Iron overload triggers redox-sensitive signals in human IMR-32 neuroblastoma cells

Excessive neuronal iron has been proposed to contribute to the pathology of several neurodegenerative diseases including Alzheimer´s and Parkinson´s diseases. This work characterized human neuroblastoma IMR-32 cells exposure to ferric ammonium citrate (FAC) as a model of neuronal iron overload and n...

ver descrição completa

Detalhes bibliográficos
Autores: Salvador, Gabriela Alejandra, Oteiza, Patricia Isabel
Formato: artículo
Estado:Versión publicada
Fecha de publicación:2011
País:Argentina
Recursos:Consejo Nacional de Investigaciones Científicas y Técnicas
Repositorio:CONICET Digital (CONICET)
Idioma:inglés
OAI Identifier:oai:ri.conicet.gov.ar:11336/6463
Acesso em linha:http://hdl.handle.net/11336/6463
Access Level:acceso abierto
Palavra-chave:Iron
Nfkb
Ap-1
Oxidative Stress
Neurotoxicity
https://purl.org/becyt/ford/3.1
https://purl.org/becyt/ford/3
id AR_b3ca62f76d06e4aba9cfbf30205ba63c
oai_identifier_str oai:ri.conicet.gov.ar:11336/6463
network_acronym_str AR
network_name_str Argentina
repository_id_str
spelling Iron overload triggers redox-sensitive signals in human IMR-32 neuroblastoma cellsSalvador, Gabriela AlejandraOteiza, Patricia IsabelIronNfkbAp-1Oxidative StressNeurotoxicityhttps://purl.org/becyt/ford/3.1https://purl.org/becyt/ford/3Excessive neuronal iron has been proposed to contribute to the pathology of several neurodegenerative diseases including Alzheimer´s and Parkinson´s diseases. This work characterized human neuroblastoma IMR-32 cells exposure to ferric ammonium citrate (FAC) as a model of neuronal iron overload and neurodegeneration. The consequences of FAC treatment on neuronal oxidative stress and on the modulation of the oxidant-sensitive transcription factors AP-1 and NF-êB were investigated. Incubation with FAC (150ìM) resulted in a time (3-72h)-dependent increase in cellular iron content, and was associated with cell oxidant increase. FAC caused a time-dependent (3-48h) increase in nuclear AP-1- and NF-êB-DNA binding. This was associated with the upstream activation of the mitogen activated kinases ERK1/2, p38 and JNK and of IêBá phosphorylation and degradation. After 72h incubation with FAC, cell viability was 40% lower than in controls. Iron overload caused apoptotic cell death. After 48-72h of incubation with FAC, caspase 3 activity was increased, and chromatin condensation and nuclear fragmentation were observed. In summary, the exposure of IMR-32 cells to FAC is associated with increased oxidant cell levels, activation of redox-sensitive signals, and apoptosis.Fil: Salvador, Gabriela Alejandra. Consejo Nacional de Investigaciones Cientificas y Técnicas. Centro Científico Tecnológico Bahia Blanca. Instituto de Investigaciones Bioquímicas Bahia Blanca (i); Argentina. Universidad Nacional del Sur; ArgentinaFil: Oteiza, Patricia Isabel. University Of California. Department Of Nutrition And Department Of Environmental Toxicology; Estados UnidosElsevier2011-05info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/6463Salvador, Gabriela Alejandra; Oteiza, Patricia Isabel; Iron overload triggers redox-sensitive signals in human IMR-32 neuroblastoma cells; Elsevier; Neurotoxicology; 32; 1; 5-2011; 75-820161-813Xenginfo:eu-repo/semantics/altIdentifier/doi/info:eu-repo/semantics/altIdentifier/doi/10.1016/j.neuro.2010.11.006info:eu-repo/semantics/altIdentifier/pmid/21130806info:eu-repo/semantics/altIdentifier/url/http://www.sciencedirect.com/science/article/pii/S0161813X1000224Xinfo:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-nd/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2024-05-08T14:15:48Zoai:ri.conicet.gov.ar:11336/6463instacron: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:34982024-05-08 14:15:49.225CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse
dc.title.none.fl_str_mv Iron overload triggers redox-sensitive signals in human IMR-32 neuroblastoma cells
