Nitric oxide, complex I, and the modulation of mitochondrial reactive species in biology and disease

Autores
Carreras, Maria Cecilia; Franco, María Clara; Peralta, Jorge Guillermo; Poderoso, Juan José
Año de publicación
2004
Idioma
inglés
Tipo de recurso
artículo
Estado
versión publicada
Descripción
Mitochondria are the specialized organelles for energy metabolism but also participate in the production of O2 active species, cell cycle regulation, apoptosis and thermogenesis. Classically, regulation of mitochondrial energy functions was based on the ADP/ATP ratio, which dynamically stimulates the transition between resting and maximal O2 uptake. However, in the last years, NO was identified as a physiologic regulator of electron transfer and ATP synthesis by inhibiting cytochrome oxidase. Additionally, NO stimulates the mitochondrial production of O 2 active species, primarily O2- and H 2O2, and, depending on NO matrix concentration, of ONOO-, which is responsible for the nitrosylation and nitration of mitochondrial components. By this means, alteration in mitochondrial complexes restricts energy output, further increases O2 active species and changes cell signaling for proliferation and apoptosis through redox effects on specific pathways. These mechanisms are prototypically operating in prevalent generalized diseases like sepsis with multiorgan failure or limited neurodegenerative disorders like Parkinson's disease. Complex I appears to be highly susceptible to ONOO- effects and nitration, which defines an acquired group of mitochondrial disorders, in addition to the genetically induced syndromes. Increase of mitochondrial NO may follow over-expression of nNOS, induction and translocation of iNOS, and activation and/or increased content of the newly described mtNOS. Likewise, mtNOS is important in the modulation of O2 uptake and cell signaling, and in mitochondrial pathology, including the effects of aging, dystrophin deficiency, hypoxia, inflammation and cancer.
Fil: Carreras, Maria Cecilia. Universidad de Buenos Aires. Facultad de Medicina. Hospital de Clínicas General San Martín. Laboratorio de Metabolismo del Oxígeno; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Inmunología, Genética y Metabolismo. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Inmunología, Genética y Metabolismo; Argentina
Fil: Franco, María Clara. Universidad de Buenos Aires. Facultad de Medicina. Hospital de Clínicas General San Martín. Laboratorio de Metabolismo del Oxígeno; Argentina
Fil: Peralta, Jorge Guillermo. Universidad de Buenos Aires. Facultad de Medicina. Hospital de Clínicas General San Martín. Laboratorio de Metabolismo del Oxígeno; Argentina
Fil: Poderoso, Juan José. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Inmunología, Genética y Metabolismo. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Inmunología, Genética y Metabolismo; Argentina. Universidad de Buenos Aires. Facultad de Medicina. Hospital de Clínicas General San Martín. Laboratorio de Metabolismo del Oxígeno; Argentina
Materia
ENOS, INOS, MTNOS AND NNOS, ENDOTELIAL, INDUCIBLE, MITOCHONDRIAL AND NEURONAL NITRIC OXIDE SYNTHASES
H2O2, HYDROGEN PEROXIDE
MN-SOD, MANGANESE-SUPEROXIDE DISMUTASE
NO, NITRIC OXIDE
NOS, NITRIC OXIDE SYNTHASE
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:11336/118275
Acceder
id CONICETDig_f67c6c0e87e8e80f9deb63830124838c
oai_identifier_str oai:ri.conicet.gov.ar:11336/118275
network_acronym_str CONICETDig
repository_id_str 3498
network_name_str CONICET Digital (CONICET)
spelling Nitric oxide, complex I, and the modulation of mitochondrial reactive species in biology and diseaseCarreras, Maria CeciliaFranco, María ClaraPeralta, Jorge GuillermoPoderoso, Juan JoséENOS, INOS, MTNOS AND NNOS, ENDOTELIAL, INDUCIBLE, MITOCHONDRIAL AND NEURONAL NITRIC OXIDE SYNTHASESH2O2, HYDROGEN PEROXIDEMN-SOD, MANGANESE-SUPEROXIDE DISMUTASENO, NITRIC OXIDENOS, NITRIC OXIDE SYNTHASEhttps://purl.org/becyt/ford/3.3https://purl.org/becyt/ford/3Mitochondria are the specialized organelles for energy metabolism but also participate in the production of O2 active species, cell cycle regulation, apoptosis and thermogenesis. Classically, regulation of mitochondrial energy functions was based on the ADP/ATP ratio, which dynamically stimulates the transition between resting and maximal O2 uptake. However, in the last years, NO was identified as a physiologic regulator of electron transfer and ATP synthesis by inhibiting cytochrome oxidase. Additionally, NO stimulates the mitochondrial production of O 2 active species, primarily O2- and H 2O2, and, depending on NO matrix concentration, of ONOO-, which is responsible for the nitrosylation and nitration of mitochondrial components. By this means, alteration in mitochondrial complexes restricts energy output, further increases O2 active species and changes cell signaling for proliferation and apoptosis through redox effects on specific pathways. These mechanisms are prototypically operating in prevalent generalized diseases like sepsis with multiorgan failure or limited neurodegenerative disorders like Parkinson's disease. Complex I appears to be highly susceptible to ONOO- effects and nitration, which defines an acquired group of mitochondrial disorders, in addition to the genetically induced syndromes. Increase of mitochondrial NO may follow over-expression of nNOS, induction and translocation of iNOS, and activation and/or increased content of the newly described mtNOS. Likewise, mtNOS is important in the modulation of O2 uptake and cell signaling, and in mitochondrial pathology, including the effects of aging, dystrophin deficiency, hypoxia, inflammation and cancer.Fil: Carreras, Maria Cecilia. Universidad de Buenos Aires. Facultad de Medicina. Hospital de Clínicas General San Martín. Laboratorio de Metabolismo del Oxígeno; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Inmunología, Genética y Metabolismo. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Inmunología, Genética y Metabolismo; ArgentinaFil: Franco, María Clara. Universidad de Buenos Aires. Facultad de Medicina. Hospital de Clínicas General San Martín. Laboratorio de Metabolismo del Oxígeno; ArgentinaFil: Peralta, Jorge Guillermo. Universidad de Buenos Aires. Facultad de Medicina. Hospital de Clínicas General San Martín. Laboratorio de Metabolismo del Oxígeno; ArgentinaFil: Poderoso, Juan José. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Inmunología, Genética y Metabolismo. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Inmunología, Genética y Metabolismo; Argentina. Universidad de Buenos Aires. Facultad de Medicina. Hospital de Clínicas General San Martín. Laboratorio de Metabolismo del Oxígeno; ArgentinaElsevier Science2004-02info: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/11336/118275Carreras, Maria Cecilia; Franco, María Clara; Peralta, Jorge Guillermo; Poderoso, Juan José; Nitric oxide, complex I, and the modulation of mitochondrial reactive species in biology and disease; Elsevier Science; Molecular Aspects Of Medicine; 25; 1-2; 2-2004; 125-1390098-2997CONICET DigitalCONICETenginfo:eu-repo/semantics/altIdentifier/doi/10.1016/j.mam.2004.02.014info:eu-repo/semantics/altIdentifier/url/https://www.sciencedirect.com/science/article/abs/pii/S0098299704000159?via%3Dihubinfo:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-sa/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-10-15T14:39:12Zoai:ri.conicet.gov.ar:11336/118275instacron: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 14:39:12.401CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse
dc.title.none.fl_str_mv Nitric oxide, complex I, and the modulation of mitochondrial reactive species in biology and disease
title Nitric oxide, complex I, and the modulation of mitochondrial reactive species in biology and disease
spellingShingle Nitric oxide, complex I, and the modulation of mitochondrial reactive species in biology and disease
Carreras, Maria Cecilia
ENOS, INOS, MTNOS AND NNOS, ENDOTELIAL, INDUCIBLE, MITOCHONDRIAL AND NEURONAL NITRIC OXIDE SYNTHASES
H2O2, HYDROGEN PEROXIDE
MN-SOD, MANGANESE-SUPEROXIDE DISMUTASE
NO, NITRIC OXIDE
NOS, NITRIC OXIDE SYNTHASE
title_short Nitric oxide, complex I, and the modulation of mitochondrial reactive species in biology and disease
title_full Nitric oxide, complex I, and the modulation of mitochondrial reactive species in biology and disease
title_fullStr Nitric oxide, complex I, and the modulation of mitochondrial reactive species in biology and disease
title_full_unstemmed Nitric oxide, complex I, and the modulation of mitochondrial reactive species in biology and disease
title_sort Nitric oxide, complex I, and the modulation of mitochondrial reactive species in biology and disease
dc.creator.none.fl_str_mv Carreras, Maria Cecilia
Franco, María Clara
Peralta, Jorge Guillermo
Poderoso, Juan José
author Carreras, Maria Cecilia
author_facet Carreras, Maria Cecilia
Franco, María Clara
Peralta, Jorge Guillermo
Poderoso, Juan José
author_role author
author2 Franco, María Clara
Peralta, Jorge Guillermo
Poderoso, Juan José
author2_role author
author
author
dc.subject.none.fl_str_mv ENOS, INOS, MTNOS AND NNOS, ENDOTELIAL, INDUCIBLE, MITOCHONDRIAL AND NEURONAL NITRIC OXIDE SYNTHASES
H2O2, HYDROGEN PEROXIDE
MN-SOD, MANGANESE-SUPEROXIDE DISMUTASE
NO, NITRIC OXIDE
NOS, NITRIC OXIDE SYNTHASE
topic ENOS, INOS, MTNOS AND NNOS, ENDOTELIAL, INDUCIBLE, MITOCHONDRIAL AND NEURONAL NITRIC OXIDE SYNTHASES
H2O2, HYDROGEN PEROXIDE
MN-SOD, MANGANESE-SUPEROXIDE DISMUTASE
NO, NITRIC OXIDE
NOS, NITRIC OXIDE SYNTHASE
purl_subject.fl_str_mv https://purl.org/becyt/ford/3.3
https://purl.org/becyt/ford/3
dc.description.none.fl_txt_mv Mitochondria are the specialized organelles for energy metabolism but also participate in the production of O2 active species, cell cycle regulation, apoptosis and thermogenesis. Classically, regulation of mitochondrial energy functions was based on the ADP/ATP ratio, which dynamically stimulates the transition between resting and maximal O2 uptake. However, in the last years, NO was identified as a physiologic regulator of electron transfer and ATP synthesis by inhibiting cytochrome oxidase. Additionally, NO stimulates the mitochondrial production of O 2 active species, primarily O2- and H 2O2, and, depending on NO matrix concentration, of ONOO-, which is responsible for the nitrosylation and nitration of mitochondrial components. By this means, alteration in mitochondrial complexes restricts energy output, further increases O2 active species and changes cell signaling for proliferation and apoptosis through redox effects on specific pathways. These mechanisms are prototypically operating in prevalent generalized diseases like sepsis with multiorgan failure or limited neurodegenerative disorders like Parkinson's disease. Complex I appears to be highly susceptible to ONOO- effects and nitration, which defines an acquired group of mitochondrial disorders, in addition to the genetically induced syndromes. Increase of mitochondrial NO may follow over-expression of nNOS, induction and translocation of iNOS, and activation and/or increased content of the newly described mtNOS. Likewise, mtNOS is important in the modulation of O2 uptake and cell signaling, and in mitochondrial pathology, including the effects of aging, dystrophin deficiency, hypoxia, inflammation and cancer.
