Exposure to decabromodiphenyl ether (BDE-209) produces mitochondrial dysfunction in rat liver and cell death
Autor(a) principal: | |
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Data de Publicação: | 2017 |
Outros Autores: | , , , , , |
Tipo de documento: | Artigo |
Idioma: | eng |
Título da fonte: | Repositório Institucional da UNESP |
Texto Completo: | http://dx.doi.org/10.1080/15287394.2017.1357370 http://hdl.handle.net/11449/164786 |
Resumo: | Polybrominated diphenyl ethers (PBDE) are ubiquitous environmental pollutants. Exposure to these chemicals has been associated with developmental neurotoxicity, endocrine dysfunctions, reproductive disorders, and hepatotoxicity. The widespread use of PBDE as flame retardants has culminated in daily exposure of humans and wildlife to these contaminants and resulted in their banned use. Thus assessment of the potential effects of each PBDE congener on living organisms has become cause for concern. The aim of this study was to (1) examine the effects of decabromodiphenyl ether (BDE)-209 on different functions of HepG2 cells and (2) investigate whether this congener is involved in mitochondrial toxicity. The use of multiple methods was employed to (i) study the influence of BDE-209 on mitochondrial permeability transition (MPT) process in mitochondria isolated from rat liver and (ii) determine the consequential cellular damage. Our results showed that BDE-209 induced matrix swelling related to MPT with 10 mu M and ATP depletion with 0.1 mu M. In addition, 0.5 mu M BDE-209 reduced HepG2 cell viability, produced collapse of membrane potential, but increased levels of reactive oxygen species (ROS) after 48 h incubation. After 24 h with 5 mu M treatment elevated levels of ROS, DNA fragmentation and cytochrome c release, accompanied by caspase 9 and caspase 3 activation was noted. Taken together, these results suggest that short-duration exposure (24 or 48 h) to 0.5 mu M or 5 mu M BDE-209 concentrations diminished HepG2 cell viability due to apoptosis associated with mitochondrial dysfunction. |
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Exposure to decabromodiphenyl ether (BDE-209) produces mitochondrial dysfunction in rat liver and cell deathPolybrominated diphenyl ethers (PBDE) are ubiquitous environmental pollutants. Exposure to these chemicals has been associated with developmental neurotoxicity, endocrine dysfunctions, reproductive disorders, and hepatotoxicity. The widespread use of PBDE as flame retardants has culminated in daily exposure of humans and wildlife to these contaminants and resulted in their banned use. Thus assessment of the potential effects of each PBDE congener on living organisms has become cause for concern. The aim of this study was to (1) examine the effects of decabromodiphenyl ether (BDE)-209 on different functions of HepG2 cells and (2) investigate whether this congener is involved in mitochondrial toxicity. The use of multiple methods was employed to (i) study the influence of BDE-209 on mitochondrial permeability transition (MPT) process in mitochondria isolated from rat liver and (ii) determine the consequential cellular damage. Our results showed that BDE-209 induced matrix swelling related to MPT with 10 mu M and ATP depletion with 0.1 mu M. In addition, 0.5 mu M BDE-209 reduced HepG2 cell viability, produced collapse of membrane potential, but increased levels of reactive oxygen species (ROS) after 48 h incubation. After 24 h with 5 mu M treatment elevated levels of ROS, DNA fragmentation and cytochrome c release, accompanied by caspase 9 and caspase 3 activation was noted. Taken together, these results suggest that short-duration exposure (24 or 48 h) to 0.5 mu M or 5 mu M BDE-209 concentrations diminished HepG2 cell viability due to apoptosis associated with mitochondrial dysfunction.Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)Univ Sao Paulo, Sch Pharmaceut Sci Ribeirao Preto, Dept Clin Anal Toxicol & Bromatol, Ribeirao Preto, SP, BrazilSao Paulo State Univ, Fac Agron Sci Botucatu, Dept Bioproc & Biotechnol, Botucatu, SP, BrazilUniv Sao Paulo, Dept Quim, Fac Filosofia Ciencias & Letras Ribeirao Preto, Ribeirao Preto, SP, BrazilUniv Coimbra, CNC Ctr Neurosci & Cell Biol, Fac Med, Coimbra, PortugalUniv Coimbra, Dept Life Sci, Coimbra, PortugalUnesp, Inst Quim, Inst Nacl Tecnol Alternat Deteccao Avaliacao Toxi, Caixa Postal 355, BR-14800900 Araraquara, SP, BrazilSao Paulo State Univ, Fac Agron Sci Botucatu, Dept Bioproc & Biotechnol, Botucatu, SP, BrazilUnesp, Inst Quim, Inst Nacl Tecnol Alternat Deteccao Avaliacao Toxi, Caixa Postal 355, BR-14800900 Araraquara, SP, BrazilFAPESP: 2009/06912-6FAPESP: 2010/02661-6FAPESP: 2012/13123-0Taylor & Francis IncUniversidade de São Paulo (USP)Universidade Estadual Paulista (Unesp)Univ CoimbraPereira, Lilian C. [UNESP]Souza, Alecsandra O.Tasso, Maria J.Oliveira, Alana M. C.Duarte, Filipe V.Palmeira, Carlos M.Dorta, Daniel J. [UNESP]2018-11-26T17:56:05Z2018-11-26T17:56:05Z2017-01-01info:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/article1129-1144application/pdfhttp://dx.doi.org/10.1080/15287394.2017.1357370Journal Of Toxicology And Environmental Health-part A-current Issues. Philadelphia: Taylor & Francis Inc, v. 80, n. 19-21, p. 1129-1144, 2017.1528-7394http://hdl.handle.net/11449/16478610.1080/15287394.2017.1357370WOS:000416348400009WOS000416348400009.pdfWeb of Sciencereponame:Repositório Institucional da UNESPinstname:Universidade Estadual Paulista (UNESP)instacron:UNESPengJournal Of Toxicology And Environmental Health-part A-current Issues0,888info:eu-repo/semantics/openAccess2024-06-24T14:51:41Zoai:repositorio.unesp.br:11449/164786Repositório InstitucionalPUBhttp://repositorio.unesp.br/oai/requestopendoar:29462024-08-05T18:01:47.152498Repositório Institucional da UNESP - Universidade Estadual Paulista (UNESP)false |
dc.title.none.fl_str_mv |
Exposure to decabromodiphenyl ether (BDE-209) produces mitochondrial dysfunction in rat liver and cell death |
title |
Exposure to decabromodiphenyl ether (BDE-209) produces mitochondrial dysfunction in rat liver and cell death |
spellingShingle |
Exposure to decabromodiphenyl ether (BDE-209) produces mitochondrial dysfunction in rat liver and cell death Pereira, Lilian C. [UNESP] |
title_short |
Exposure to decabromodiphenyl ether (BDE-209) produces mitochondrial dysfunction in rat liver and cell death |
title_full |
Exposure to decabromodiphenyl ether (BDE-209) produces mitochondrial dysfunction in rat liver and cell death |
title_fullStr |
Exposure to decabromodiphenyl ether (BDE-209) produces mitochondrial dysfunction in rat liver and cell death |
title_full_unstemmed |
Exposure to decabromodiphenyl ether (BDE-209) produces mitochondrial dysfunction in rat liver and cell death |
title_sort |
Exposure to decabromodiphenyl ether (BDE-209) produces mitochondrial dysfunction in rat liver and cell death |
author |
Pereira, Lilian C. [UNESP] |
author_facet |
Pereira, Lilian C. [UNESP] Souza, Alecsandra O. Tasso, Maria J. Oliveira, Alana M. C. Duarte, Filipe V. Palmeira, Carlos M. Dorta, Daniel J. [UNESP] |
author_role |
author |
author2 |
Souza, Alecsandra O. Tasso, Maria J. Oliveira, Alana M. C. Duarte, Filipe V. Palmeira, Carlos M. Dorta, Daniel J. [UNESP] |
author2_role |
author author author author author author |
dc.contributor.none.fl_str_mv |
Universidade de São Paulo (USP) Universidade Estadual Paulista (Unesp) Univ Coimbra |
dc.contributor.author.fl_str_mv |
