Doxorubicin increases the susceptibility of brain mitochondria to Ca2+-induced permeability transition and oxidative damage

Detalhes bibliográficos
Autor(a) principal: Cardoso, Susana
Data de Publicação: 2008
Outros Autores: Santos, Renato X., Carvalho, Cristina, Correia, Sónia, Pereira, Gonçalo C., Pereira, Susana S., Oliveira, Paulo J., Santos, Maria S., Proença, Teresa, Moreira, Paula I.
Tipo de documento: Artigo
Idioma: eng
Título da fonte: Repositório Científico de Acesso Aberto de Portugal (Repositórios Cientìficos)
Texto Completo: http://hdl.handle.net/10316/10086
https://doi.org/10.1016/j.freeradbiomed.2008.08.008
Resumo: This study was aimed at investigating the effects of subchronic administration of doxorubicin (DOX) on brain mitochondrial bioenergetics and oxidative status. Rats were treated with seven weekly injections of vehicle (sc, saline solution) or DOX (sc, 2 mg kg−1), and 1 week after the last administration of the drug the animals were sacrificed and brain mitochondrial fractions were obtained. Several parameters were analyzed: respiratory chain, phosphorylation system, induction of the permeability transition pore (PTP), mitochondrial aconitase activity, lipid peroxidation markers, and nonenzymatic antioxidant defenses. DOX treatment induced an increase in thiobarbituric acid-reactive substances and vitamin E levels and a decrease in reduced glutathione content and aconitase activity. Furthermore, DOX potentiated PTP induced by Ca2+. No statistical differences were observed in the other parameters analyzed. Altogether our results show that DOX treatment increases the susceptibility of brain mitochondria to Ca2+-induced PTP opening and oxidative stress, predisposing brain cells to degeneration and death
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spelling Doxorubicin increases the susceptibility of brain mitochondria to Ca2+-induced permeability transition and oxidative damageDoxorubicinMitochondriaOxidative stressPermeability transition poreFree radicalsbrainAnimalsAntioxidantsBrainCalciumDoxorubicinGlutathioneMaleMitochondriaMitochondrial Membrane Transport ProteinsMitochondrial Permeability Transition PoreOxidation-ReductionOxidative StressRatsRats, WistarVitamin EThis study was aimed at investigating the effects of subchronic administration of doxorubicin (DOX) on brain mitochondrial bioenergetics and oxidative status. Rats were treated with seven weekly injections of vehicle (sc, saline solution) or DOX (sc, 2 mg kg−1), and 1 week after the last administration of the drug the animals were sacrificed and brain mitochondrial fractions were obtained. Several parameters were analyzed: respiratory chain, phosphorylation system, induction of the permeability transition pore (PTP), mitochondrial aconitase activity, lipid peroxidation markers, and nonenzymatic antioxidant defenses. DOX treatment induced an increase in thiobarbituric acid-reactive substances and vitamin E levels and a decrease in reduced glutathione content and aconitase activity. Furthermore, DOX potentiated PTP induced by Ca2+. No statistical differences were observed in the other parameters analyzed. Altogether our results show that DOX treatment increases the susceptibility of brain mitochondria to Ca2+-induced PTP opening and oxidative stress, predisposing brain cells to degeneration and deathThe work was funded by the Portuguese Foundation for Science and Technology (PTDC-SAU-OSM-64084-2006). Referenceshttp://www.sciencedirect.com/science/article/B6T38-4T7087K-3/2/399a0c99d1e73842d49f885883fb79d72008info:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/articlehttp://hdl.handle.net/10316/10086http://hdl.handle.net/10316/10086https://doi.org/10.1016/j.freeradbiomed.2008.08.008engFree Radical Biology and Medicine. 45:10 (2008) 1395-14020891-5849Cardoso, SusanaSantos, Renato X.Carvalho, CristinaCorreia, SóniaPereira, Gonçalo C.Pereira, Susana S.Oliveira, Paulo J.Santos, Maria S.Proença, TeresaMoreira, Paula I.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:RCAAP2022-09-01T15:42:41Zoai:estudogeral.uc.pt:10316/10086Portal AgregadorONGhttps://www.rcaap.pt/oai/openaireopendoar:71602024-03-19T20:55:24.327015Repositório 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 Doxorubicin increases the susceptibility of brain mitochondria to Ca2+-induced permeability transition and oxidative damage
title Doxorubicin increases the susceptibility of brain mitochondria to Ca2+-induced permeability transition and oxidative damage
spellingShingle Doxorubicin increases the susceptibility of brain mitochondria to Ca2+-induced permeability transition and oxidative damage
Cardoso, Susana
Doxorubicin
Mitochondria
Oxidative stress
Permeability transition pore
Free radicals
brain
Animals
Antioxidants
Brain
Calcium
Doxorubicin
Glutathione
Male
Mitochondria
Mitochondrial Membrane Transport Proteins
Mitochondrial Permeability Transition Pore
Oxidation-Reduction
Oxidative Stress
Rats
Rats, Wistar
Vitamin E
title_short Doxorubicin increases the susceptibility of brain mitochondria to Ca2+-induced permeability transition and oxidative damage
title_full Doxorubicin increases the susceptibility of brain mitochondria to Ca2+-induced permeability transition and oxidative damage
title_fullStr Doxorubicin increases the susceptibility of brain mitochondria to Ca2+-induced permeability transition and oxidative damage
title_full_unstemmed Doxorubicin increases the susceptibility of brain mitochondria to Ca2+-induced permeability transition and oxidative damage
title_sort Doxorubicin increases the susceptibility of brain mitochondria to Ca2+-induced permeability transition and oxidative damage
author Cardoso, Susana
author_facet Cardoso, Susana
Santos, Renato X.
