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Article

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

Neurobiology of disease - 1 Aug 2003

Beretta Simone, Sala Gessica, Mattavelli Laura, Ceresa Chiara, Casciati Arianna, Ferri Alberto, Carrì Maria Teresa, Ferrarese Carlo

Abstract excerpt

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) production in human neuroblastoma SH-SY5Y cells compared to cells overexpressing wild-type SOD1 and untransfected cells....

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Identifiers

PMID: 12901835
DOI: 10.1016/s0969-9961(03)00043-3

Genes

SOD1

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PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-08.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

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