Liver preconditioning induced by iron in a rat model of ischemia/reperfusion

Autores
Galleano, Mónica Liliana; Tapia, Gladys; Puntarulo, Susana Ángela; Varela, Patricia; Videla, Luis A.; Fernández, Virginia
Año de publicación
2011
Idioma
inglés
Tipo de recurso
artículo
Estado
versión publicada
Descripción
Aims: Liver preconditioning against ischemia-reperfusion (IR) injury is a major area of experimental research, in which regulation of gene expression with cytoprotective responses due to transient oxidative stress development has been reported. Considering that significant cytoprotection occurs after exposure to low levels of iron (Fe), we tested the hypothesis that sub-chronic administration of Fe to rats underlying transient oxidative stress preconditions the liver against IR injury. Main methods: Animals received six doses (50 mg Fe-dextran/kg ip) every second day during 10 days, before partial IR (vascular clamping) or sham laparotomy (control). Transient oxidative stress was defined by liver glutathione and protein carbonyl contents (24, 48, and 72 h after Fe treatment). Plasma and liver Fe status and ferritin content (western blot) were assessed in animals not subjected to IR. Liver injury and inflammatory response were evaluated by serum transaminases, liver morphology and serum TNF-α. Fe preconditioning against IR injury was correlated with liver glutathione content and the redox-sensitive NF-κB signaling pathway (EMSA) and western blot analysis of haptoglobin. Key findings: Significant hepatoprotection against IR injury, underlying transient oxidative stress and enhancement in the total and labile Fe pools, was achieved by Fe administration. Abrogation of IR injury is related to reduced TNF-α response (91%), abolishment of the IR-induced liver glutathione depletion and recovery of the NF-κB signaling pathway (75%), lost during IR. Significance: Sub-chronic Fe administration protects the liver against IR injury through antioxidant and anti-inflammatory responses, with recovery of NF-κB activation and related acute-phase response signaling.
Fil: Galleano, Mónica Liliana. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Bioquímica y Medicina Molecular. Universidad de Buenos Aires. Facultad Medicina. Instituto de Bioquímica y Medicina Molecular; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Programa de Radicales Libres; Argentina
Fil: Tapia, Gladys. Universidad de Chile; Chile
Fil: Puntarulo, Susana Ángela. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Bioquímica y Medicina Molecular. Universidad de Buenos Aires. Facultad Medicina. Instituto de Bioquímica y Medicina Molecular; Argentina
Fil: Varela, Patricia. Universidad de Chile; Chile
Fil: Videla, Luis A.. Universidad de Chile; Chile
Fil: Fernández, Virginia. Universidad de Chile; Chile
Materia
ACUTE-PHASE RESPONSE
FREE RADICALS
IRON ADMINISTRATION
ISCHEMIA-REPERFUSION INJURY
LIVER PRECONDITIONING
NUCLEAR FACTOR-ΚB
OXIDATIVE STRESS
Nivel de accesibilidad
acceso abierto
Condiciones de uso
https://creativecommons.org/licenses/by-nc-nd/2.5/ar/
Repositorio
CONICET Digital (CONICET)
Institución
Consejo Nacional de Investigaciones Científicas y Técnicas
OAI Identificador
oai:ri.conicet.gov.ar:11336/151515

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network_acronym_str CONICETDig
repository_id_str 3498
network_name_str CONICET Digital (CONICET)
spelling Liver preconditioning induced by iron in a rat model of ischemia/reperfusionGalleano, Mónica LilianaTapia, GladysPuntarulo, Susana ÁngelaVarela, PatriciaVidela, Luis A.Fernández, VirginiaACUTE-PHASE RESPONSEFREE RADICALSIRON ADMINISTRATIONISCHEMIA-REPERFUSION INJURYLIVER PRECONDITIONINGNUCLEAR FACTOR-ΚBOXIDATIVE STRESShttps://purl.org/becyt/ford/3.1https://purl.org/becyt/ford/3Aims: Liver preconditioning against ischemia-reperfusion (IR) injury is a major area of experimental research, in which regulation of gene expression with cytoprotective responses due to transient oxidative stress development has been reported. Considering that significant cytoprotection occurs after exposure to low levels of iron (Fe), we tested the hypothesis that sub-chronic administration of Fe