Oxidative stress and cell damage in a model of precancerouslesions and advanced hepatocellular carcinoma in rats
Autor(a) principal: | |
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Data de Publicação: | 2015 |
Outros Autores: | , , , , , , |
Tipo de documento: | Artigo |
Idioma: | eng |
Título da fonte: | Repositório Institucional da UFRGS |
Texto Completo: | http://hdl.handle.net/10183/201454 |
Resumo: | Hepatocellular carcinoma (HCC) is the third most frequent cause of cancer deaths through-out the world. This study was aimed to analyze oxidative stress and cell damage in amultistage model of liver carcinogenesis induced by diethylnitrosamine (DEN) in rats.Male Wistar rats weighing 145–150 g were divided into three groups: control, precan-cerous lesions (PL) (which received 100 mg DEN once a week every 6 weeks up to 28weeks), and advanced HCC (50 mg DEN once/twice per week up to 19 weeks). Lipid per-oxidation (TBARS), superoxide dismutase (SOD) activity, and expression of transforminggrowth factor-1 beta (TGF)-1 , endothelial and inducible nitric oxide syntahese (eNOS,iNOS), NADPH quinone oxireductase (NQO)-1, nuclear factor erythroid 2-related factor(NrF)2, kelch-like ECH-associated protein (Keap)1 and heat shock protein (HSP)70 weremeasured. TBARS concentration was augmented in the PL and advanced HCC groups. SODactivity, TGF-1 and Nrf2 expression were higher in animals with precancerous lesions.In advanced HCC, expression of NQO1 and iNOS increased while there was a decrease inHPS70 expression. Data obtained provide evidence for the differential activation of pro-teins involved in oxidative stress and cell damage during progression of carcinogenesis inan animal model of HCC. |
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Moreira, Andréa JanzRodrigues, GraziellaBona, Silvia ReginaCerski, Carlos Thadeu SchmidtMarroni, Claudio AugustoMauriz, José LuizGonzález-Gallego, JavierMarroni, Norma Anair Possa2019-11-08T03:44:23Z20152214-7500http://hdl.handle.net/10183/201454001070471Hepatocellular carcinoma (HCC) is the third most frequent cause of cancer deaths through-out the world. This study was aimed to analyze oxidative stress and cell damage in amultistage model of liver carcinogenesis induced by diethylnitrosamine (DEN) in rats.Male Wistar rats weighing 145–150 g were divided into three groups: control, precan-cerous lesions (PL) (which received 100 mg DEN once a week every 6 weeks up to 28weeks), and advanced HCC (50 mg DEN once/twice per week up to 19 weeks). Lipid per-oxidation (TBARS), superoxide dismutase (SOD) activity, and expression of transforminggrowth factor-1 beta (TGF)-1 , endothelial and inducible nitric oxide syntahese (eNOS,iNOS), NADPH quinone oxireductase (NQO)-1, nuclear factor erythroid 2-related factor(NrF)2, kelch-like ECH-associated protein (Keap)1 and heat shock protein (HSP)70 weremeasured. TBARS concentration was augmented in the PL and advanced HCC groups. SODactivity, TGF-1 and Nrf2 expression were higher in animals with precancerous lesions.In advanced HCC, expression of NQO1 and iNOS increased while there was a decrease inHPS70 expression. Data obtained provide evidence for the differential activation of pro-teins involved in oxidative stress and cell damage during progression of carcinogenesis inan animal model of HCC.application/pdfengToxicology reports. [Ireland]. Vol. 2 (2015), p. 333-340Estresse oxidativoCarcinoma hepatocelularÓxido nítrico sintaseDietilnitrosaminaAnimaisRatos WistarOxidative stress and cell damage in a model of precancerouslesions and advanced hepatocellular carcinoma in ratsEstrangeiroinfo:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/openAccessreponame:Repositório Institucional da UFRGSinstname:Universidade Federal do Rio Grande do Sul (UFRGS)instacron:UFRGSTEXT001070471.pdf.txt001070471.pdf.txtExtracted Texttext/plain43493http://www.lume.ufrgs.br/bitstream/10183/201454/2/001070471.pdf.txtef9a2af1171161e58a5310e6059193e4MD52ORIGINAL001070471.pdfTexto completo (inglês)application/pdf1341546http://www.lume.ufrgs.br/bitstream/10183/201454/1/001070471.pdfe8f148de4663b69babd46ae888923c89MD5110183/2014542019-11-09 04:51:37.255991oai:www.lume.ufrgs.br:10183/201454Repositório de PublicaçõesPUBhttps://lume.ufrgs.br/oai/requestopendoar:2019-11-09T06:51:37Repositório Institucional da UFRGS - Universidade Federal do Rio Grande do Sul (UFRGS)false |
