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Mice with a partial deficiency of manganese superoxide dismutase show increased vulnerability to the mitochondrial toxins malonate, 3-nitropropionic acid, and MPTP.

Experimental neurology - 1 Jan 2001

Andreassen O A, Ferrante R J, Dedeoglu A, Albers D W, Klivenyi P, Carlson E J, Epstein C J, Beal M F

Abstract excerpt

There is substantial evidence implicating mitochondrial dysfunction and free radical generation as major mechanisms of neuronal death in neurodegenerative diseases. The major free radical scavenging enzyme in mitochondria is manganese superoxide dismutase (SOD2). In the present study we investigated the susceptibility of mice with a partial deficiency of SOD2 to the neurotoxins...

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Identifiers

PMID: 11161607
DOI: 10.1006/exnr.2000.7525

Genes

SOD2

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PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-07.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

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