Distribution of oligodendrocyte loss and mitochondrial toxicity in the cuprizone-induced experimental demyelination model

P. Acs, M. A. Selak, S. Komoly, B. Kálmán

Research output: Contribution to journalArticle

28 Citations (Scopus)

Abstract

Cuprizone is a copper-chelating mitochondrial toxin that causes oligodendrocyte apoptosis and demyelination preferentially in the corpus callosum (CC) and the superior cerebellar peduncles, but not in the spinal cord (SC) of C57BL/6 mice. Here we aimed to determine the activities of copper-containing enzymes in correlation with the distribution of demyelination during exposure to cuprizone. The study revealed mitochondrial complex IV and superoxide dismutase activity alterations in both the pathology-affected CC and the non-affected SC. This observation raises the possibility that regionally different subcellular molecular interactions lead to the selective oligodendrocyte loss induced by the nonselective mitochondrial toxin, cuprizone.

Original languageEnglish
Pages (from-to)128-131
Number of pages4
JournalJournal of Neuroimmunology
Volume262
Issue number1-2
DOIs
Publication statusPublished - 2013

Fingerprint

Cuprizone
Oligodendroglia
Demyelinating Diseases
Theoretical Models
Corpus Callosum
Copper
Spinal Cord
Inbred C57BL Mouse
Superoxide Dismutase
Apoptosis
Pathology
Enzymes

Keywords

  • Copper chelation
  • Cuprizone
  • Demyelination
  • Mitochondrial toxicity
  • Multiple sclerosis
  • Selective vulnerability

ASJC Scopus subject areas

  • Immunology
  • Clinical Neurology
  • Immunology and Allergy
  • Neurology

Cite this

Distribution of oligodendrocyte loss and mitochondrial toxicity in the cuprizone-induced experimental demyelination model. / Acs, P.; Selak, M. A.; Komoly, S.; Kálmán, B.

In: Journal of Neuroimmunology, Vol. 262, No. 1-2, 2013, p. 128-131.

Research output: Contribution to journalArticle

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