Time course and mechanism of brain oxidative stress and damage for redox active and inactive transition metals overload

Autores
Ferrarotti, Nidia Fatima; Musacco Sebio, Rosario Natalia; Saporito Magriñá, Christian Martín; Acosta, Juan Manuel; Repetto, Marisa Gabriela
Año de publicación
2016
Idioma
inglés
Tipo de recurso
artículo
Estado
versión publicada
Descripción
The objective of this work was to study the in vivo time course of biochemical processes of oxidative damage in the brain of Sprague-Dawley rats that received an acute overload of the redox active metals iron (Fe) and copper (Cu), and the redox inactive cobalt (Co) and nickel (Ni). Oxidative stress indicators (phospholipid and protein oxidation), glutathione (GSH), antioxidant enzymes and NADPH oxidase activities, and the plasma inflammatory cytokine (IL-6) were measured. The results showed that in brain oxidative mechanisms for both sets of metal are different, however in both cases are irreversible. The mechanism for Fe and Cu oxidative damage is mediated by the generation of the free radical hydroxyl (Fenton reaction and homolytic cleavage of hydroperoxides). Two events of antioxidant protection prior to oxidation of phospholipids and proteins by Fe and Cu are considered. The first process is the use of GSH and the second is the increased activity of the Cu, Zn-SOD and catalase enzymes. The oxidative mechanism for metal redox inactive is the consumption of GSH, NADPH oxidase activation and inflammatory response mediated by IL-6. Co increased protein oxidation as a result of the inflammatory process. Ni produced increments of phospholipid oxidation and SOD activity.
Fil: Ferrarotti, Nidia Fatima. 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: Musacco Sebio, Rosario Natalia. 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: Saporito Magriñá, Christian Martín. 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: Acosta, Juan Manuel. 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: Repetto, Marisa Gabriela. 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
Materia
METALS
OXIDATIVE DAMAGE
OXIDATIVE STRESS
LIPID PEROXIDATION
Nivel de accesibilidad
acceso abierto
Condiciones de uso
https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
Repositorio
CONICET Digital (CONICET)
Institución
Consejo Nacional de Investigaciones Científicas y Técnicas
OAI Identificador
oai:ri.conicet.gov.ar:11336/127289
Acceder
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oai_identifier_str oai:ri.conicet.gov.ar:11336/127289
network_acronym_str CONICETDig
repository_id_str 3498
network_name_str CONICET Digital (CONICET)
spelling Time course and mechanism of brain oxidative stress and damage for redox active and inactive transition metals overloadFerrarotti, Nidia FatimaMusacco Sebio, Rosario NataliaSaporito Magriñá, Christian MartínAcosta, Juan ManuelRepetto, Marisa GabrielaMETALSOXIDATIVE DAMAGEOXIDATIVE STRESSLIPID PEROXIDATIONhttps://purl.org/becyt/ford/1.6https://purl.org/becyt/ford/1The objective of this work was to study the in vivo time course of biochemical processes of oxidative damage in the brain of Sprague-Dawley rats that received an acute overload of the redox active metals iron (Fe) and copper (Cu), and the redox inactive cobalt (Co) and nickel (Ni). Oxidative stress indicators (phospholipid and protein oxidation), glutathione (GSH), antioxidant enzymes and NADPH oxidase activities, and the plasma inflammatory cytokine (IL-6) were measured. The results showed that in brain oxidative mechanisms for both sets of metal are different, however in both cases are irreversible. The mechanism for Fe and Cu oxidative damage is mediated by the generation of the free radical hydroxyl (Fenton reaction and homolytic cleavage of hydroperoxides). Two events of antioxidant protection prior to oxidation of phospholipids and proteins by Fe and Cu are considered. The first process is the use of GSH and the second is the increased activity of the Cu, Zn-SOD and catalase enzymes. The oxidative mechanism for metal redox inactive is the consumption of GSH, NADPH oxidase activation and inflammatory response mediated by IL-6. Co increased protein oxidation as a result of the inflammatory process. Ni produced increments of phospholipid oxidation and SOD activity.Fil: Ferrarotti, Nidia Fatima. 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: Musacco Sebio, Rosario Natalia. 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: Saporito Magriñá, Christian Martín. 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: Acosta, Juan Manuel. 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: Repetto, Marisa Gabriela. 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; ArgentinaInstituto de Histología y Embriología2016-04info: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/11336/127289Ferrarotti, Nidia Fatima; Musacco Sebio, Rosario Natalia; Saporito Magriñá, Christian Martín; Acosta, Juan Manuel; Repetto, Marisa Gabriela; Time course and mechanism of brain oxidative stress and damage for redox active and inactive transition metals overload; Instituto de Histología y Embriología; Biocell; 40; 1; 4-2016; 19-220327-95451667-5746CONICET DigitalCONICETenginfo:eu-repo/semantics/altIdentifier/url/https://www.techscience.com/biocell/v40n1/33989info:eu-repo/semantics/altIdentifier/doi/10.32604/biocell.2016.40.019info:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-sa/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-10-15T14:37:38Zoai:ri.conicet.gov.ar:11336/127289instacron: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:34982025-10-15 14:37:38.366CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse
dc.title.none.fl_str_mv Time course and mechanism of brain oxidative stress and damage for redox active and inactive transition metals overload
title Time course and mechanism of brain oxidative stress and damage for redox active and inactive transition metals overload
spellingShingle Time course and mechanism of brain oxidative stress and damage for redox active and inactive transition metals overload