Fil: Carreras, Maria Cecilia. Universidad de Buenos Aires. Facultad de Medicina. Hospital de Clínicas General San Martín. Laboratorio de Metabolismo del Oxígeno; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Inmunología, Genética y Metabolismo. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Inmunología, Genética y Metabolismo; Argentina
Fil: Franco, María Clara. Universidad de Buenos Aires. Facultad de Medicina. Hospital de Clínicas General San Martín. Laboratorio de Metabolismo del Oxígeno; Argentina
Fil: Peralta, Jorge Guillermo. Universidad de Buenos Aires. Facultad de Medicina. Hospital de Clínicas General San Martín. Laboratorio de Metabolismo del Oxígeno; Argentina
Fil: Poderoso, Juan José. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Inmunología, Genética y Metabolismo. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Inmunología, Genética y Metabolismo; Argentina. Universidad de Buenos Aires. Facultad de Medicina. Hospital de Clínicas General San Martín. Laboratorio de Metabolismo del Oxígeno; Argentina
description Mitochondria are the specialized organelles for energy metabolism but also participate in the production of O2 active species, cell cycle regulation, apoptosis and thermogenesis. Classically, regulation of mitochondrial energy functions was based on the ADP/ATP ratio, which dynamically stimulates the transition between resting and maximal O2 uptake. However, in the last years, NO was identified as a physiologic regulator of electron transfer and ATP synthesis by inhibiting cytochrome oxidase. Additionally, NO stimulates the mitochondrial production of O 2 active species, primarily O2- and H 2O2, and, depending on NO matrix concentration, of ONOO-, which is responsible for the nitrosylation and nitration of mitochondrial components. By this means, alteration in mitochondrial complexes restricts energy output, further increases O2 active species and changes cell signaling for proliferation and apoptosis through redox effects on specific pathways. These mechanisms are prototypically operating in prevalent generalized diseases like sepsis with multiorgan failure or limited neurodegenerative disorders like Parkinson's disease. Complex I appears to be highly susceptible to ONOO- effects and nitration, which defines an acquired group of mitochondrial disorders, in addition to the genetically induced syndromes. Increase of mitochondrial NO may follow over-expression of nNOS, induction and translocation of iNOS, and activation and/or increased content of the newly described mtNOS. Likewise, mtNOS is important in the modulation of O2 uptake and cell signaling, and in mitochondrial pathology, including the effects of aging, dystrophin deficiency, hypoxia, inflammation and cancer.
publishDate 2004
dc.date.none.fl_str_mv 2004-02
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/11336/118275
Carreras, Maria Cecilia; Franco, María Clara; Peralta, Jorge Guillermo; Poderoso, Juan José; Nitric oxide, complex I, and the modulation of mitochondrial reactive species in biology and disease; Elsevier Science; Molecular Aspects Of Medicine; 25; 1-2; 2-2004; 125-139
0098-2997
CONICET Digital
CONICET
url http://hdl.handle.net/11336/118275
identifier_str_mv Carreras, Maria Cecilia; Franco, María Clara; Peralta, Jorge Guillermo; Poderoso, Juan José; Nitric oxide, complex I, and the modulation of mitochondrial reactive species in biology and disease; Elsevier Science; Molecular Aspects Of Medicine; 25; 1-2; 2-2004; 125-139
0098-2997
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.mam.2004.02.014
info:eu-repo/semantics/altIdentifier/url/https://www.sciencedirect.com/science/article/abs/pii/S0098299704000159?via%3Dihub
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 Elsevier Science
publisher.none.fl_str_mv Elsevier Science
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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