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Copper and zinc dismetabolism in the mouse brain upon chronic cuprizone treatment
Authors:P. Zatta  M. Raso  P. Zambenedetti  W. Wittkowski  L. Messori  F. Piccioli  P. L. Mauri  M. Beltramini
Affiliation:(1) CNR-Institute for Biomedical Technologies, Metalloproteins Unit, Department of Biology, University of Padua, Viale G. Colombo, 3, 3512 Padua, Italy;(2) Department of Biology, University of Padua, Padua, Italy;(3) Pathology Division, Dolo General Hospital, Venice, Italy;(4) Institute of Anatomy, University of Munster, Munster, Germany;(5) Department of Chemistry, University of Florence, Florence, Italy;(6) CNR-Institute for Biomedical Technologies, Milan, Italy
Abstract:
Recent reports describe successful treatment using copper chelation therapy in neurodegenerative animal models. However, the success claimed for chelation therapy in neurodegenerative diseases is still rather controversial. To acquire new information on copper metabolism/homeostasis, we utilized cuprizone, a very sensitive and selective copper-chelating agent with well-known neurotoxic properties, as a relevant chemical model in mice. Upon cuprizone treatment, mice developed a pronounced astrocytosis, with brain oedema and spongiosis characterised by vacuolisations of the neuropil predominantly in the white matter. In addition, cuprizone treatment severely altered copper and zinc homeostasis in the central nervous system (CNS) as well as in all other tissues examined, with increasing metal ion concentrations particularly in the CNS. Concomitant with this increase in the Cu and Zn concentration in the brain, metallothionein-I and -II were also highly immunoreactive in astrocyte, consistent with the astrocytosis and demyelination observed in our and other laboratories.Received 23 February 2005; received after revision 3 May 2005; accepted 13 May 2005
Keywords:Cuprizone  metallothionein  copper  zinc  myelin  astrocyte  mouse brain  prion disease
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