Ferrarotti, Nidia Fatima
METALS
OXIDATIVE DAMAGE
OXIDATIVE STRESS
LIPID PEROXIDATION
title_short Time course and mechanism of brain oxidative stress and damage for redox active and inactive transition metals overload
title_full Time course and mechanism of brain oxidative stress and damage for redox active and inactive transition metals overload
title_fullStr Time course and mechanism of brain oxidative stress and damage for redox active and inactive transition metals overload
title_full_unstemmed Time course and mechanism of brain oxidative stress and damage for redox active and inactive transition metals overload
title_sort Time course and mechanism of brain oxidative stress and damage for redox active and inactive transition metals overload
dc.creator.none.fl_str_mv Ferrarotti, Nidia Fatima
Musacco Sebio, Rosario Natalia
Saporito Magriñá, Christian Martín
Acosta, Juan Manuel
Repetto, Marisa Gabriela
author Ferrarotti, Nidia Fatima
author_facet Ferrarotti, Nidia Fatima
Musacco Sebio, Rosario Natalia
Saporito Magriñá, Christian Martín
Acosta, Juan Manuel
Repetto, Marisa Gabriela
author_role author
author2 Musacco Sebio, Rosario Natalia
Saporito Magriñá, Christian Martín
Acosta, Juan Manuel
Repetto, Marisa Gabriela
author2_role author
author
author
author
dc.subject.none.fl_str_mv METALS
OXIDATIVE DAMAGE
OXIDATIVE STRESS
LIPID PEROXIDATION
topic METALS
OXIDATIVE DAMAGE
OXIDATIVE STRESS
LIPID PEROXIDATION
purl_subject.fl_str_mv https://purl.org/becyt/ford/1.6
https://purl.org/becyt/ford/1
dc.description.none.fl_txt_mv The objective of this work was to study the in vivo time course of biochemical processes of oxidative damage in the brain of Sprague-Dawley rats that received an acute overload of the redox active metals iron (Fe) and copper (Cu), and the redox inactive cobalt (Co) and nickel (Ni). Oxidative stress indicators (phospholipid and protein oxidation), glutathione (GSH), antioxidant enzymes and NADPH oxidase activities, and the plasma inflammatory cytokine (IL-6) were measured. The results showed that in brain oxidative mechanisms for both sets of metal are different, however in both cases are irreversible. The mechanism for Fe and Cu oxidative damage is mediated by the generation of the free radical hydroxyl (Fenton reaction and homolytic cleavage of hydroperoxides). Two events of antioxidant protection prior to oxidation of phospholipids and proteins by Fe and Cu are considered. The first process is the use of GSH and the second is the increased activity of the Cu, Zn-SOD and catalase enzymes. The oxidative mechanism for metal redox inactive is the consumption of GSH, NADPH oxidase activation and inflammatory response mediated by IL-6. Co increased protein oxidation as a result of the inflammatory process. Ni produced increments of phospholipid oxidation and SOD activity.
Fil: Ferrarotti, Nidia Fatima. 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: Musacco Sebio, Rosario Natalia. 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: Saporito Magriñá, Christian Martín. 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: Acosta, Juan Manuel. 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: Repetto, Marisa Gabriela. 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
description The objective of this work was to study the in vivo time course of biochemical processes of oxidative damage in the brain of Sprague-Dawley rats that received an acute overload of the redox active metals iron (Fe) and copper (Cu), and the redox inactive cobalt (Co) and nickel (Ni). Oxidative stress indicators (phospholipid and protein oxidation), glutathione (GSH), antioxidant enzymes and NADPH oxidase activities, and the plasma inflammatory cytokine (IL-6) were measured. The results showed that in brain oxidative mechanisms for both sets of metal are different, however in both cases are irreversible. The mechanism for Fe and Cu oxidative damage is mediated by the generation of the free radical hydroxyl (Fenton reaction and homolytic cleavage of hydroperoxides). Two events of antioxidant protection prior to oxidation of phospholipids and proteins by Fe and Cu are considered. The first process is the use of GSH and the second is the increased activity of the Cu, Zn-SOD and catalase enzymes. The oxidative mechanism for metal redox inactive is the consumption of GSH, NADPH oxidase activation and inflammatory response mediated by IL-6. Co increased protein oxidation as a result of the inflammatory process. Ni produced increments of phospholipid oxidation and SOD activity.
publishDate 2016
dc.date.none.fl_str_mv 2016-04
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/11336/127289
Ferrarotti, Nidia Fatima; Musacco Sebio, Rosario Natalia; Saporito Magriñá, Christian Martín; Acosta, Juan Manuel; Repetto, Marisa Gabriela; Time course and mechanism of brain oxidative stress and damage for redox active and inactive transition metals overload; Instituto de Histología y Embriología; Biocell; 40; 1; 4-2016; 19-22
0327-9545
1667-5746
CONICET Digital
CONICET
url http://hdl.handle.net/11336/127289
identifier_str_mv Ferrarotti, Nidia Fatima; Musacco Sebio, Rosario Natalia; Saporito Magriñá, Christian Martín; Acosta, Juan Manuel; Repetto, Marisa Gabriela; Time course and mechanism of brain oxidative stress and damage for redox active and inactive transition metals overload; Instituto de Histología y Embriología; Biocell; 40; 1; 4-2016; 19-22
0327-9545
1667-5746
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.techscience.com/biocell/v40n1/33989
info:eu-repo/semantics/altIdentifier/doi/10.32604/biocell.2016.40.019
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
application/pdf
dc.publisher.none.fl_str_mv Instituto de Histología y Embriología
publisher.none.fl_str_mv Instituto de Histología y Embriología
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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score 13.22299

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