Iron in neuronal function and dysfunction
- Autores
- Salvador, Gabriela Alejandra
- Año de publicación
- 2010
- Idioma
- inglés
- Tipo de recurso
- artículo
- Estado
- versión publicada
- Descripción
- Iron (Fe) is an essential element for many metabolic processes, serving as a cofactor for heme and nonheme proteins. Cellular iron deficiency arrests cell growth and leads to cell death; however, like most transition metals, an excess of intracellular iron is toxic. The ability of Fe to accept and donate electrons can lead to the formation of reactive nitrogen and oxygen species, and oxidative damage to tissue components; contributing to disease and, perhaps, aging itself. It has also been suggested that iron-induced oxidative stress can play a key role in the pathogenesis of several neurodegenerative diseases. Iron progressively accumulates in the brain both during normal aging and neurodegenerative processes. However, iron accumulation occurs without the concomitant increase in tissue ferritin, which could increase the risk of oxidative stress. Moreover, high iron concentrations in the brain have been consistently observed in Alzheimer´s disease (AD) and Parkinson´s disease (PD). In this regard, metalloneurobiology has become extremely important in understanding the role of iron in the onset and progression of neurodegenerative diseases. Neurons have developed several protective mechanisms against oxidative stress, among them the activation of cellular signaling pathways. The final response will depend on the identity, intensity, and persistence of the oxidative insult. The characterization of the mechanisms involved in high iron induced in neuronal dysfunction and death is central to understanding the pathology of a number of neurodegenerative disorders.
Fil: Salvador, Gabriela Alejandra. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Bahía Blanca. Instituto de Investigaciones Bioquímicas de Bahía Blanca. Universidad Nacional del Sur. Instituto de Investigaciones Bioquímicas de Bahía Blanca; Argentina - Materia
-
Iron
Oxidative Stress
Neurotoxicity
Nervous System - Nivel de accesibilidad
- acceso abierto
- Condiciones de uso
- https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
- Repositorio
- Institución
- Consejo Nacional de Investigaciones Científicas y Técnicas
- OAI Identificador
- oai:ri.conicet.gov.ar:11336/42111
Ver los metadatos del registro completo
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Iron in neuronal function and dysfunctionSalvador, Gabriela AlejandraIronOxidative StressNeurotoxicityNervous Systemhttps://purl.org/becyt/ford/3.3https://purl.org/becyt/ford/3Iron (Fe) is an essential element for many metabolic processes, serving as a cofactor for heme and nonheme proteins. Cellular iron deficiency arrests cell growth and leads to cell death; however, like most transition metals, an excess of intracellular iron is toxic. The ability of Fe to accept and donate electrons can lead to the formation of reactive nitrogen and oxygen species, and oxidative damage to tissue components; contributing to disease and, perhaps, aging itself. It has also been suggested that iron-induced oxidative stress can play a key role in the pathogenesis of several neurodegenerative diseases. Iron progressively accumulates in the brain both during normal aging and neurodegenerative processes. However, iron accumulation occurs without the concomitant increase in tissue ferritin, which could increase the risk of oxidative stress. Moreover, high iron concentrations in the brain have been consistently observed in Alzheimer´s disease (AD) and Parkinson´s disease (PD). In this regard, metalloneurobiology has become extremely important in understanding the role of iron in the onset and progression of neurodegenerative diseases. Neurons have developed several protective mechanisms against oxidative stress, among them the activation of cellular signaling pathways. The final response will depend on the identity, intensity, and persistence of the oxidative insult. The characterization of the mechanisms involved in high iron induced in neuronal dysfunction and death is central to understanding the pathology of a number of neurodegenerative disorders.Fil: Salvador, Gabriela Alejandra. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Bahía Blanca. Instituto de Investigaciones Bioquímicas de Bahía Blanca. Universidad Nacional del Sur. Instituto de Investigaciones Bioquímicas de Bahía Blanca; ArgentinaIOS Press2010-03info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/42111Salvador, Gabriela Alejandra; Iron in neuronal function and dysfunction; IOS Press; Biofactors; 36; 2; 3-2010; 103-1100951-6433CONICET DigitalCONICETenginfo:eu-repo/semantics/altIdentifier/doi/10.1002/biof.80info:eu-repo/semantics/altIdentifier/url/https://iubmb.onlinelibrary.wiley.com/doi/abs/10.1002/biof.80info:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-sa/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-09-29T10:47:32Zoai:ri.conicet.gov.ar:11336/42111instacron: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:34982025-09-29 10:47:32.368CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse |
dc.title.none.fl_str_mv |
Iron in neuronal function and dysfunction |
title |
Iron in neuronal function and dysfunction |
spellingShingle |
Iron in neuronal function and dysfunction Salvador, Gabriela Alejandra Iron Oxidative Stress Neurotoxicity Nervous System |
title_short |
Iron in neuronal function and dysfunction |
title_full |
Iron in neuronal function and dysfunction |
title_fullStr |
Iron in neuronal function and dysfunction |
title_full_unstemmed |
Iron in neuronal function and dysfunction |
title_sort |
