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DC Field | Value | Language |
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dc.contributor | Sistema FMUSP-HC: Faculdade de Medicina da Universidade de São Paulo (FMUSP) e Hospital das Clínicas da FMUSP | |
dc.contributor.author | MATIAS, Andreza C. | |
dc.contributor.author | MANIERI, Tania M. | |
dc.contributor.author | CIPRIANO, Samantha S. | |
dc.contributor.author | CARIONI, Vivian M. O. | |
dc.contributor.author | NOMURA, Cassiana S. | |
dc.contributor.author | MACHADO, Camila M. L. | |
dc.contributor.author | CERCHIARO, Giselle | |
dc.date.accessioned | 2013-09-23T16:55:51Z | |
dc.date.available | 2013-09-23T16:55:51Z | |
dc.date.issued | 2013 | |
dc.identifier.citation | TOXICOLOGY IN VITRO, v.27, n.1, p.349-357, 2013 | |
dc.identifier.issn | 0887-2333 | |
dc.identifier.uri | https://observatorio.fm.usp.br/handle/OPI/2443 | |
dc.description.abstract | Dithiocarbamates are nitrogen- and sulfur-containing compounds commonly used in pharmacology, medicine and agriculture. The molecular effects of dithiocarbamates on neuronal cell systems are not fully understood, especially in terms of their ability to accumulate copper ions inside the cell. In this work, the molecular effects of N,N-diethyldithiocarbamate (DEDTC) were studied in human SH-SY5Y neuroblastoma cells to determine the role of copper in the DEDTC toxicity and the pathway trigged in cell by the complex Cu-DEDTC. From concentration-dependent studies, we found that 5 mu M of this compound induced a drastic decrease in viable cells with a concomitant accumulation in intracellular copper resulted from complexation with DEDTC, measured by atomic absorption spectroscopy. The mechanism of DEDTC-induced apoptosis in neuronal model cells is thought to occur through the death receptor signaling triggered by DEDTC-copper complex in low concentration that is associated with the activation of caspase 8. Our results indicated that the mechanism of cell death involves cytochrome c release forming the apoptosome together with Apaf-1 and caspase 9, converting the caspase 9 into its active form, allowing it to activate caspase 3 as observed by immunofluorescence. This pathway is induced by the cytotoxic effects that occur when DEDTC forms a complex with the copper ions present in the culture medium and transports them into the cell, suggesting that the DEDTC by itself was not able to cause cell death and the major effect is from its copper-complex in neuroblastoma cells. The present study suggests a role for the influence of copper by low concentrations of DEDTC in the extracellular media, the absorption and accumulation of copper in the cell and apoptotic events, induced by the cytotoxic effects that occur when DEDTC forms a complex with the copper ions. | |
dc.description.sponsorship | Sao Paulo Research Foundation (FAPESP - Fundacao de Amparo a Pesquisa do Estado de Sao Paulo) | |
dc.description.sponsorship | National Council for Scientific and Technological Development (CNPq - Conselho Nacional de Desenvolvimento Cientifico e Tecnologico) | |
dc.language.iso | eng | |
dc.publisher | PERGAMON-ELSEVIER SCIENCE LTD | |
dc.relation.ispartof | Toxicology in Vitro | |
dc.rights | restrictedAccess | |
dc.subject | Diethyldithiocarbamate | |
dc.subject | Copper uptake | |
dc.subject | Copper toxicity | |
dc.subject | Apoptosis | |
dc.subject | DEDTC | |
dc.subject | Cytochrome c release | |
dc.subject | Neuroblastoma | |
dc.subject | SH-SY5Y | |
dc.subject.other | oxidative stress | |
dc.subject.other | pyrrolidine dithiocarbamate | |
dc.subject.other | lipid oxidation | |
dc.subject.other | myelin injury | |
dc.subject.other | n,n-diethyldithiocarbamate | |
dc.subject.other | accumulation | |
dc.subject.other | involvement | |
dc.subject.other | complexes | |
dc.subject.other | damage | |
dc.subject.other | death | |
dc.title | Diethyldithiocarbamate induces apoptosis in neuroblastoma cells by raising the intracellular copper level, triggering cytochrome c release and caspase activation | |
dc.type | article | |
dc.rights.holder | Copyright PERGAMON-ELSEVIER SCIENCE LTD | |
dc.identifier.doi | 10.1016/j.tiv.2012.08.017 | |
dc.identifier.pmid | 22951949 | |
dc.subject.wos | Toxicology | |
dc.type.category | original article | |
dc.type.version | publishedVersion | |
hcfmusp.author.external | MATIAS, Andreza C.:Fed Univ ABC UFABC, Ctr Nat Sci & Humanities, BR-09210170 Santo Andre, SP, Brazil | |
hcfmusp.author.external | MANIERI, Tania M.:Fed Univ ABC UFABC, Ctr Nat Sci & Humanities, BR-09210170 Santo Andre, SP, Brazil | |
hcfmusp.author.external | CIPRIANO, Samantha S.:Fed Univ ABC UFABC, Ctr Nat Sci & Humanities, BR-09210170 Santo Andre, SP, Brazil | |
hcfmusp.author.external | CARIONI, Vivian M. O.:Fed Univ ABC UFABC, Ctr Nat Sci & Humanities, BR-09210170 Santo Andre, SP, Brazil | |
hcfmusp.author.external | NOMURA, Cassiana S.:Univ Sao Paulo, Inst Chem, BR-05508000 Sao Paulo, Brazil | |
hcfmusp.author.external | CERCHIARO, Giselle:Fed Univ ABC UFABC, Ctr Nat Sci & Humanities, BR-09210170 Santo Andre, SP, Brazil | |
hcfmusp.description.beginpage | 349 | |
hcfmusp.description.endpage | 357 | |
hcfmusp.description.issue | 1 | |
hcfmusp.description.volume | 27 | |
hcfmusp.origem | WOS | |
hcfmusp.origem.id | 2-s2.0-85027924086 | |
hcfmusp.origem.id | WOS:000314371600041 | |
hcfmusp.publisher.city | OXFORD | |
hcfmusp.publisher.country | ENGLAND | |
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dc.description.index | MEDLINE | |
hcfmusp.remissive.sponsorship | CNPq | |
hcfmusp.remissive.sponsorship | FAPESP | |
hcfmusp.citation.scopus | 35 | - |
hcfmusp.scopus.lastupdate | 2024-03-29 | - |
Appears in Collections: | Artigos e Materiais de Revistas Científicas - LIM/43 Artigos e Materiais de Revistas Científicas - ODS/03 |
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