Rat liver mitochondrial dysfunction by addition of copper(II) or iron(III) ions

Autores
Saporito Magriñá, Christian Martín; Musacco Sebio, Rosario Natalia; Acosta, Juan Manuel; Bajicoff, Sofía; Paredes Fleitas, Paola; Boveris, Alberto Antonio; Repetto, Marisa Gabriela
Año de publicación
2017
Idioma
inglés
Tipo de recurso
artículo
Estado
versión publicada
Descripción
Increased copper (Cu) and iron (Fe) levels in liver and brain are associated to oxidative stress and damage with increased phospholipid oxidation process. The aim of this work was to assess the toxic effects of Cu2 + and Fe3 + addition to rat liver mitochondria by determining mitochondrial respiration in states 3 (active respiration) and 4 (resting respiration), and phospholipid peroxidation. Both, Cu2 + and Fe3 + produced decreases in O2 consumption in a concentration-dependent manner in active state 3: both ions by 42% with malate-glutamate as complex I substrate (concentration for half maximal response (C50) 60 μM Cu2 + and 1.25 mM Fe3 +), and with succinate as complex II substrate: 64?69% with C50 of 50 μM Cu2 + and with C50 of 1.25 mM of Fe3 +. Respiratory control decreased with Cu2 + (C50 50 μM) and Fe3 + (C50 1.25-1-75 mM) with both substrates. Cu2 + produced a 2-fold increase and Fe3 + a 5-fold increase of thiobarbituric acid-reactive substances (TBARS) content from 25 μM Cu2 + (C50 40 μM) and from 100 μM Fe3 + (C50 1.75 mM). Supplementations with Cu2 + and Fe3 + ions induce mitochondrial dysfunction with phospholipid peroxidation in rat liver mitochondria. Although is proved that a Fenton/Haber Weiss mechanism of oxidative damage occurs in metal-ion induced mitochondrial toxicity, slightly different responses to the metal ions suggest some differences in the mechanism of intracellular toxicity. The decreased rates of mitochondrial respiration and the alteration of mitochondrial function by phospholipid and protein oxidations lead to mitochondrial dysfunction, cellular dyshomeostasis and cell death.
Fil: Saporito Magriñá, Christian Martín. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Departamento de Química Analítica y Fisicoquímica. Cátedra de Química General e Inorgánica; Argentina
Fil: Musacco Sebio, Rosario Natalia. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Departamento de Química Analítica y Fisicoquímica. Cátedra de Química General e Inorgánica; Argentina
Fil: Acosta, Juan Manuel. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Departamento de Química Analítica y Fisicoquímica. Cátedra de Química General e Inorgánica; Argentina
Fil: Bajicoff, Sofía. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Departamento de Química Analítica y Fisicoquímica. Cátedra de Química General e Inorgánica; Argentina
Fil: Paredes Fleitas, Paola. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Departamento de Química Analítica y Fisicoquímica. Cátedra de Química General e Inorgánica; Argentina
Fil: Boveris, Alberto Antonio. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Departamento de Química Analítica y Fisicoquímica. Cátedra de Química General e Inorgánica; Argentina
Fil: Repetto, Marisa Gabriela. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Departamento de Química Analítica y Fisicoquímica. Cátedra de Química General e Inorgánica; Argentina
Materia
Copper Ions
Iron Ions
Liver Oxidative Stress And Damage
Metal Toxicity
Mitochondria
Oxygen Consumption
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:11336/66281
Acceder
id CONICETDig_9db7534ca069c91242d9fd8f65365f50
oai_identifier_str oai:ri.conicet.gov.ar:11336/66281
network_acronym_str CONICETDig
repository_id_str 3498
network_name_str CONICET Digital (CONICET)
