Protective effects of mito-TEMPO against doxorubicin cardiotoxicity in mice
Autor(a) principal: | |
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Data de Publicação: | 2016 |
Outros Autores: | , , , , , , , , , |
Tipo de documento: | Artigo |
Idioma: | eng |
Título da fonte: | Repositório Institucional da UNIFESP |
Texto Completo: | http://dx.doi.org/10.1007/s00280-015-2949-7 https://repositorio.unifesp.br/handle/11600/57908 |
Resumo: | Doxorubicin (DOX) is a chemotherapeutic that is widely used for the treatment of many human tumors. However, the development of cardiotoxicity has limited its use. The aim of the present study was to evaluate the possible efficacy of mito-TEMPO (mito-T) as a protective agent against DOX-induced cardiotoxicity in mice. C57BL/6 mice were treated twice with mito-T at low (5 mg/kg body weight) or high (20 mg/kg body weight) dose and once with DOX (24 mg/kg body weight) or saline (0.1 mL/20 g body weight) by means of intraperitoneal injections. The levels of malondialdehyde (MLDA), a marker of lipid peroxidation, and serum levels of creatine kinase were evaluated 48 h after the injection of DOX. DOX induced lipid peroxidation in heart mitochondria (p < 0.001), and DOX-treated mice receiving mito-T at low dose had levels of MLDA significantly lower than the mice that received only DOX (p < 0.01). Furthermore, administration of mito-T alone did not cause any significant changes from control values. Additionally, DOX-treated mice treated with mito-T at high dose showed decrease in serum levels of total CK compared to mice treated with DOX alone (p < 0.05). Our results indicate that mito-T protects mice against DOX-induced cardiotoxicity. |
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Protective effects of mito-TEMPO against doxorubicin cardiotoxicity in miceDoxorubicinCardiotoxicityMitochondriaMito-TEMPODoxorubicin (DOX) is a chemotherapeutic that is widely used for the treatment of many human tumors. However, the development of cardiotoxicity has limited its use. The aim of the present study was to evaluate the possible efficacy of mito-TEMPO (mito-T) as a protective agent against DOX-induced cardiotoxicity in mice. C57BL/6 mice were treated twice with mito-T at low (5 mg/kg body weight) or high (20 mg/kg body weight) dose and once with DOX (24 mg/kg body weight) or saline (0.1 mL/20 g body weight) by means of intraperitoneal injections. The levels of malondialdehyde (MLDA), a marker of lipid peroxidation, and serum levels of creatine kinase were evaluated 48 h after the injection of DOX. DOX induced lipid peroxidation in heart mitochondria (p < 0.001), and DOX-treated mice receiving mito-T at low dose had levels of MLDA significantly lower than the mice that received only DOX (p < 0.01). Furthermore, administration of mito-T alone did not cause any significant changes from control values. Additionally, DOX-treated mice treated with mito-T at high dose showed decrease in serum levels of total CK compared to mice treated with DOX alone (p < 0.05). Our results indicate that mito-T protects mice against DOX-induced cardiotoxicity.Fundacao Oswaldo Cruz, Goncallo Moniz Res Ctr, Rua Waldemar Falcao 121, BR-40296710 Salvador, BA, BrazilUniv Fed Sao Paulo, Lab Imunol Celular & Bioquim Fungos & Protozoario, Sao Paulo, BrazilUCL, London, EnglandUniv Fed Sao Paulo, Lab Imunol Celular & Bioquim Fungos & Protozoario, Sao Paulo, BrazilWeb of ScienceFundacao de Amparo a Pesquisa do Estado da Bahia-FAPESB, State Government of Bahia, BrazilFundacao Oswaldo Cruz, BrazilConselho Nacional de Desenvolvimento Cientifico e Tecnologico-CNPq, Ministry of Science and Technology, BrazilSpringer2020-08-21T17:00:12Z2020-08-21T17:00:12Z2016info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersion659-662application/pdfhttp://dx.doi.org/10.1007/s00280-015-2949-7Cancer Chemotherapy And Pharmacology. New York, v. 77, n. 3, p. 659-662, 2016.10.1007/s00280-015-2949-7WOS000371246100023.pdf0344-5704https://repositorio.unifesp.br/handle/11600/57908WOS:000371246100023engCancer Chemotherapy And PharmacologyNew Yorkinfo:eu-repo/semantics/openAccessJunqueira Rocha, Viviane Costade Aragao Franca, Luciana Souzade Araujo, Cintia FigueiredoNg, Ayling Martinsde Andrade, Candace MachadoAndrade, Andre Cronemberger [UNIFESP]Santos, Emanuelle de SouzaBorges-Silva, Mariana da CruzMacambira, Simone GarciaNoronha-Dutra, Alberto AugustoPontes-de-Carvalho, Lain Carlosreponame:Repositório Institucional da UNIFESPinstname:Universidade Federal de São Paulo (UNIFESP)instacron:UNIFESP2024-08-09T08:00:09Zoai:repositorio.unifesp.br/:11600/57908Repositório InstitucionalPUBhttp://www.repositorio.unifesp.br/oai/requestbiblioteca.csp@unifesp.bropendoar:34652024-08-09T08:00:09Repositório Institucional da UNIFESP - Universidade Federal de São Paulo (UNIFESP)false |
dc.title.none.fl_str_mv |
Protective effects of mito-TEMPO against doxorubicin cardiotoxicity in mice |
title |
Protective effects of mito-TEMPO against doxorubicin cardiotoxicity in mice |
