O Nicorandil preserva a funcionalidade do sistema fosforilativo e oxidativo mitocondrial num modelo animal de isquémia-reperfusão global
Autor(a) principal: | |
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Data de Publicação: | 2007 |
Outros Autores: | , , |
Tipo de documento: | Artigo |
Idioma: | por |
Título da fonte: | Repositório Científico de Acesso Aberto de Portugal (Repositórios Cientìficos) |
Texto Completo: | http://hdl.handle.net/10400.4/866 |
Resumo: | Ischemia followed by reperfusion (IR) negatively affects mitochondrial function. At the level of the oxidative-phosphorylative system, IR inhibits the respiratory complexes and ATP synthase, and increases the passive leak of protons through the inner mitochondrial membrane, uncoupling respiration from phosphorylation, decreasing mitochondrial potential and, consequently, ATP production. Drugs that minimize the mitochondrial damage induced by IR may prove to be clinically effective. In the present work, we analyzed the impact of nicorandil, a mitochondrial ATP-sensitive potassium channel agonist, on mitochondrial dysfunction at the level of the oxidative-phosphorylative system of rat hearts subjected to IR. The decrease in the respiratory control ratio (RCR) induced by IR leads to the conclusion that IR has a negative impact on the activity of the mitochondrial respiratory system, uncoupling oxidation from phosphorylation. This effect is reversed by nicorandil, which increases not only RCR, but also the ADP/O ratio. Regarding respiratory rate, state 3 rate was approximately the same for all the experimental groups, while state 4 rate was lower for the group where IR was induced in the presence of nicorandil. This result is in accordance with the data obtained for the RCR and ADP/O. State 4 rate is most affected by uncoupling, given that it is controlled by proton leak. Mitochondria subjected to IR in the presence of nicorandil have a lower state 4 rate, i.e. they are less uncoupled. From these results we conclude that nicorandil preserves the function of mitochondria subjected to IR in terms of both respiration and phosphorylative capacity. |
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O Nicorandil preserva a funcionalidade do sistema fosforilativo e oxidativo mitocondrial num modelo animal de isquémia-reperfusão globalNicorandil preserves the function of the mitochondrial phosphorylative and oxidative system in an animal model of global ischemia-reperfusionMitocôndriaNicorandilRatosLesão de ReperfusãoIschemia followed by reperfusion (IR) negatively affects mitochondrial function. At the level of the oxidative-phosphorylative system, IR inhibits the respiratory complexes and ATP synthase, and increases the passive leak of protons through the inner mitochondrial membrane, uncoupling respiration from phosphorylation, decreasing mitochondrial potential and, consequently, ATP production. Drugs that minimize the mitochondrial damage induced by IR may prove to be clinically effective. In the present work, we analyzed the impact of nicorandil, a mitochondrial ATP-sensitive potassium channel agonist, on mitochondrial dysfunction at the level of the oxidative-phosphorylative system of rat hearts subjected to IR. The decrease in the respiratory control ratio (RCR) induced by IR leads to the conclusion that IR has a negative impact on the activity of the mitochondrial respiratory system, uncoupling oxidation from phosphorylation. This effect is reversed by nicorandil, which increases not only RCR, but also the ADP/O ratio. Regarding respiratory rate, state 3 rate was approximately the same for all the experimental groups, while state 4 rate was lower for the group where IR was induced in the presence of nicorandil. This result is in accordance with the data obtained for the RCR and ADP/O. State 4 rate is most affected by uncoupling, given that it is controlled by proton leak. Mitochondria subjected to IR in the presence of nicorandil have a lower state 4 rate, i.e. they are less uncoupled. From these results we conclude that nicorandil preserves the function of mitochondria subjected to IR in terms of both respiration and phosphorylative capacity.Sociedade Portuguesa de CardiologiaRIHUCCarreira, RMonteiro, PGonçalves, LProvidência, LA2010-12-07T12:17:46Z20072007-01-01T00:00:00Zinfo:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/articleapplication/pdfhttp://hdl.handle.net/10400.4/866porRev Port Cardiol. 2007 May;26(5):521-8.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:RCAAP2023-07-11T14:22:03Zoai:rihuc.huc.min-saude.pt:10400.4/866Portal AgregadorONGhttps://www.rcaap.pt/oai/openaireopendoar:71602024-03-19T18:03:24.419534Repositório Científico de Acesso Aberto de Portugal (Repositórios Cientìficos) - Agência para a Sociedade do Conhecimento (UMIC) - FCT - Sociedade da Informaçãofalse |