spelling Rat liver mitochondrial dysfunction by addition of copper(II) or iron(III) ionsSaporito Magriñá, Christian MartínMusacco Sebio, Rosario NataliaAcosta, Juan ManuelBajicoff, SofíaParedes Fleitas, PaolaBoveris, Alberto AntonioRepetto, Marisa GabrielaCopper IonsIron IonsLiver Oxidative Stress And DamageMetal ToxicityMitochondriaOxygen Consumptionhttps://purl.org/becyt/ford/1.6https://purl.org/becyt/ford/1Increased copper (Cu) and iron (Fe) levels in liver and brain are associated to oxidative stress and damage with increased phospholipid oxidation process. The aim of this work was to assess the toxic effects of Cu2 + and Fe3 + addition to rat liver mitochondria by determining mitochondrial respiration in states 3 (active respiration) and 4 (resting respiration), and phospholipid peroxidation. Both, Cu2 + and Fe3 + produced decreases in O2 consumption in a concentration-dependent manner in active state 3: both ions by 42% with malate-glutamate as complex I substrate (concentration for half maximal response (C50) 60 μM Cu2 + and 1.25 mM Fe3 +), and with succinate as complex II substrate: 64?69% with C50 of 50 μM Cu2 + and with C50 of 1.25 mM of Fe3 +. Respiratory control decreased with Cu2 + (C50 50 μM) and Fe3 + (C50 1.25-1-75 mM) with both substrates. Cu2 + produced a 2-fold increase and Fe3 + a 5-fold increase of thiobarbituric acid-reactive substances (TBARS) content from 25 μM Cu2 + (C50 40 μM) and from 100 μM Fe3 + (C50 1.75 mM). Supplementations with Cu2 + and Fe3 + ions induce mitochondrial dysfunction with phospholipid peroxidation in rat liver mitochondria. Although is proved that a Fenton/Haber Weiss mechanism of oxidative damage occurs in metal-ion induced mitochondrial toxicity, slightly different responses to the metal ions suggest some differences in the mechanism of intracellular toxicity. The decreased rates of mitochondrial respiration and the alteration of mitochondrial function by phospholipid and protein oxidations lead to mitochondrial dysfunction, cellular dyshomeostasis and cell death.Fil: Saporito Magriñá, Christian Martín. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Departamento de Química Analítica y Fisicoquímica. Cátedra de Química General e Inorgánica; ArgentinaFil: Musacco Sebio, Rosario Natalia. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Departamento de Química Analítica y Fisicoquímica. Cátedra de Química General e Inorgánica; ArgentinaFil: Acosta, Juan Manuel. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Departamento de Química Analítica y Fisicoquímica. Cátedra de Química General e Inorgánica; ArgentinaFil: Bajicoff, Sofía. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Departamento de Química Analítica y Fisicoquímica. Cátedra de Química General e Inorgánica; ArgentinaFil: Paredes Fleitas, Paola. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Departamento de Química Analítica y Fisicoquímica. Cátedra de Química General e Inorgánica; ArgentinaFil: Boveris, Alberto Antonio. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Departamento de Química Analítica y Fisicoquímica. Cátedra de Química General e Inorgánica; ArgentinaFil: Repetto, Marisa Gabriela. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Departamento de Química Analítica y Fisicoquímica. Cátedra de Química General e Inorgánica; ArgentinaElsevier Science Inc2017-01info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfapplication/pdfapplication/pdfapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/66281Saporito Magriñá, Christian Martín; Musacco Sebio, Rosario Natalia; Acosta, Juan Manuel; Bajicoff, Sofía; Paredes Fleitas, Paola; et al.; Rat liver mitochondrial dysfunction by addition of copper(II) or iron(III) ions; Elsevier Science Inc; Journal of Inorganic Biochemistry; 166; 1-2017; 5-110162-0134CONICET DigitalCONICETenginfo:eu-repo/semantics/altIdentifier/doi/10.1016/j.jinorgbio.2016.10.009info:eu-repo/semantics/altIdentifier/url/https://linkinghub.elsevier.com/retrieve/pii/S0162013416303385info:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-sa/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-09-29T09:35:45Zoai:ri.conicet.gov.ar:11336/66281instacron: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 09:35:45.847CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse
