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

  • 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