Sub-chronic administration of doxorubicin to Wistar rats results in oxidative stress and unaltered apoptotic signaling in the lung

Detalhes bibliográficos
Autor(a) principal: Machado, Nuno G.
Data de Publicação: 2010
Outros Autores: Baldeiras, Inês, Pereira, Gonçalo C., Pereira, Susana P., Oliveira, Paulo J.
Tipo de documento: Artigo
Idioma: eng
Título da fonte: Repositório Científico de Acesso Aberto de Portugal (Repositórios Cientìficos)
Texto Completo: http://hdl.handle.net/10316/47552
https://doi.org/10.1016/j.cbi.2010.09.027
Resumo: Despite the vast published data on cardiac toxicity, there is still little work done regarding the toxicity of the antineoplastic agent Doxorubicin (DOX) in the lung. The aim of the present work was to determine if DOX causes alterations in selected apoptotic proteins and oxidative stress in the lung, in a similar manner to what occurs in the heart. For that purpose, lungs from Wistar-Han rats sub-chronically treated with vehicle or DOX for seven weeks were collected and analyzed concerning several proteins involved in mitochondrial permeabilization and apoptotic pathways, including p53, Bax and Bcl-2 and different oxidative stress markers. After sub-chronic DOX treatment, no alterations in lung proteins involved in mitochondrial membrane permeabilization or caspase 3 and 9-like activities were found. Nevertheless, an increase in malondialdehyde levels and a decrease in the lung concentration of vitamin E were detected, despite no alterations in reduced and oxidized glutathione. The results obtained indicate for the first time that lungs from DOX-treated rats appear to be susceptible to increased lipid peroxidation, which can explain some cases of DOX-induced lung toxicity.
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spelling Sub-chronic administration of doxorubicin to Wistar rats results in oxidative stress and unaltered apoptotic signaling in the lungAnimalsApoptosisBody WeightCaspase 3Caspase 9DoxorubicinLungMaleMalondialdehydeMitochondrial ADP, ATP TranslocasesOxidative StressRatsRats, WistarSignal TransductionTime FactorsToxicity TestsTumor Suppressor Protein p53Vitamin EVoltage-Dependent Anion Channelsbcl-2-Associated X ProteinDespite the vast published data on cardiac toxicity, there is still little work done regarding the toxicity of the antineoplastic agent Doxorubicin (DOX) in the lung. The aim of the present work was to determine if DOX causes alterations in selected apoptotic proteins and oxidative stress in the lung, in a similar manner to what occurs in the heart. For that purpose, lungs from Wistar-Han rats sub-chronically treated with vehicle or DOX for seven weeks were collected and analyzed concerning several proteins involved in mitochondrial permeabilization and apoptotic pathways, including p53, Bax and Bcl-2 and different oxidative stress markers. After sub-chronic DOX treatment, no alterations in lung proteins involved in mitochondrial membrane permeabilization or caspase 3 and 9-like activities were found. Nevertheless, an increase in malondialdehyde levels and a decrease in the lung concentration of vitamin E were detected, despite no alterations in reduced and oxidized glutathione. The results obtained indicate for the first time that lungs from DOX-treated rats appear to be susceptible to increased lipid peroxidation, which can explain some cases of DOX-induced lung toxicity.2010-12-05info:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/articlehttp://hdl.handle.net/10316/47552http://hdl.handle.net/10316/47552https://doi.org/10.1016/j.cbi.2010.09.027engMachado, Nuno G.Baldeiras, InêsPereira, Gonçalo C.Pereira, Susana P.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:RCAAP2021-10-11T09:23:40ZPortal AgregadorONG
dc.title.none.fl_str_mv Sub-chronic administration of doxorubicin to Wistar rats results in oxidative stress and unaltered apoptotic signaling in the lung
title Sub-chronic administration of doxorubicin to Wistar rats results in oxidative stress and unaltered apoptotic signaling in the lung
spellingShingle Sub-chronic administration of doxorubicin to Wistar rats results in oxidative stress and unaltered apoptotic signaling in the lung
Machado, Nuno G.