dc.title.none.fl_str_mv Rat liver mitochondrial dysfunction by addition of copper(II) or iron(III) ions
title Rat liver mitochondrial dysfunction by addition of copper(II) or iron(III) ions
spellingShingle Rat liver mitochondrial dysfunction by addition of copper(II) or iron(III) ions
Saporito Magriñá, Christian Martín
Copper Ions
Iron Ions
Liver Oxidative Stress And Damage
Metal Toxicity
Mitochondria
Oxygen Consumption
title_short Rat liver mitochondrial dysfunction by addition of copper(II) or iron(III) ions
title_full Rat liver mitochondrial dysfunction by addition of copper(II) or iron(III) ions
title_fullStr Rat liver mitochondrial dysfunction by addition of copper(II) or iron(III) ions
title_full_unstemmed Rat liver mitochondrial dysfunction by addition of copper(II) or iron(III) ions
title_sort Rat liver mitochondrial dysfunction by addition of copper(II) or iron(III) ions
dc.creator.none.fl_str_mv Saporito Magriñá, Christian Martín
Musacco Sebio, Rosario Natalia
Acosta, Juan Manuel
Bajicoff, Sofía
Paredes Fleitas, Paola
Boveris, Alberto Antonio
Repetto, Marisa Gabriela
author Saporito Magriñá, Christian Martín
author_facet Saporito Magriñá, Christian Martín
Musacco Sebio, Rosario Natalia
Acosta, Juan Manuel
Bajicoff, Sofía
Paredes Fleitas, Paola
Boveris, Alberto Antonio
Repetto, Marisa Gabriela
author_role author
author2 Musacco Sebio, Rosario Natalia
Acosta, Juan Manuel
Bajicoff, Sofía
Paredes Fleitas, Paola
Boveris, Alberto Antonio
Repetto, Marisa Gabriela
author2_role author
author
author
author
author
author
dc.subject.none.fl_str_mv Copper Ions
Iron Ions
Liver Oxidative Stress And Damage
Metal Toxicity
Mitochondria
Oxygen Consumption
topic Copper Ions
Iron Ions
Liver Oxidative Stress And Damage
Metal Toxicity
Mitochondria
Oxygen Consumption
purl_subject.fl_str_mv https://purl.org/becyt/ford/1.6
https://purl.org/becyt/ford/1
dc.description.none.fl_txt_mv Increased copper (Cu) and iron (Fe) levels in liver and brain are associated to oxidative stress and damage with increased phospholipid oxidation process. The aim of this work was to assess the toxic effects of Cu2 + and Fe3 + addition to rat liver mitochondria by determining mitochondrial respiration in states 3 (active respiration) and 4 (resting respiration), and phospholipid peroxidation. Both, Cu2 + and Fe3 + produced decreases in O2 consumption in a concentration-dependent manner in active state 3: both ions by 42% with malate-glutamate as complex I substrate (concentration for half maximal response (C50) 60 μM Cu2 + and 1.25 mM Fe3 +), and with succinate as complex II substrate: 64?69% with C50 of 50 μM Cu2 + and with C50 of 1.25 mM of Fe3 +. Respiratory control decreased with Cu2 + (C50 50 μM) and Fe3 + (C50 1.25-1-75 mM) with both substrates. Cu2 + produced a 2-fold increase and Fe3 + a 5-fold increase of thiobarbituric acid-reactive substances (TBARS) content from 25 μM Cu2 + (C50 40 μM) and from 100 μM Fe3 + (C50 1.75 mM). Supplementations with Cu2 + and Fe3 + ions induce mitochondrial dysfunction with phospholipid peroxidation in rat liver mitochondria. Although is proved that a Fenton/Haber Weiss mechanism of oxidative damage occurs in metal-ion induced mitochondrial toxicity, slightly different responses to the metal ions suggest some differences in the mechanism of intracellular toxicity. The decreased rates of mitochondrial respiration and the alteration of mitochondrial function by phospholipid and protein oxidations lead to mitochondrial dysfunction, cellular dyshomeostasis and cell death.
