Oxidative stress and cell damage in a model of precancerouslesions and advanced hepatocellular carcinoma in rats

Detalhes bibliográficos
Autor(a) principal: Moreira, Andréa Janz
Data de Publicação: 2015
Outros Autores: Rodrigues, Graziella, Bona, Silvia Regina, Cerski, Carlos Thadeu Schmidt, Marroni, Claudio Augusto, Mauriz, José Luiz, González-Gallego, Javier, Marroni, Norma Anair Possa
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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spelling 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
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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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