Characterization of copper transport in gill cells of a mangrove crab Ucides cordatus

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dc.contributor.author Sa, M. G.
dc.contributor.author Zanotto, F. P. [UNIFESP]
dc.date.accessioned 2016-01-24T14:34:43Z
dc.date.available 2016-01-24T14:34:43Z
dc.date.issued 2013-11-15
dc.identifier http://dx.doi.org/10.1016/j.aquatox.2013.10.018
dc.identifier.citation Aquatic Toxicology. Amsterdam: Elsevier B.V., v. 144, p. 275-283, 2013.
dc.identifier.issn 0166-445X
dc.identifier.uri http://repositorio.unifesp.br/handle/11600/36981
dc.description.abstract The branchial epithelium of crustaceans is exposed to the environment and is the first site affected by metal pollution. the aim of this work was to characterize copper (Cu) transport using a fluorescent dye, Phen Green, in gill cells of a hypo-hyper-regulator mangrove crab Ucides cordatus. the results showed that added extracellular CuCl2 (0, 0.025, 0.150, 0.275, 0.550 and 1.110 mu M) showed typical Michaelis-Menten transport for Cu in anterior and posterior gill cells (V-max for anterior and posterior gills: 0.41 +/- 0.12 and 1.76 +/- 0.27 intracellular Cu in mu M x 22.10(4) cells(-1) x 300 s(-1) respectively and K-m values: 0.44 +/- 0.04 and 0.32 +/- 0.13 mu M, respectively). Intracellular Cu was significantly higher for posterior gill cells compared to anterior gill cells, suggesting differential accumulation for each gill type. Extracellular Ca at 20 mM decreased cellular Cu transport for both anterior and posterior gill cells. Nifedipine and verapamil, calcium channel inhibitors from plasma membrane, decreased Cu transport and affected K-m for both gills. These results could be due to a competition between Cu and Ca. Amiloride, a Na/Ca exchanger inhibitor, as well as bafilomycin, a proton pump inhibitor, caused a decrease of intracellular Cu compared to control. Ouabain and KB-R 7943, acting on Na homeostasis, similarly decreased intracellular Cu in both gill cells. Besides that, gill cells exposed to ATP and Cu simultaneously, showed an increase in intracellular copper, which was inhibited by vanadate, an inhibitor of P-type ATPase. These results suggest either the presence of a Cu-ATPase in crab gill cells, responsible for Cu influx, or the effect of a change in electrochemical membrane potential that could also drive Cu to the gill cell interior. Caffeine increased intracellular Cu, suggesting that intracellular Ca could be affecting Cu uptake. Overall the results show that copper uptake in gill cells of crabs is regulated by intracellular Ca, Ca channels and by Na exchangers. This is the first report of Cu transport characterization in whole gill cells of crabs. (C) 2013 Elsevier B.V. All rights reserved. en
dc.description.sponsorship Mackpesquisa
dc.description.sponsorship Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)
dc.description.sponsorship Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
dc.format.extent 275-283
dc.language.iso eng
dc.publisher Elsevier B.V.
dc.relation.ispartof Aquatic Toxicology
dc.rights Acesso restrito
dc.subject Ucides cordatus en
dc.subject Cu transport en
dc.subject Gill cells en
dc.subject ATP en
dc.subject Caffeine en
dc.subject Bafilomycin en
dc.subject Cu-ATPase en
dc.title Characterization of copper transport in gill cells of a mangrove crab Ucides cordatus en
dc.type Artigo
dc.rights.license http://www.elsevier.com/about/open-access/open-access-policies/article-posting-policy
dc.contributor.institution Universidade de São Paulo (USP)
dc.contributor.institution Universidade Federal de São Paulo (UNIFESP)
dc.description.affiliation Univ São Paulo, Dept Physiol, Biosci Inst, BR-05508900 São Paulo, Brazil
dc.description.affiliation Universidade Federal de São Paulo, Escola Paulista Med, Dept Biophys, BR-04044020 São Paulo, Brazil
dc.description.affiliationUnifesp Universidade Federal de São Paulo, Escola Paulista Med, Dept Biophys, BR-04044020 São Paulo, Brazil
dc.description.sponsorshipID FAPESP: 2009/15546-3
dc.identifier.doi 10.1016/j.aquatox.2013.10.018
dc.description.source Web of Science
dc.identifier.wos WOS:000330817200029



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