Iron in neuronal function and dysfunction |
dc.creator.none.fl_str_mv |
Salvador, Gabriela Alejandra |
author |
Salvador, Gabriela Alejandra |
author_facet |
Salvador, Gabriela Alejandra |
author_role |
author |
dc.subject.none.fl_str_mv |
Iron Oxidative Stress Neurotoxicity Nervous System |
topic |
Iron Oxidative Stress Neurotoxicity Nervous System |
purl_subject.fl_str_mv |
https://purl.org/becyt/ford/3.3 https://purl.org/becyt/ford/3 |
dc.description.none.fl_txt_mv |
Iron (Fe) is an essential element for many metabolic processes, serving as a cofactor for heme and nonheme proteins. Cellular iron deficiency arrests cell growth and leads to cell death; however, like most transition metals, an excess of intracellular iron is toxic. The ability of Fe to accept and donate electrons can lead to the formation of reactive nitrogen and oxygen species, and oxidative damage to tissue components; contributing to disease and, perhaps, aging itself. It has also been suggested that iron-induced oxidative stress can play a key role in the pathogenesis of several neurodegenerative diseases. Iron progressively accumulates in the brain both during normal aging and neurodegenerative processes. However, iron accumulation occurs without the concomitant increase in tissue ferritin, which could increase the risk of oxidative stress. Moreover, high iron concentrations in the brain have been consistently observed in Alzheimer´s disease (AD) and Parkinson´s disease (PD). In this regard, metalloneurobiology has become extremely important in understanding the role of iron in the onset and progression of neurodegenerative diseases. Neurons have developed several protective mechanisms against oxidative stress, among them the activation of cellular signaling pathways. The final response will depend on the identity, intensity, and persistence of the oxidative insult. The characterization of the mechanisms involved in high iron induced in neuronal dysfunction and death is central to understanding the pathology of a number of neurodegenerative disorders. Fil: Salvador, Gabriela Alejandra. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Bahía Blanca. Instituto de Investigaciones Bioquímicas de Bahía Blanca. Universidad Nacional del Sur. Instituto de Investigaciones Bioquímicas de Bahía Blanca; Argentina |
description |
Iron (Fe) is an essential element for many metabolic processes, serving as a cofactor for heme and nonheme proteins. Cellular iron deficiency arrests cell growth and leads to cell death; however, like most transition metals, an excess of intracellular iron is toxic. The ability of Fe to accept and donate electrons can lead to the formation of reactive nitrogen and oxygen species, and oxidative damage to tissue components; contributing to disease and, perhaps, aging itself. It has also been suggested that iron-induced oxidative stress can play a key role in the pathogenesis of several neurodegenerative diseases. Iron progressively accumulates in the brain both during normal aging and neurodegenerative processes. However, iron accumulation occurs without the concomitant increase in tissue ferritin, which could increase the risk of oxidative stress. Moreover, high iron concentrations in the brain have been consistently observed in Alzheimer´s disease (AD) and Parkinson´s disease (PD). In this regard, metalloneurobiology has become extremely important in understanding the role of iron in the onset and progression of neurodegenerative diseases. Neurons have developed several protective mechanisms against oxidative stress, among them the activation of cellular signaling pathways. The final response will depend on the identity, intensity, and persistence of the oxidative insult. The characterization of the mechanisms involved in high iron induced in neuronal dysfunction and death is central to understanding the pathology of a number of neurodegenerative disorders. |
publishDate |
2010 |
dc.date.none.fl_str_mv |
2010-03 |
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/11336/42111 Salvador, Gabriela Alejandra; Iron in neuronal function and dysfunction; IOS Press; Biofactors; 36; 2; 3-2010; 103-110 0951-6433 CONICET Digital CONICET |
url |
http://hdl.handle.net/11336/42111 |
identifier_str_mv |
Salvador, Gabriela Alejandra; Iron in neuronal function and dysfunction; IOS Press; Biofactors; 36; 2; 3-2010; 103-110 0951-6433 CONICET Digital CONICET |
dc.language.none.fl_str_mv |
eng |
language |
eng |
dc.relation.none.fl_str_mv |
info:eu-repo/semantics/altIdentifier/doi/10.1002/biof.80 info:eu-repo/semantics/altIdentifier/url/https://iubmb.onlinelibrary.wiley.com/doi/abs/10.1002/biof.80 |
dc.rights.none.fl_str_mv |
info:eu-repo/semantics/openAccess https://creativecommons.org/licenses/by-nc-sa/2.5/ar/ |
eu_rights_str_mv |
openAccess |
rights_invalid_str_mv |
https://creativecommons.org/licenses/by-nc-sa/2.5/ar/ |
dc.format.none.fl_str_mv |
application/pdf application/pdf |
dc.publisher.none.fl_str_mv |
IOS Press |
publisher.none.fl_str_mv |
IOS Press |
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reponame:CONICET Digital (CONICET) instname:Consejo Nacional de Investigaciones Científicas y Técnicas |
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CONICET Digital (CONICET) |
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CONICET Digital (CONICET) |
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Consejo Nacional de Investigaciones Científicas y Técnicas |
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CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicas |
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dasensio@conicet.gov.ar; lcarlino@conicet.gov.ar |
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13.070432 |