TY - JOUR
T1 - Monitoring systemic oxidative stress in an animal model of amyotrophic lateral sclerosis
AU - Miana-Mena, Francisco Javier
AU - González-Mingot, Cristina
AU - Larrodé, Pilar
AU - Muñoz, María Jesús
AU - Oliván, Sara
AU - Fuentes-Broto, Lorena
AU - Martínez-Ballarín, Enrique
AU - Reiter, Russel J.
AU - Osta, Rosario
AU - García, Joaquín José
PY - 2011/5/1
Y1 - 2011/5/1
N2 - 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.
AB - 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.
KW - Amyotrophic lateral sclerosis
KW - G93A
KW - Lipid peroxidation
KW - Oxidative stress
KW - Protein oxidation
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U2 - 10.1007/s00415-010-5825-8
DO - 10.1007/s00415-010-5825-8
M3 - Article
C2 - 21108037
AN - SCOPUS:79959967416
VL - 258
SP - 762
EP - 769
JO - Deutsche Zeitschrift fur Nervenheilkunde
JF - Deutsche Zeitschrift fur Nervenheilkunde
SN - 0340-5354
IS - 5
ER -