to rats underlying transient oxidative stress preconditions the liver against IR injury. Main methods: Animals received six doses (50 mg Fe-dextran/kg ip) every second day during 10 days, before partial IR (vascular clamping) or sham laparotomy (control). Transient oxidative stress was defined by liver glutathione and protein carbonyl contents (24, 48, and 72 h after Fe treatment). Plasma and liver Fe status and ferritin content (western blot) were assessed in animals not subjected to IR. Liver injury and inflammatory response were evaluated by serum transaminases, liver morphology and serum TNF-α. Fe preconditioning against IR injury was correlated with liver glutathione content and the redox-sensitive NF-κB signaling pathway (EMSA) and western blot analysis of haptoglobin. Key findings: Significant hepatoprotection against IR injury, underlying transient oxidative stress and enhancement in the total and labile Fe pools, was achieved by Fe administration. Abrogation of IR injury is related to reduced TNF-α response (91%), abolishment of the IR-induced liver glutathione depletion and recovery of the NF-κB signaling pathway (75%), lost during IR. Significance: Sub-chronic Fe administration protects the liver against IR injury through antioxidant and anti-inflammatory responses, with recovery of NF-κB activation and related acute-phase response signaling.Fil: Galleano, Mónica Liliana. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Bioquímica y Medicina Molecular. Universidad de Buenos Aires. Facultad Medicina. Instituto de Bioquímica y Medicina Molecular; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Programa de Radicales Libres; ArgentinaFil: Tapia, Gladys. Universidad de Chile; ChileFil: Puntarulo, Susana Ángela. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Bioquímica y Medicina Molecular. Universidad de Buenos Aires. Facultad Medicina. Instituto de Bioquímica y Medicina Molecular; ArgentinaFil: Varela, Patricia. Universidad de Chile; ChileFil: Videla, Luis A.. Universidad de Chile; ChileFil: Fernández, Virginia. Universidad de Chile; ChilePergamon-Elsevier Science Ltd2011-08info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/151515Galleano, Mónica Liliana; Tapia, Gladys; Puntarulo, Susana Ángela; Varela, Patricia; Videla, Luis A.; et al.; Liver preconditioning induced by iron in a rat model of ischemia/reperfusion; Pergamon-Elsevier Science Ltd; Life Sciences; 89; 7-8; 8-2011; 221-2280024-3205CONICET DigitalCONICETenginfo:eu-repo/semantics/altIdentifier/url/https://www.sciencedirect.com/science/article/abs/pii/S0024320511002736info:eu-repo/semantics/altIdentifier/doi/10.1016/j.lfs.2011.06.005info:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-nd/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-09-03T09:55:45Zoai:ri.conicet.gov.ar:11336/151515instacron:CONICETInstitucionalhttp://ri.conicet.gov.ar/Organismo científico-tecnológicoNo correspondehttp://ri.conicet.gov.ar/oai/requestdasensio@conicet.gov.ar; lcarlino@conicet.gov.arArgentinaNo correspondeNo correspondeNo correspondeopendoar:34982025-09-03 09:55:45.647CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse
dc.title.none.fl_str_mv Liver preconditioning induced by iron in a rat model of ischemia/reperfusion
title Liver preconditioning induced by iron in a rat model of ischemia/reperfusion
spellingShingle Liver preconditioning induced by iron in a rat model of ischemia/reperfusion
Galleano, Mónica Liliana
ACUTE-PHASE RESPONSE
FREE RADICALS
IRON ADMINISTRATION
ISCHEMIA-REPERFUSION INJURY
LIVER PRECONDITIONING
NUCLEAR FACTOR-ΚB
OXIDATIVE STRESS
title_short Liver preconditioning induced by iron in a rat model of ischemia/reperfusion
title_full Liver preconditioning induced by iron in a rat model of ischemia/reperfusion
title_fullStr Liver preconditioning induced by iron in a rat model of ischemia/reperfusion
title_full_unstemmed Liver preconditioning induced by iron in a rat model of ischemia/reperfusion
title_sort Liver preconditioning induced by iron in a rat model of ischemia/reperfusion
dc.creator.none.fl_str_mv Galleano, Mónica Liliana
Tapia, Gladys
Puntarulo, Susana Ángela
Varela, Patricia
Videla, Luis A.
