Zinc supplementation does not prevent cuprizone toxicity in the brain of mice

Marina D. Jeyasingham, Harcharan K. Rooprai, David Dexter, Oliver E. Pratt, Samuel Komoly

Research output: Contribution to journalArticle

2 Citations (Scopus)

Abstract

The metal ion chelator cuprizone (bis(cyclohexanone)oxalyldihydrazone) is an effective agent for inducing experimental demyelination in rodents. The current work was undertaken to assess whether this demyelination was a result of the ability of cuprizone to sequester metal ions thereby leading to a reduction of tissue concentrations of essential trace metals. After cuprizone administration, demyelination in mouse brain was followed using biochemical techniques and it was shown that mice fed cuprizone for 49 days had reduced blood concentrations of copper, zinc and iron but that the brain contents of these cations were not decreased. Also, that loss of carbonic anhydrase activity (CAII) (a zinc metalloenzyme) in cuprizone fed mice could not be prevented by the feeding of a zinc supplemented diet. Indeed, zinc supplementation itself had an deletrious effect on kidney CAII activity. The findings are discussed in relation to possible roles for CA in the CNS and kidney.

Original languageEnglish
Pages (from-to)181-187
Number of pages7
JournalNeuroscience Research Communications
Volume22
Issue number3
DOIs
Publication statusPublished - May 1 1998

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Keywords

  • Carbonic anhydrase
  • Copper
  • Cuprizone
  • Demyelination
  • Iron
  • Zinc

ASJC Scopus subject areas

  • Neuroscience(all)

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