Dioxin-induced acute cardiac mitochondrial oxidative damage and increased activity of ATP-sensitive potassium channels in Wistar rats
Autor(a) principal: | |
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Data de Publicação: | 2013 |
Outros Autores: | , , , , , , , |
Tipo de documento: | Artigo |
Idioma: | eng |
Título da fonte: | Repositório Científico de Acesso Aberto de Portugal (Repositórios Cientìficos) |
Texto Completo: | http://hdl.handle.net/10316/25767 https://doi.org/10.1016/j.envpol.2013.05.049 |
Resumo: | The environmental dioxin 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) is classified as a Group 1 human carcinogen and teratogenic agent.We hypothesize that TCDD-induced oxidative stress may also interfere with mitochondrial ATP-sensitive potassium channels (mitoKATP), which are known to regulate and to be regulated by mitochondrial redox state. We investigated the effects of an acute treatment of male Wistar rats with TCDD (50 mg/kg i.p.) and measured the regulation of cardiac mitoKATP. While the function of cardiac mitochondria was slightly depressed, mitoKATP activity was 52% higher in animals treated with TCDD. The same effects were not observed in liver mitochondria isolated from the same animals. Our data also shows that regulation of mitochondrial ROS production by mitoKATP activity is different in both groups. To our knowledge, this is the first report to show that TCDD increases mitoKATP activity in the heart, which may counteract the increased oxidative stress caused by the dioxin during acute exposure. |
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Dioxin-induced acute cardiac mitochondrial oxidative damage and increased activity of ATP-sensitive potassium channels in Wistar ratsBioenergeticsDioxinmitoKATPMitochondriaROSTCDDThe environmental dioxin 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) is classified as a Group 1 human carcinogen and teratogenic agent.We hypothesize that TCDD-induced oxidative stress may also interfere with mitochondrial ATP-sensitive potassium channels (mitoKATP), which are known to regulate and to be regulated by mitochondrial redox state. We investigated the effects of an acute treatment of male Wistar rats with TCDD (50 mg/kg i.p.) and measured the regulation of cardiac mitoKATP. While the function of cardiac mitochondria was slightly depressed, mitoKATP activity was 52% higher in animals treated with TCDD. The same effects were not observed in liver mitochondria isolated from the same animals. Our data also shows that regulation of mitochondrial ROS production by mitoKATP activity is different in both groups. To our knowledge, this is the first report to show that TCDD increases mitoKATP activity in the heart, which may counteract the increased oxidative stress caused by the dioxin during acute exposure.SPP and GCP are supported by a Portuguese Foundation for Science and Technology (FCT) Ph.D. fellowship (SFRH/BD/64247/ 2009 and SFRH/BD/36938/2007). The present work is supported by FCT grants PTDC-SAU-OSM-64084-2006 and PTDC/QUI-QUI/ 101409/2008 (to PO) and PEst-C/SAU/LA0001/2011 (to CNC) cofunded by FEDER, COMPETE and the Portuguese National Funds.Elsevier Ltd.2013info:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/articlehttp://hdl.handle.net/10316/25767http://hdl.handle.net/10316/25767https://doi.org/10.1016/j.envpol.2013.05.049enghttp://www.sciencedirect.com/science/article/pii/S0269749113003084Pereira, Susana P.Pereira, Gonçalo C.Pereira, Cláudia V.Carvalho, Filipa S.Cordeiro, Marília H.Mota, Paula C.Ramalho-Santos, J.Moreno, A. J. M.Oliveira, Paulo J.info:eu-repo/semantics/openAccessreponame:Repositório Científico de Acesso Aberto de Portugal (Repositórios Cientìficos)instname:Agência para a Sociedade do Conhecimento (UMIC) - FCT - Sociedade da Informaçãoinstacron:RCAAP2022-07-27T13:29:36ZPortal AgregadorONG |
dc.title.none.fl_str_mv |
Dioxin-induced acute cardiac mitochondrial oxidative damage and increased activity of ATP-sensitive potassium channels in Wistar rats |
title |
Dioxin-induced acute cardiac mitochondrial oxidative damage and increased activity of ATP-sensitive potassium channels in Wistar rats |
spellingShingle |