Fil: Saporito Magriñá, Christian Martín. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Departamento de Química Analítica y Fisicoquímica. Cátedra de Química General e Inorgánica; Argentina
Fil: Musacco Sebio, Rosario Natalia. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Departamento de Química Analítica y Fisicoquímica. Cátedra de Química General e Inorgánica; Argentina
Fil: Acosta, Juan Manuel. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Departamento de Química Analítica y Fisicoquímica. Cátedra de Química General e Inorgánica; Argentina
Fil: Bajicoff, Sofía. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Departamento de Química Analítica y Fisicoquímica. Cátedra de Química General e Inorgánica; Argentina
Fil: Paredes Fleitas, Paola. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Departamento de Química Analítica y Fisicoquímica. Cátedra de Química General e Inorgánica; Argentina
Fil: Boveris, Alberto Antonio. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Departamento de Química Analítica y Fisicoquímica. Cátedra de Química General e Inorgánica; Argentina
Fil: Repetto, Marisa Gabriela. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Departamento de Química Analítica y Fisicoquímica. Cátedra de Química General e Inorgánica; Argentina
description Increased copper (Cu) and iron (Fe) levels in liver and brain are associated to oxidative stress and damage with increased phospholipid oxidation process. The aim of this work was to assess the toxic effects of Cu2 + and Fe3 + addition to rat liver mitochondria by determining mitochondrial respiration in states 3 (active respiration) and 4 (resting respiration), and phospholipid peroxidation. Both, Cu2 + and Fe3 + produced decreases in O2 consumption in a concentration-dependent manner in active state 3: both ions by 42% with malate-glutamate as complex I substrate (concentration for half maximal response (C50) 60 μM Cu2 + and 1.25 mM Fe3 +), and with succinate as complex II substrate: 64?69% with C50 of 50 μM Cu2 + and with C50 of 1.25 mM of Fe3 +. Respiratory control decreased with Cu2 + (C50 50 μM) and Fe3 + (C50 1.25-1-75 mM) with both substrates. Cu2 + produced a 2-fold increase and Fe3 + a 5-fold increase of thiobarbituric acid-reactive substances (TBARS) content from 25 μM Cu2 + (C50 40 μM) and from 100 μM Fe3 + (C50 1.75 mM). Supplementations with Cu2 + and Fe3 + ions induce mitochondrial dysfunction with phospholipid peroxidation in rat liver mitochondria. Although is proved that a Fenton/Haber Weiss mechanism of oxidative damage occurs in metal-ion induced mitochondrial toxicity, slightly different responses to the metal ions suggest some differences in the mechanism of intracellular toxicity. The decreased rates of mitochondrial respiration and the alteration of mitochondrial function by phospholipid and protein oxidations lead to mitochondrial dysfunction, cellular dyshomeostasis and cell death.
publishDate 2017
dc.date.none.fl_str_mv 2017-01
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/11336/66281
Saporito Magriñá, Christian Martín; Musacco Sebio, Rosario Natalia; Acosta, Juan Manuel; Bajicoff, Sofía; Paredes Fleitas, Paola; et al.; Rat liver mitochondrial dysfunction by addition of copper(II) or iron(III) ions; Elsevier Science Inc; Journal of Inorganic Biochemistry; 166; 1-2017; 5-11
0162-0134
CONICET Digital
CONICET
url http://hdl.handle.net/11336/66281
identifier_str_mv Saporito Magriñá, Christian Martín; Musacco Sebio, Rosario Natalia; Acosta, Juan Manuel; Bajicoff, Sofía; Paredes Fleitas, Paola; et al.; Rat liver mitochondrial dysfunction by addition of copper(II) or iron(III) ions; Elsevier Science Inc; Journal of Inorganic Biochemistry; 166; 1-2017; 5-11
0162-0134
CONICET Digital
CONICET
dc.language.none.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv info:eu-repo/semantics/altIdentifier/doi/10.1016/j.jinorgbio.2016.10.009
info:eu-repo/semantics/altIdentifier/url/https://linkinghub.elsevier.com/retrieve/pii/S0162013416303385
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
application/pdf
application/pdf
dc.publisher.none.fl_str_mv Elsevier Science Inc
publisher.none.fl_str_mv Elsevier Science Inc
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 13.070432

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