Cuprizone neurotoxicity, copper deficiency and neurodegeneration.

Abstract:

:Cuprizone is used to obtain demyelination in mice. Cuprizone-treated mice show symptoms similar to several neurodegenerative disorders such as severe status spongiosus. Although it has a simple chemical formula, its neurotoxic mechanism is still unknown. In this work, we examined both physico-chemical properties and biological effects of cuprizone. Our results indicate that cuprizone has very complicated and misunderstood solution chemistry. Moreover, we show here the inability of cuprizone to cross neither the intestinal epithelial barrier nor the neuronal cell membrane, as well its high tolerability by cultured neurons. If added to mice diet, cuprizone does not accumulate in liver or in brain. Therefore, its neurotoxic effect is explainable only in terms of its capability to chelate copper, leading to chronic copper deficiency.

journal_name

Neurotoxicology

journal_title

Neurotoxicology

authors

Benetti F,Ventura M,Salmini B,Ceola S,Carbonera D,Mammi S,Zitolo A,D'Angelo P,Urso E,Maffia M,Salvato B,Spisni E

doi

10.1016/j.neuro.2010.05.008

subject

Has Abstract

pub_date

2010-09-01 00:00:00

pages

509-17

issue

5

eissn

0161-813X

issn

1872-9711

pii

S0161-813X(10)00096-3

journal_volume

31

pub_type

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