Dioxin-induced acute cardiac mitochondrial oxidative damage and increased activity of ATP-sensitive potassium channels in Wistar rats Pereira, Susana P. Bioenergetics Dioxin mitoKATP Mitochondria ROS TCDD |
title_short |
Dioxin-induced acute cardiac mitochondrial oxidative damage and increased activity of ATP-sensitive potassium channels in Wistar rats |
title_full |
Dioxin-induced acute cardiac mitochondrial oxidative damage and increased activity of ATP-sensitive potassium channels in Wistar rats |
title_fullStr |
Dioxin-induced acute cardiac mitochondrial oxidative damage and increased activity of ATP-sensitive potassium channels in Wistar rats |
title_full_unstemmed |
Dioxin-induced acute cardiac mitochondrial oxidative damage and increased activity of ATP-sensitive potassium channels in Wistar rats |
title_sort |
Dioxin-induced acute cardiac mitochondrial oxidative damage and increased activity of ATP-sensitive potassium channels in Wistar rats |
author |
Pereira, Susana P. |
author_facet |
Pereira, Susana P. Pereira, Gonçalo C. Pereira, Cláudia V. Carvalho, Filipa S. Cordeiro, Marília H. Mota, Paula C. Ramalho-Santos, J. Moreno, A. J. M. Oliveira, Paulo J. |
author_role |
author |
author2 |
Pereira, Gonçalo C. Pereira, Cláudia V. Carvalho, Filipa S. Cordeiro, Marília H. Mota, Paula C. Ramalho-Santos, J. Moreno, A. J. M. Oliveira, Paulo J. |
author2_role |
author author author author author author author author |
dc.contributor.author.fl_str_mv |
Pereira, Susana P. Pereira, Gonçalo C. Pereira, Cláudia V. Carvalho, Filipa S. Cordeiro, Marília H. Mota, Paula C. Ramalho-Santos, J. Moreno, A. J. M. Oliveira, Paulo J. |
dc.subject.por.fl_str_mv |
Bioenergetics Dioxin mitoKATP Mitochondria ROS TCDD |
topic |
Bioenergetics Dioxin mitoKATP Mitochondria ROS TCDD |
description |
The environmental dioxin 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) is classified as a Group 1 human carcinogen and teratogenic agent.We hypothesize that TCDD-induced oxidative stress may also interfere with mitochondrial ATP-sensitive potassium channels (mitoKATP), which are known to regulate and to be regulated by mitochondrial redox state. We investigated the effects of an acute treatment of male Wistar rats with TCDD (50 mg/kg i.p.) and measured the regulation of cardiac mitoKATP. While the function of cardiac mitochondria was slightly depressed, mitoKATP activity was 52% higher in animals treated with TCDD. The same effects were not observed in liver mitochondria isolated from the same animals. Our data also shows that regulation of mitochondrial ROS production by mitoKATP activity is different in both groups. To our knowledge, this is the first report to show that TCDD increases mitoKATP activity in the heart, which may counteract the increased oxidative stress caused by the dioxin during acute exposure. |
publishDate |
2013 |
dc.date.none.fl_str_mv |
2013 |
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://hdl.handle.net/10316/25767 http://hdl.handle.net/10316/25767 https://doi.org/10.1016/j.envpol.2013.05.049 |
url |
http://hdl.handle.net/10316/25767 https://doi.org/10.1016/j.envpol.2013.05.049 |
dc.language.iso.fl_str_mv |
eng |
language |
eng |
dc.relation.none.fl_str_mv |
http://www.sciencedirect.com/science/article/pii/S0269749113003084 |
dc.rights.driver.fl_str_mv |
info:eu-repo/semantics/openAccess |
eu_rights_str_mv |
openAccess |
dc.publisher.none.fl_str_mv |
Elsevier Ltd. |
publisher.none.fl_str_mv |
Elsevier Ltd. |
dc.source.none.fl_str_mv |
reponame:Repositório Científico de Acesso Aberto de Portugal (Repositórios Cientìficos) instname:Agência para a Sociedade do Conhecimento (UMIC) - FCT - Sociedade da Informação instacron:RCAAP |
instname_str |
Agência para a Sociedade do Conhecimento (UMIC) - FCT - Sociedade da Informação |
instacron_str |
RCAAP |
institution |
RCAAP |
reponame_str |
Repositório Científico de Acesso Aberto de Portugal (Repositórios Cientìficos) |
collection |
Repositório Científico de Acesso Aberto de Portugal (Repositórios Cientìficos) |
repository.name.fl_str_mv |
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repository.mail.fl_str_mv |
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1777302659279093760 |