Fernández, Virginia
author Galleano, Mónica Liliana
author_facet Galleano, Mónica Liliana
Tapia, Gladys
Puntarulo, Susana Ángela
Varela, Patricia
Videla, Luis A.
Fernández, Virginia
author_role author
author2 Tapia, Gladys
Puntarulo, Susana Ángela
Varela, Patricia
Videla, Luis A.
Fernández, Virginia
author2_role author
author
author
author
author
dc.subject.none.fl_str_mv ACUTE-PHASE RESPONSE
FREE RADICALS
IRON ADMINISTRATION
ISCHEMIA-REPERFUSION INJURY
LIVER PRECONDITIONING
NUCLEAR FACTOR-ΚB
OXIDATIVE STRESS
topic ACUTE-PHASE RESPONSE
FREE RADICALS
IRON ADMINISTRATION
ISCHEMIA-REPERFUSION INJURY
LIVER PRECONDITIONING
NUCLEAR FACTOR-ΚB
OXIDATIVE STRESS
purl_subject.fl_str_mv https://purl.org/becyt/ford/3.1
https://purl.org/becyt/ford/3
dc.description.none.fl_txt_mv Aims: Liver preconditioning against ischemia-reperfusion (IR) injury is a major area of experimental research, in which regulation of gene expression with cytoprotective responses due to transient oxidative stress development has been reported. Considering that significant cytoprotection occurs after exposure to low levels of iron (Fe), we tested the hypothesis that sub-chronic administration of Fe to rats underlying transient oxidative stress preconditions the liver against IR injury. Main methods: Animals received six doses (50 mg Fe-dextran/kg ip) every second day during 10 days, before partial IR (vascular clamping) or sham laparotomy (control). Transient oxidative stress was defined by liver glutathione and protein carbonyl contents (24, 48, and 72 h after Fe treatment). Plasma and liver Fe status and ferritin content (western blot) were assessed in animals not subjected to IR. Liver injury and inflammatory response were evaluated by serum transaminases, liver morphology and serum TNF-α. Fe preconditioning against IR injury was correlated with liver glutathione content and the redox-sensitive NF-κB signaling pathway (EMSA) and western blot analysis of haptoglobin. Key findings: Significant hepatoprotection against IR injury, underlying transient oxidative stress and enhancement in the total and labile Fe pools, was achieved by Fe administration. Abrogation of IR injury is related to reduced TNF-α response (91%), abolishment of the IR-induced liver glutathione depletion and recovery of the NF-κB signaling pathway (75%), lost during IR. Significance: Sub-chronic Fe administration protects the liver against IR injury through antioxidant and anti-inflammatory responses, with recovery of NF-κB activation and related acute-phase response signaling.