dc.title.none.fl_str_mv |
O Nicorandil preserva a funcionalidade do sistema fosforilativo e oxidativo mitocondrial num modelo animal de isquémia-reperfusão global Nicorandil preserves the function of the mitochondrial phosphorylative and oxidative system in an animal model of global ischemia-reperfusion |
title |
O Nicorandil preserva a funcionalidade do sistema fosforilativo e oxidativo mitocondrial num modelo animal de isquémia-reperfusão global |
spellingShingle |
O Nicorandil preserva a funcionalidade do sistema fosforilativo e oxidativo mitocondrial num modelo animal de isquémia-reperfusão global Carreira, R Mitocôndria Nicorandil Ratos Lesão de Reperfusão |
title_short |
O Nicorandil preserva a funcionalidade do sistema fosforilativo e oxidativo mitocondrial num modelo animal de isquémia-reperfusão global |
title_full |
O Nicorandil preserva a funcionalidade do sistema fosforilativo e oxidativo mitocondrial num modelo animal de isquémia-reperfusão global |
title_fullStr |
O Nicorandil preserva a funcionalidade do sistema fosforilativo e oxidativo mitocondrial num modelo animal de isquémia-reperfusão global |
title_full_unstemmed |
O Nicorandil preserva a funcionalidade do sistema fosforilativo e oxidativo mitocondrial num modelo animal de isquémia-reperfusão global |
title_sort |
O Nicorandil preserva a funcionalidade do sistema fosforilativo e oxidativo mitocondrial num modelo animal de isquémia-reperfusão global |
author |
Carreira, R |
author_facet |
Carreira, R Monteiro, P Gonçalves, L Providência, LA |
author_role |
author |
author2 |
Monteiro, P Gonçalves, L Providência, LA |
author2_role |
author author author |
dc.contributor.none.fl_str_mv |
RIHUC |
dc.contributor.author.fl_str_mv |
Carreira, R Monteiro, P Gonçalves, L Providência, LA |
dc.subject.por.fl_str_mv |
Mitocôndria Nicorandil Ratos Lesão de Reperfusão |
topic |
Mitocôndria Nicorandil Ratos Lesão de Reperfusão |
description |
Ischemia followed by reperfusion (IR) negatively affects mitochondrial function. At the level of the oxidative-phosphorylative system, IR inhibits the respiratory complexes and ATP synthase, and increases the passive leak of protons through the inner mitochondrial membrane, uncoupling respiration from phosphorylation, decreasing mitochondrial potential and, consequently, ATP production. Drugs that minimize the mitochondrial damage induced by IR may prove to be clinically effective. In the present work, we analyzed the impact of nicorandil, a mitochondrial ATP-sensitive potassium channel agonist, on mitochondrial dysfunction at the level of the oxidative-phosphorylative system of rat hearts subjected to IR. The decrease in the respiratory control ratio (RCR) induced by IR leads to the conclusion that IR has a negative impact on the activity of the mitochondrial respiratory system, uncoupling oxidation from phosphorylation. This effect is reversed by nicorandil, which increases not only RCR, but also the ADP/O ratio. Regarding respiratory rate, state 3 rate was approximately the same for all the experimental groups, while state 4 rate was lower for the group where IR was induced in the presence of nicorandil. This result is in accordance with the data obtained for the RCR and ADP/O. State 4 rate is most affected by uncoupling, given that it is controlled by proton leak. Mitochondria subjected to IR in the presence of nicorandil have a lower state 4 rate, i.e. they are less uncoupled. From these results we conclude that nicorandil preserves the function of mitochondria subjected to IR in terms of both respiration and phosphorylative capacity. |
publishDate |
2007 |
dc.date.none.fl_str_mv |
2007 2007-01-01T00:00:00Z 2010-12-07T12:17:46Z |
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/10400.4/866 |
url |
http://hdl.handle.net/10400.4/866 |
dc.language.iso.fl_str_mv |
por |
language |
por |
dc.relation.none.fl_str_mv |
Rev Port Cardiol. 2007 May;26(5):521-8. |
dc.rights.driver.fl_str_mv |
info:eu-repo/semantics/openAccess |
eu_rights_str_mv |
openAccess |
dc.format.none.fl_str_mv |
application/pdf |
dc.publisher.none.fl_str_mv |
Sociedade Portuguesa de Cardiologia |
publisher.none.fl_str_mv |
Sociedade Portuguesa de Cardiologia |
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 |
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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) |
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Repositório Científico de Acesso Aberto de Portugal (Repositórios Cientìficos) - Agência para a Sociedade do Conhecimento (UMIC) - FCT - Sociedade da Informação |
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