Pereira, Lilian C. [UNESP] Souza, Alecsandra O. Tasso, Maria J. Oliveira, Alana M. C. Duarte, Filipe V. Palmeira, Carlos M. Dorta, Daniel J. [UNESP] |
description |
Polybrominated diphenyl ethers (PBDE) are ubiquitous environmental pollutants. Exposure to these chemicals has been associated with developmental neurotoxicity, endocrine dysfunctions, reproductive disorders, and hepatotoxicity. The widespread use of PBDE as flame retardants has culminated in daily exposure of humans and wildlife to these contaminants and resulted in their banned use. Thus assessment of the potential effects of each PBDE congener on living organisms has become cause for concern. The aim of this study was to (1) examine the effects of decabromodiphenyl ether (BDE)-209 on different functions of HepG2 cells and (2) investigate whether this congener is involved in mitochondrial toxicity. The use of multiple methods was employed to (i) study the influence of BDE-209 on mitochondrial permeability transition (MPT) process in mitochondria isolated from rat liver and (ii) determine the consequential cellular damage. Our results showed that BDE-209 induced matrix swelling related to MPT with 10 mu M and ATP depletion with 0.1 mu M. In addition, 0.5 mu M BDE-209 reduced HepG2 cell viability, produced collapse of membrane potential, but increased levels of reactive oxygen species (ROS) after 48 h incubation. After 24 h with 5 mu M treatment elevated levels of ROS, DNA fragmentation and cytochrome c release, accompanied by caspase 9 and caspase 3 activation was noted. Taken together, these results suggest that short-duration exposure (24 or 48 h) to 0.5 mu M or 5 mu M BDE-209 concentrations diminished HepG2 cell viability due to apoptosis associated with mitochondrial dysfunction. |
publishDate |
2017 |
dc.date.none.fl_str_mv |
2017-01-01 2018-11-26T17:56:05Z 2018-11-26T17:56:05Z |
dc.type.status.fl_str_mv |
info:eu-repo/semantics/publishedVersion |
dc.type.driver.fl_str_mv |
info:eu-repo/semantics/article |
format |
article |
status_str |
publishedVersion |
dc.identifier.uri.fl_str_mv |
http://dx.doi.org/10.1080/15287394.2017.1357370 Journal Of Toxicology And Environmental Health-part A-current Issues. Philadelphia: Taylor & Francis Inc, v. 80, n. 19-21, p. 1129-1144, 2017. 1528-7394 http://hdl.handle.net/11449/164786 10.1080/15287394.2017.1357370 WOS:000416348400009 WOS000416348400009.pdf |
url |
http://dx.doi.org/10.1080/15287394.2017.1357370 http://hdl.handle.net/11449/164786 |
identifier_str_mv |
Journal Of Toxicology And Environmental Health-part A-current Issues. Philadelphia: Taylor & Francis Inc, v. 80, n. 19-21, p. 1129-1144, 2017. 1528-7394 10.1080/15287394.2017.1357370 WOS:000416348400009 WOS000416348400009.pdf |
dc.language.iso.fl_str_mv |
eng |
language |
eng |
dc.relation.none.fl_str_mv |
Journal Of Toxicology And Environmental Health-part A-current Issues 0,888 |
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info:eu-repo/semantics/openAccess |
eu_rights_str_mv |
openAccess |
dc.format.none.fl_str_mv |
1129-1144 application/pdf |
dc.publisher.none.fl_str_mv |
Taylor & Francis Inc |
publisher.none.fl_str_mv |
Taylor & Francis Inc |
dc.source.none.fl_str_mv |
Web of Science reponame:Repositório Institucional da UNESP instname:Universidade Estadual Paulista (UNESP) instacron:UNESP |
instname_str |
Universidade Estadual Paulista (UNESP) |
instacron_str |
UNESP |
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UNESP |
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Repositório Institucional da UNESP |
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Repositório Institucional da UNESP |
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Repositório Institucional da UNESP - Universidade Estadual Paulista (UNESP) |
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