Animals
Apoptosis
Body Weight
Caspase 3
Caspase 9
Doxorubicin
Lung
Male
Malondialdehyde
Mitochondrial ADP, ATP Translocases
Oxidative Stress
Rats
Rats, Wistar
Signal Transduction
Time Factors
Toxicity Tests
Tumor Suppressor Protein p53
Vitamin E
Voltage-Dependent Anion Channels
bcl-2-Associated X Protein
title_short Sub-chronic administration of doxorubicin to Wistar rats results in oxidative stress and unaltered apoptotic signaling in the lung
title_full Sub-chronic administration of doxorubicin to Wistar rats results in oxidative stress and unaltered apoptotic signaling in the lung
title_fullStr Sub-chronic administration of doxorubicin to Wistar rats results in oxidative stress and unaltered apoptotic signaling in the lung
title_full_unstemmed Sub-chronic administration of doxorubicin to Wistar rats results in oxidative stress and unaltered apoptotic signaling in the lung
title_sort Sub-chronic administration of doxorubicin to Wistar rats results in oxidative stress and unaltered apoptotic signaling in the lung
author Machado, Nuno G.
author_facet Machado, Nuno G.
Baldeiras, Inês
Pereira, Gonçalo C.
Pereira, Susana P.
Oliveira, Paulo J.
author_role author
author2 Baldeiras, Inês
Pereira, Gonçalo C.
Pereira, Susana P.
Oliveira, Paulo J.
author2_role author
author
author
author
dc.contributor.author.fl_str_mv Machado, Nuno G.
Baldeiras, Inês
Pereira, Gonçalo C.
Pereira, Susana P.
Oliveira, Paulo J.
dc.subject.por.fl_str_mv Animals
Apoptosis
Body Weight
Caspase 3
Caspase 9
Doxorubicin
Lung
Male
Malondialdehyde
Mitochondrial ADP, ATP Translocases
Oxidative Stress
Rats
Rats, Wistar
Signal Transduction
Time Factors
Toxicity Tests
Tumor Suppressor Protein p53
Vitamin E
Voltage-Dependent Anion Channels
bcl-2-Associated X Protein
topic Animals
Apoptosis
Body Weight
Caspase 3
Caspase 9
Doxorubicin
Lung
Male
Malondialdehyde
Mitochondrial ADP, ATP Translocases
Oxidative Stress
Rats
Rats, Wistar
Signal Transduction
Time Factors
Toxicity Tests
Tumor Suppressor Protein p53
Vitamin E
Voltage-Dependent Anion Channels
bcl-2-Associated X Protein
description Despite the vast published data on cardiac toxicity, there is still little work done regarding the toxicity of the antineoplastic agent Doxorubicin (DOX) in the lung. The aim of the present work was to determine if DOX causes alterations in selected apoptotic proteins and oxidative stress in the lung, in a similar manner to what occurs in the heart. For that purpose, lungs from Wistar-Han rats sub-chronically treated with vehicle or DOX for seven weeks were collected and analyzed concerning several proteins involved in mitochondrial permeabilization and apoptotic pathways, including p53, Bax and Bcl-2 and different oxidative stress markers. After sub-chronic DOX treatment, no alterations in lung proteins involved in mitochondrial membrane permeabilization or caspase 3 and 9-like activities were found. Nevertheless, an increase in malondialdehyde levels and a decrease in the lung concentration of vitamin E were detected, despite no alterations in reduced and oxidized glutathione. The results obtained indicate for the first time that lungs from DOX-treated rats appear to be susceptible to increased lipid peroxidation, which can explain some cases of DOX-induced lung toxicity.
publishDate 2010
dc.date.none.fl_str_mv 2010-12-05
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/10316/47552
http://hdl.handle.net/10316/47552
https://doi.org/10.1016/j.cbi.2010.09.027
url http://hdl.handle.net/10316/47552
https://doi.org/10.1016/j.cbi.2010.09.027
dc.language.iso.fl_str_mv eng
language eng
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
repository.mail.fl_str_mv
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