spellingShingle |
Protective effects of mito-TEMPO against doxorubicin cardiotoxicity in mice Junqueira Rocha, Viviane Costa Doxorubicin Cardiotoxicity Mitochondria Mito-TEMPO |
title_short |
Protective effects of mito-TEMPO against doxorubicin cardiotoxicity in mice |
title_full |
Protective effects of mito-TEMPO against doxorubicin cardiotoxicity in mice |
title_fullStr |
Protective effects of mito-TEMPO against doxorubicin cardiotoxicity in mice |
title_full_unstemmed |
Protective effects of mito-TEMPO against doxorubicin cardiotoxicity in mice |
title_sort |
Protective effects of mito-TEMPO against doxorubicin cardiotoxicity in mice |
author |
Junqueira Rocha, Viviane Costa |
author_facet |
Junqueira Rocha, Viviane Costa de Aragao Franca, Luciana Souza de Araujo, Cintia Figueiredo Ng, Ayling Martins de Andrade, Candace Machado Andrade, Andre Cronemberger [UNIFESP] Santos, Emanuelle de Souza Borges-Silva, Mariana da Cruz Macambira, Simone Garcia Noronha-Dutra, Alberto Augusto Pontes-de-Carvalho, Lain Carlos |
author_role |
author |
author2 |
de Aragao Franca, Luciana Souza de Araujo, Cintia Figueiredo Ng, Ayling Martins de Andrade, Candace Machado Andrade, Andre Cronemberger [UNIFESP] Santos, Emanuelle de Souza Borges-Silva, Mariana da Cruz Macambira, Simone Garcia Noronha-Dutra, Alberto Augusto Pontes-de-Carvalho, Lain Carlos |
author2_role |
author author author author author author author author author author |
dc.contributor.author.fl_str_mv |
Junqueira Rocha, Viviane Costa de Aragao Franca, Luciana Souza de Araujo, Cintia Figueiredo Ng, Ayling Martins de Andrade, Candace Machado Andrade, Andre Cronemberger [UNIFESP] Santos, Emanuelle de Souza Borges-Silva, Mariana da Cruz Macambira, Simone Garcia Noronha-Dutra, Alberto Augusto Pontes-de-Carvalho, Lain Carlos |
dc.subject.por.fl_str_mv |
Doxorubicin Cardiotoxicity Mitochondria Mito-TEMPO |
topic |
Doxorubicin Cardiotoxicity Mitochondria Mito-TEMPO |
description |
Doxorubicin (DOX) is a chemotherapeutic that is widely used for the treatment of many human tumors. However, the development of cardiotoxicity has limited its use. The aim of the present study was to evaluate the possible efficacy of mito-TEMPO (mito-T) as a protective agent against DOX-induced cardiotoxicity in mice. C57BL/6 mice were treated twice with mito-T at low (5 mg/kg body weight) or high (20 mg/kg body weight) dose and once with DOX (24 mg/kg body weight) or saline (0.1 mL/20 g body weight) by means of intraperitoneal injections. The levels of malondialdehyde (MLDA), a marker of lipid peroxidation, and serum levels of creatine kinase were evaluated 48 h after the injection of DOX. DOX induced lipid peroxidation in heart mitochondria (p < 0.001), and DOX-treated mice receiving mito-T at low dose had levels of MLDA significantly lower than the mice that received only DOX (p < 0.01). Furthermore, administration of mito-T alone did not cause any significant changes from control values. Additionally, DOX-treated mice treated with mito-T at high dose showed decrease in serum levels of total CK compared to mice treated with DOX alone (p < 0.05). Our results indicate that mito-T protects mice against DOX-induced cardiotoxicity. |
publishDate |
2016 |
dc.date.none.fl_str_mv |
2016 2020-08-21T17:00:12Z 2020-08-21T17:00:12Z |
dc.type.driver.fl_str_mv |
info:eu-repo/semantics/article |
dc.type.status.fl_str_mv |
info:eu-repo/semantics/publishedVersion |
format |
article |
status_str |
publishedVersion |
dc.identifier.uri.fl_str_mv |
http://dx.doi.org/10.1007/s00280-015-2949-7 Cancer Chemotherapy And Pharmacology. New York, v. 77, n. 3, p. 659-662, 2016. 10.1007/s00280-015-2949-7 WOS000371246100023.pdf 0344-5704 https://repositorio.unifesp.br/handle/11600/57908 WOS:000371246100023 |
url |
http://dx.doi.org/10.1007/s00280-015-2949-7 https://repositorio.unifesp.br/handle/11600/57908 |
identifier_str_mv |
Cancer Chemotherapy And Pharmacology. New York, v. 77, n. 3, p. 659-662, 2016. 10.1007/s00280-015-2949-7 WOS000371246100023.pdf 0344-5704 WOS:000371246100023 |
dc.language.iso.fl_str_mv |
eng |
language |
eng |
dc.relation.none.fl_str_mv |
Cancer Chemotherapy And Pharmacology |
dc.rights.driver.fl_str_mv |
info:eu-repo/semantics/openAccess |
eu_rights_str_mv |
openAccess |
dc.format.none.fl_str_mv |
659-662 application/pdf |
dc.coverage.none.fl_str_mv |
New York |
dc.publisher.none.fl_str_mv |
Springer |
publisher.none.fl_str_mv |
Springer |
dc.source.none.fl_str_mv |
reponame:Repositório Institucional da UNIFESP instname:Universidade Federal de São Paulo (UNIFESP) instacron:UNIFESP |
instname_str |
Universidade Federal de São Paulo (UNIFESP) |
instacron_str |
UNIFESP |
institution |
UNIFESP |
reponame_str |
Repositório Institucional da UNIFESP |
collection |
Repositório Institucional da UNIFESP |
repository.name.fl_str_mv |
Repositório Institucional da UNIFESP - Universidade Federal de São Paulo (UNIFESP) |
repository.mail.fl_str_mv |
biblioteca.csp@unifesp.br |
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1814268378535165952 |