Mitochondrial dysfunction due to mutant copper/zinc superoxide dismutase associated with amyotrophic lateral sclerosis is reversed by N-acetylcysteine

Mitochondrial dysfunction due to mutant copper/zinc superoxide dismutase associated with amyotrophic lateral sclerosis is reversed by N-acetylcysteine

We report that the expression of mutant G93A copper/zinc superoxide dismutase (SOD1), associated with familial amyotrophic lateral sclerosis, specifically causes a decrease in MTT reduction rate and ATP levels and an increase in both cytosolic and mitochondrial reactive oxygen species (ROS) producti...

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Bibliographic Details
Main Authors: Simone Beretta, Gessica Sala, Laura Mattavelli, Chiara Ceresa, Arianna Casciati, Alberto Ferri, Maria Teresa Carrì, Carlo Ferrarese
Format: Article
Language:English
Published: Elsevier 2003-08-01
Series:Neurobiology of Disease
Subjects:
Amyotrophic lateral sclerosis
SOD1
Oxidative stress
Mitochondrial function
n-Acetylcysteine
Online Access:http://www.sciencedirect.com/science/article/pii/S0969996103000433

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http://www.sciencedirect.com/science/article/pii/S0969996103000433

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