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dc.contributor.authorKudrin, AVen_US
dc.contributor.authorGromova, OAen_US
dc.date.accessioned2018-09-17T15:15:10Z
dc.date.issued2003en_US
dc.identifier1en_US
dc.identifier.citationTRACE ELEMENTS AND ELECTROLYTES, 2003, 20 pp. 1 - 4en_US
dc.identifier.issn0946-2104en_US
dc.identifier.urihttps://repository.icr.ac.uk/handle/internal/2734
dc.description.abstractZinc plays an essential role in the brain by participating in the bulk of enzymatic and regulatory events. However, zinc may become deleterious for brain cells in excessive amounts that may be released following stress, seizures or ischemic conditions. The mechanism of zinc-mediated neurotoxicity has appeared to be rather complex not only because of concentration effects on the level of receptors to the various neuromediators but also owing to the variety of zinc functions throughout the brain and its involvement in maintaining the cytokine network, nitric oxide production and cell signalling pathways. This review highlights a hypothetical mechanism that postulates the presence of 2 main sites of zinc turnover in the brain with slightly different functional roles.en_US
dc.format.extent1 - 4en_US
dc.titleTwo faces of zinc in the brainen_US
dc.typeJournal Article
rioxxterms.licenseref.startdate2003en_US
rioxxterms.typeJournal Article/Reviewen_US
dc.relation.isPartOfTRACE ELEMENTS AND ELECTROLYTESen_US
pubs.notesresearcherid-numbers: Gromova, Olga/J-4946-2017 orcid-numbers: Gromova, Olga/0000-0002-7663-710X unique-id: ISI:000180741900001en_US
pubs.notesNot knownen_US
pubs.organisational-group/ICR
pubs.volume20en_US
pubs.embargo.termsNot knownen_US
dc.contributor.icrauthorKudrin,en_US


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