Brain zinc chelation by diethyldithiocarbamate increased the behavioral and mitochondrial damages in zebrafish subjected to hypoxia
dc.contributor.author | Braga, Marcos Martins | pt_BR |
dc.contributor.author | Silva, Emerson Santos da | pt_BR |
dc.contributor.author | Moraes, Tarsila Barros | pt_BR |
dc.contributor.author | Schirmbeck, Gabriel Henrique | pt_BR |
dc.contributor.author | Rico, Eduardo Pacheco | pt_BR |
dc.contributor.author | Pinto, Charles Budaszewski | pt_BR |
dc.contributor.author | Rosemberg, Denis Broock | pt_BR |
dc.contributor.author | Dutra Filho, Carlos Severo | pt_BR |
dc.contributor.author | Dias, Renato Dutra | pt_BR |
dc.contributor.author | Oliveira, Diogo Losch de | pt_BR |
dc.contributor.author | Rocha, Joao Batista Teixeira da | pt_BR |
dc.contributor.author | Souza, Diogo Onofre Gomes de | pt_BR |
dc.date.accessioned | 2021-08-11T04:48:13Z | pt_BR |
dc.date.issued | 2016 | pt_BR |
dc.identifier.issn | 2045-2322 | pt_BR |
dc.identifier.uri | http://hdl.handle.net/10183/225540 | pt_BR |
dc.description.abstract | The increase in brain levels of chelatable zinc (Zn) in dysfunctions involving oxygen deprivation has stimulated the treatment with Zn chelators, such as diethyldithiocarbamate (DEDTC). However, DEDTC is a redox-active compound and it should be better evaluated during hypoxia. We use the hypoxia model in zebrafish to evaluate DEDTC effects. The exploratory behavior, chelatable Zn content, activities of mitochondrial dehydrogenases, reactive species levels (nitric oxide, superoxide anion, hydroxyl radical scavenger capacity) and cellular antioxidants (sulfhydryl, superoxide dismutase) of zebrafish brain were assessed after recovery, with or without 0.2mM DEDTC. The increased brain levels of chelatable Zn induced by hypoxia were mitigated by DEDTC. However, the novel tank task indicated that DEDTC did further enhance the exploratory deficit caused by hypoxia. Furthermore, these behavioral impairments caused by DEDTC were more associated with a negative action on mitochondrial activity and brain oxidative balance. Thus, due to apparent pro-oxidant action of DEDTC, our data do not support its use for neuroprotection in neuropathologies involving oxygen deprivation. | en |
dc.format.mimetype | application/pdf | pt_BR |
dc.language.iso | eng | pt_BR |
dc.relation.ispartof | Scientific reports. London. Vol. 6, article 20279, [9] p. | pt_BR |
dc.rights | Open Access | en |
dc.subject | Zinco | pt_BR |
dc.subject | Cerebrovascular disorders | en |
dc.subject | Hipóxia | pt_BR |
dc.subject | Diseases of the nervous system | en |
dc.subject | Ditiocarb | pt_BR |
dc.title | Brain zinc chelation by diethyldithiocarbamate increased the behavioral and mitochondrial damages in zebrafish subjected to hypoxia | pt_BR |
dc.type | Artigo de periódico | pt_BR |
dc.identifier.nrb | 001018683 | pt_BR |
dc.type.origin | Estrangeiro | pt_BR |
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