dc.title.pt_BR.fl_str_mv |
Oxidative stress and cell damage in a model of precancerouslesions and advanced hepatocellular carcinoma in rats |
title |
Oxidative stress and cell damage in a model of precancerouslesions and advanced hepatocellular carcinoma in rats |
spellingShingle |
Oxidative stress and cell damage in a model of precancerouslesions and advanced hepatocellular carcinoma in rats Moreira, Andréa Janz Estresse oxidativo Carcinoma hepatocelular Óxido nítrico sintase Dietilnitrosamina Animais Ratos Wistar |
title_short |
Oxidative stress and cell damage in a model of precancerouslesions and advanced hepatocellular carcinoma in rats |
title_full |
Oxidative stress and cell damage in a model of precancerouslesions and advanced hepatocellular carcinoma in rats |
title_fullStr |
Oxidative stress and cell damage in a model of precancerouslesions and advanced hepatocellular carcinoma in rats |
title_full_unstemmed |
Oxidative stress and cell damage in a model of precancerouslesions and advanced hepatocellular carcinoma in rats |
title_sort |
Oxidative stress and cell damage in a model of precancerouslesions and advanced hepatocellular carcinoma in rats |
author |
Moreira, Andréa Janz |
author_facet |
Moreira, Andréa Janz Rodrigues, Graziella Bona, Silvia Regina Cerski, Carlos Thadeu Schmidt Marroni, Claudio Augusto Mauriz, José Luiz González-Gallego, Javier Marroni, Norma Anair Possa |
author_role |
author |
author2 |
Rodrigues, Graziella Bona, Silvia Regina Cerski, Carlos Thadeu Schmidt Marroni, Claudio Augusto Mauriz, José Luiz González-Gallego, Javier Marroni, Norma Anair Possa |
author2_role |
author author author author author author author |
dc.contributor.author.fl_str_mv |
Moreira, Andréa Janz Rodrigues, Graziella Bona, Silvia Regina Cerski, Carlos Thadeu Schmidt Marroni, Claudio Augusto Mauriz, José Luiz González-Gallego, Javier Marroni, Norma Anair Possa |
dc.subject.por.fl_str_mv |
Estresse oxidativo Carcinoma hepatocelular Óxido nítrico sintase Dietilnitrosamina Animais Ratos Wistar |
topic |
Estresse oxidativo Carcinoma hepatocelular Óxido nítrico sintase Dietilnitrosamina Animais Ratos Wistar |
description |
Hepatocellular carcinoma (HCC) is the third most frequent cause of cancer deaths through-out the world. This study was aimed to analyze oxidative stress and cell damage in amultistage model of liver carcinogenesis induced by diethylnitrosamine (DEN) in rats.Male Wistar rats weighing 145–150 g were divided into three groups: control, precan-cerous lesions (PL) (which received 100 mg DEN once a week every 6 weeks up to 28weeks), and advanced HCC (50 mg DEN once/twice per week up to 19 weeks). Lipid per-oxidation (TBARS), superoxide dismutase (SOD) activity, and expression of transforminggrowth factor-1 beta (TGF)-1 , endothelial and inducible nitric oxide syntahese (eNOS,iNOS), NADPH quinone oxireductase (NQO)-1, nuclear factor erythroid 2-related factor(NrF)2, kelch-like ECH-associated protein (Keap)1 and heat shock protein (HSP)70 weremeasured. TBARS concentration was augmented in the PL and advanced HCC groups. SODactivity, TGF-1 and Nrf2 expression were higher in animals with precancerous lesions.In advanced HCC, expression of NQO1 and iNOS increased while there was a decrease inHPS70 expression. Data obtained provide evidence for the differential activation of pro-teins involved in oxidative stress and cell damage during progression of carcinogenesis inan animal model of HCC. |
publishDate |
2015 |
dc.date.issued.fl_str_mv |
2015 |
dc.date.accessioned.fl_str_mv |
2019-11-08T03:44:23Z |
dc.type.driver.fl_str_mv |
Estrangeiro info:eu-repo/semantics/article |
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http://hdl.handle.net/10183/201454 |
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2214-7500 |
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001070471 |
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http://hdl.handle.net/10183/201454 |
dc.language.iso.fl_str_mv |
eng |
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dc.relation.ispartof.pt_BR.fl_str_mv |
Toxicology reports. [Ireland]. Vol. 2 (2015), p. 333-340 |
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info:eu-repo/semantics/openAccess |
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openAccess |
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