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.
Autore Pugliese
Tutti gli autori
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F. BENETTI , M. VENTURA , B. SALMINI , S. CEOLA , D. CARBONERA , S. MAMMI , A. ZITOLO , P. D'ANGELO , E. URSO , M. MAFFIA , B. SALVATO , E. SPISNI
Titolo volume/Rivista
NEUROTOXICOLOGY
Anno di pubblicazione
2010
ISSN
0161-813X
ISBN
Non Disponibile
Numero di citazioni Wos
23
Ultimo Aggiornamento Citazioni
22/04/2018
Numero di citazioni Scopus
26
Ultimo Aggiornamento Citazioni
22/04/2018
Settori ERC
Non Disponibile
Codici ASJC
Non Disponibile
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