Bile acids are toxic for isolated cardiac mitochondria

Detalhes bibliográficos
Autor(a) principal: Ferreira, Manuela
Data de Publicação: 2005
Outros Autores: Coxito, Pedro, Sardão, Vilma, Palmeira, Carlos, Oliveira, Paulo
Tipo de documento: Artigo
Idioma: eng
Título da fonte: Repositório Científico de Acesso Aberto de Portugal (Repositórios Cientìficos)
Texto Completo: http://hdl.handle.net/10316/7824
https://doi.org/10.1385/CT:5:1:063
Resumo: Cholestasis and other liver diseases may affect the heart through the toxic effects of the retained bile acids on cardiac mitochondria, which could explain the origin of hepatic-derived cardiomyopathies. The objective of this work was to test the hypothesis that bile acids are toxic to heart mitochondria for concentrations that are relevant for cholestasis. Heart mitochondria were isolated from rat and subjected to incubation with selected bile acids (litocholic acid [LCA], deoxycholic acid [DCA], chenodeoxycholic acid [CDCA], glycochenodeoxycholic acid [GCDC], taurodeoxycholic acid [CDCA], and glycoursodeoxycholic acid [GUDC]). We observed that the most toxic bile acids were also the most lipophilic ones (LCA, DCA, and CDCA), inducing a decrease on state 3 respiration, respiratory control ratio, and membrane potential and causing the induction of the mitochondrial permeability transition. GUDC was the bile acid with lower indexes of toxicity on isolated heart mitochondria. The results of this research indicate that attoxicologically relevant concentrations, most bile acids (mainly the most lipophilic) alter mitochondrial bioenergetics. The impairment of cardiac mitochondrial function may be an important cause for the observed cardiac alterations during cholestasis.
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spelling Bile acids are toxic for isolated cardiac mitochondriaCholestasis and other liver diseases may affect the heart through the toxic effects of the retained bile acids on cardiac mitochondria, which could explain the origin of hepatic-derived cardiomyopathies. The objective of this work was to test the hypothesis that bile acids are toxic to heart mitochondria for concentrations that are relevant for cholestasis. Heart mitochondria were isolated from rat and subjected to incubation with selected bile acids (litocholic acid [LCA], deoxycholic acid [DCA], chenodeoxycholic acid [CDCA], glycochenodeoxycholic acid [GCDC], taurodeoxycholic acid [CDCA], and glycoursodeoxycholic acid [GUDC]). We observed that the most toxic bile acids were also the most lipophilic ones (LCA, DCA, and CDCA), inducing a decrease on state 3 respiration, respiratory control ratio, and membrane potential and causing the induction of the mitochondrial permeability transition. GUDC was the bile acid with lower indexes of toxicity on isolated heart mitochondria. The results of this research indicate that attoxicologically relevant concentrations, most bile acids (mainly the most lipophilic) alter mitochondrial bioenergetics. The impairment of cardiac mitochondrial function may be an important cause for the observed cardiac alterations during cholestasis.2005info:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/articlehttp://hdl.handle.net/10316/7824http://hdl.handle.net/10316/7824https://doi.org/10.1385/CT:5:1:063engCardiovascular Toxicology. 5:1 (2005) 63-73Ferreira, ManuelaCoxito, PedroSardão, VilmaPalmeira, CarlosOliveira, Pauloinfo: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:RCAAP2022-08-17T13:42:30Zoai:estudogeral.uc.pt:10316/7824Portal AgregadorONGhttps://www.rcaap.pt/oai/openaireopendoar:71602024-03-19T20:55:33.533984Repositório 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 Bile acids are toxic for isolated cardiac mitochondria
title Bile acids are toxic for isolated cardiac mitochondria
spellingShingle Bile acids are toxic for isolated cardiac mitochondria
Ferreira, Manuela
title_short Bile acids are toxic for isolated cardiac mitochondria
title_full Bile acids are toxic for isolated cardiac mitochondria
title_fullStr Bile acids are toxic for isolated cardiac mitochondria
title_full_unstemmed Bile acids are toxic for isolated cardiac mitochondria
title_sort Bile acids are toxic for isolated cardiac mitochondria
author Ferreira, Manuela
author_facet Ferreira, Manuela
Coxito, Pedro
Sardão, Vilma
Palmeira, Carlos
Oliveira, Paulo
author_role author
author2 Coxito, Pedro
Sardão, Vilma
Palmeira, Carlos
Oliveira, Paulo
author2_role author
author
author
author
dc.contributor.author.fl_str_mv Ferreira, Manuela
Coxito, Pedro
Sardão, Vilma
Palmeira, Carlos
Oliveira, Paulo
description Cholestasis and other liver diseases may affect the heart through the toxic effects of the retained bile acids on cardiac mitochondria, which could explain the origin of hepatic-derived cardiomyopathies. The objective of this work was to test the hypothesis that bile acids are toxic to heart mitochondria for concentrations that are relevant for cholestasis. Heart mitochondria were isolated from rat and subjected to incubation with selected bile acids (litocholic acid [LCA], deoxycholic acid [DCA], chenodeoxycholic acid [CDCA], glycochenodeoxycholic acid [GCDC], taurodeoxycholic acid [CDCA], and glycoursodeoxycholic acid [GUDC]). We observed that the most toxic bile acids were also the most lipophilic ones (LCA, DCA, and CDCA), inducing a decrease on state 3 respiration, respiratory control ratio, and membrane potential and causing the induction of the mitochondrial permeability transition. GUDC was the bile acid with lower indexes of toxicity on isolated heart mitochondria. The results of this research indicate that attoxicologically relevant concentrations, most bile acids (mainly the most lipophilic) alter mitochondrial bioenergetics. The impairment of cardiac mitochondrial function may be an important cause for the observed cardiac alterations during cholestasis.
publishDate 2005
dc.date.none.fl_str_mv 2005
dc.type.status.fl_str_mv info:eu-repo/semantics/publishedVersion
dc.type.driver.fl_str_mv info:eu-repo/semantics/article
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dc.identifier.uri.fl_str_mv http://hdl.handle.net/10316/7824
http://hdl.handle.net/10316/7824
https://doi.org/10.1385/CT:5:1:063
url http://hdl.handle.net/10316/7824
https://doi.org/10.1385/CT:5:1:063
dc.language.iso.fl_str_mv eng
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dc.relation.none.fl_str_mv Cardiovascular Toxicology. 5:1 (2005) 63-73
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