title Iron overload triggers redox-sensitive signals in human IMR-32 neuroblastoma cells
spellingShingle Iron overload triggers redox-sensitive signals in human IMR-32 neuroblastoma cells
Salvador, Gabriela Alejandra
Iron
Nfkb
Ap-1
Oxidative Stress
Neurotoxicity
https://purl.org/becyt/ford/3.1
https://purl.org/becyt/ford/3
title_short Iron overload triggers redox-sensitive signals in human IMR-32 neuroblastoma cells
title_full Iron overload triggers redox-sensitive signals in human IMR-32 neuroblastoma cells
title_fullStr Iron overload triggers redox-sensitive signals in human IMR-32 neuroblastoma cells
title_full_unstemmed Iron overload triggers redox-sensitive signals in human IMR-32 neuroblastoma cells
title_sort Iron overload triggers redox-sensitive signals in human IMR-32 neuroblastoma cells
dc.creator.none.fl_str_mv Salvador, Gabriela Alejandra
Oteiza, Patricia Isabel
author Salvador, Gabriela Alejandra
author_facet Salvador, Gabriela Alejandra
Oteiza, Patricia Isabel
author_role author
author2 Oteiza, Patricia Isabel
author2_role author
dc.subject.none.fl_str_mv Iron
Nfkb
Ap-1
Oxidative Stress
Neurotoxicity
https://purl.org/becyt/ford/3.1
https://purl.org/becyt/ford/3
topic Iron
Nfkb
Ap-1
Oxidative Stress
Neurotoxicity
https://purl.org/becyt/ford/3.1
https://purl.org/becyt/ford/3
description Excessive neuronal iron has been proposed to contribute to the pathology of several neurodegenerative diseases including Alzheimer´s and Parkinson´s diseases. This work characterized human neuroblastoma IMR-32 cells exposure to ferric ammonium citrate (FAC) as a model of neuronal iron overload and neurodegeneration. The consequences of FAC treatment on neuronal oxidative stress and on the modulation of the oxidant-sensitive transcription factors AP-1 and NF-êB were investigated. Incubation with FAC (150ìM) resulted in a time (3-72h)-dependent increase in cellular iron content, and was associated with cell oxidant increase. FAC caused a time-dependent (3-48h) increase in nuclear AP-1- and NF-êB-DNA binding. This was associated with the upstream activation of the mitogen activated kinases ERK1/2, p38 and JNK and of IêBá phosphorylation and degradation. After 72h incubation with FAC, cell viability was 40% lower than in controls. Iron overload caused apoptotic cell death. After 48-72h of incubation with FAC, caspase 3 activity was increased, and chromatin condensation and nuclear fragmentation were observed. In summary, the exposure of IMR-32 cells to FAC is associated with increased oxidant cell levels, activation of redox-sensitive signals, and apoptosis.
publishDate 2011
dc.date.none.fl_str_mv 2011-05
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/11336/6463
Salvador, Gabriela Alejandra; Oteiza, Patricia Isabel; Iron overload triggers redox-sensitive signals in human IMR-32 neuroblastoma cells; Elsevier; Neurotoxicology; 32; 1; 5-2011; 75-82
0161-813X
url http://hdl.handle.net/11336/6463
identifier_str_mv Salvador, Gabriela Alejandra; Oteiza, Patricia Isabel; Iron overload triggers redox-sensitive signals in human IMR-32 neuroblastoma cells; Elsevier; Neurotoxicology; 32; 1; 5-2011; 75-82
0161-813X
dc.language.none.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv info:eu-repo/semantics/altIdentifier/doi/
info:eu-repo/semantics/altIdentifier/doi/10.1016/j.neuro.2010.11.006
info:eu-repo/semantics/altIdentifier/pmid/21130806
info:eu-repo/semantics/altIdentifier/url/http://www.sciencedirect.com/science/article/pii/S0161813X1000224X
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
dc.publisher.none.fl_str_mv Elsevier
publisher.none.fl_str_mv Elsevier
dc.source.none.fl_str_mv reponame:CONICET Digital (CONICET)
instname:Consejo Nacional de Investigaciones Científicas y Técnicas
instname_str Consejo Nacional de Investigaciones Científicas y Técnicas
reponame_str CONICET Digital (CONICET)
collection CONICET Digital (CONICET)
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
_version_ 1799196132078780416
score 15,811543

Registos relacionados