Fil: Galleano, Mónica Liliana. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Bioquímica y Medicina Molecular. Universidad de Buenos Aires. Facultad Medicina. Instituto de Bioquímica y Medicina Molecular; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Programa de Radicales Libres; Argentina
Fil: Tapia, Gladys. Universidad de Chile; Chile
Fil: Puntarulo, Susana Ángela. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Bioquímica y Medicina Molecular. Universidad de Buenos Aires. Facultad Medicina. Instituto de Bioquímica y Medicina Molecular; Argentina
Fil: Varela, Patricia. Universidad de Chile; Chile
Fil: Videla, Luis A.. Universidad de Chile; Chile
Fil: Fernández, Virginia. Universidad de Chile; Chile
description Aims: Liver preconditioning against ischemia-reperfusion (IR) injury is a major area of experimental research, in which regulation of gene expression with cytoprotective responses due to transient oxidative stress development has been reported. Considering that significant cytoprotection occurs after exposure to low levels of iron (Fe), we tested the hypothesis that sub-chronic administration of Fe to rats underlying transient oxidative stress preconditions the liver against IR injury. Main methods: Animals received six doses (50 mg Fe-dextran/kg ip) every second day during 10 days, before partial IR (vascular clamping) or sham laparotomy (control). Transient oxidative stress was defined by liver glutathione and protein carbonyl contents (24, 48, and 72 h after Fe treatment). Plasma and liver Fe status and ferritin content (western blot) were assessed in animals not subjected to IR. Liver injury and inflammatory response were evaluated by serum transaminases, liver morphology and serum TNF-α. Fe preconditioning against IR injury was correlated with liver glutathione content and the redox-sensitive NF-κB signaling pathway (EMSA) and western blot analysis of haptoglobin. Key findings: Significant hepatoprotection against IR injury, underlying transient oxidative stress and enhancement in the total and labile Fe pools, was achieved by Fe administration. Abrogation of IR injury is related to reduced TNF-α response (91%), abolishment of the IR-induced liver glutathione depletion and recovery of the NF-κB signaling pathway (75%), lost during IR. Significance: Sub-chronic Fe administration protects the liver against IR injury through antioxidant and anti-inflammatory responses, with recovery of NF-κB activation and related acute-phase response signaling.
publishDate 2011
dc.date.none.fl_str_mv 2011-08
dc.type.none.fl_str_mv info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
http://purl.org/coar/resource_type/c_6501
info:ar-repo/semantics/articulo
format article
status_str publishedVersion
dc.identifier.none.fl_str_mv http://hdl.handle.net/11336/151515
Galleano, Mónica Liliana; Tapia, Gladys; Puntarulo, Susana Ángela; Varela, Patricia; Videla, Luis A.; et al.; Liver preconditioning induced by iron in a rat model of ischemia/reperfusion; Pergamon-Elsevier Science Ltd; Life Sciences; 89; 7-8; 8-2011; 221-228
0024-3205
CONICET Digital
CONICET
url http://hdl.handle.net/11336/151515
identifier_str_mv Galleano, Mónica Liliana; Tapia, Gladys; Puntarulo, Susana Ángela; Varela, Patricia; Videla, Luis A.; et al.; Liver preconditioning induced by iron in a rat model of ischemia/reperfusion; Pergamon-Elsevier Science Ltd; Life Sciences; 89; 7-8; 8-2011; 221-228
0024-3205
CONICET Digital
CONICET
dc.language.none.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv info:eu-repo/semantics/altIdentifier/url/https://www.sciencedirect.com/science/article/abs/pii/S0024320511002736
info:eu-repo/semantics/altIdentifier/doi/10.1016/j.lfs.2011.06.005
dc.rights.none.fl_str_mv info:eu-repo/semantics/openAccess
https://creativecommons.org/licenses/by-nc-nd/2.5/ar/
eu_rights_str_mv openAccess
rights_invalid_str_mv https://creativecommons.org/licenses/by-nc-nd/2.5/ar/
dc.format.none.fl_str_mv application/pdf
application/pdf
application/pdf
dc.publisher.none.fl_str_mv Pergamon-Elsevier Science Ltd
publisher.none.fl_str_mv Pergamon-Elsevier Science Ltd
dc.source.none.fl_str_mv reponame:CONICET Digital (CONICET)
instname:Consejo Nacional de Investigaciones Científicas y Técnicas
reponame_str CONICET Digital (CONICET)
collection CONICET Digital (CONICET)
instname_str Consejo Nacional de Investigaciones Científicas y Técnicas
repository.name.fl_str_mv CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicas
repository.mail.fl_str_mv dasensio@conicet.gov.ar; lcarlino@conicet.gov.ar
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