Carvalho, Cristina
Correia, Sónia
Pereira, Gonçalo C.
Pereira, Susana S.
Oliveira, Paulo J.
Santos, Maria S.
Proença, Teresa
Moreira, Paula I.
author_role author
author2 Santos, Renato X.
Carvalho, Cristina
Correia, Sónia
Pereira, Gonçalo C.
Pereira, Susana S.
Oliveira, Paulo J.
Santos, Maria S.
Proença, Teresa
Moreira, Paula I.
author2_role author
author
author
author
author
author
author
author
author
dc.contributor.author.fl_str_mv Cardoso, Susana
Santos, Renato X.
Carvalho, Cristina
Correia, Sónia
Pereira, Gonçalo C.
Pereira, Susana S.
Oliveira, Paulo J.
Santos, Maria S.
Proença, Teresa
Moreira, Paula I.
dc.subject.por.fl_str_mv Doxorubicin
Mitochondria
Oxidative stress
Permeability transition pore
Free radicals
brain
Animals
Antioxidants
Brain
Calcium
Doxorubicin
Glutathione
Male
Mitochondria
Mitochondrial Membrane Transport Proteins
Mitochondrial Permeability Transition Pore
Oxidation-Reduction
Oxidative Stress
Rats
Rats, Wistar
Vitamin E
topic Doxorubicin
Mitochondria
Oxidative stress
Permeability transition pore
Free radicals
brain
Animals
Antioxidants
Brain
Calcium
Doxorubicin
Glutathione
Male
Mitochondria
Mitochondrial Membrane Transport Proteins
Mitochondrial Permeability Transition Pore
Oxidation-Reduction
Oxidative Stress
Rats
Rats, Wistar
Vitamin E
description This study was aimed at investigating the effects of subchronic administration of doxorubicin (DOX) on brain mitochondrial bioenergetics and oxidative status. Rats were treated with seven weekly injections of vehicle (sc, saline solution) or DOX (sc, 2 mg kg−1), and 1 week after the last administration of the drug the animals were sacrificed and brain mitochondrial fractions were obtained. Several parameters were analyzed: respiratory chain, phosphorylation system, induction of the permeability transition pore (PTP), mitochondrial aconitase activity, lipid peroxidation markers, and nonenzymatic antioxidant defenses. DOX treatment induced an increase in thiobarbituric acid-reactive substances and vitamin E levels and a decrease in reduced glutathione content and aconitase activity. Furthermore, DOX potentiated PTP induced by Ca2+. No statistical differences were observed in the other parameters analyzed. Altogether our results show that DOX treatment increases the susceptibility of brain mitochondria to Ca2+-induced PTP opening and oxidative stress, predisposing brain cells to degeneration and death
publishDate 2008
dc.date.none.fl_str_mv 2008
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/10316/10086
http://hdl.handle.net/10316/10086
https://doi.org/10.1016/j.freeradbiomed.2008.08.008
url http://hdl.handle.net/10316/10086
https://doi.org/10.1016/j.freeradbiomed.2008.08.008
dc.language.iso.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv Free Radical Biology and Medicine. 45:10 (2008) 1395-1402
0891-5849
dc.rights.driver.fl_str_mv info:eu-repo/semantics/openAccess
eu_rights_str_mv openAccess
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 Repositório Científico de Acesso Aberto de Portugal (Repositórios Cientìficos) - Agência para a Sociedade do Conhecimento (UMIC) - FCT - Sociedade da Informação
repository.mail.fl_str_mv
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