophic lateral sclerosis

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

Research output: Contribution to journalArticlepeer-review

29 Scopus citations


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 SOD G39A 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 SOD G93A 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.

Original languageEnglish (US)
Pages (from-to)762-769
Number of pages8
JournalJournal of Neurology
Issue number5
StatePublished - May 2011
Externally publishedYes


  • Amyotrophic lateral sclerosis
  • G93A
  • Lipid peroxidation
  • Oxidative stress
  • Protein oxidation

ASJC Scopus subject areas

  • Clinical Neurology
  • Neurology


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