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.
|Number of pages||7|
|Journal||Neuroscience Research Communications|
|Publication status||Published - máj. 1 1998|
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