Complex I syndrome in striatum and frontal cortex in a rat model of Parkinson disease

Autores
Valdez, Laura Batriz; Zaobornyj, Tamara; Bández, Manuel J.; López Cepero, José María; Boveris, Alberto Antonio; Navarro, Ana
Año de publicación
2019
Idioma
inglés
Tipo de recurso
artículo
Estado
versión publicada
Descripción
Mitochondrial dysfunction named complex I syndrome was observed in striatum mitochondria of rotenone treated rats (2 mg rotenone/kg, i. p., for 30 or 60 days) in an animal model of Parkinson disease. After 60 days of rotenone treatment, the animals showed: (a) 6-fold increased bradykinesia and 60% decreased locomotor activity; (b) 35-34% decreases in striatum O 2 uptake and in state 3 mitochondrial respiration with malate-glutamate as substrate; (c) 43–57% diminished striatum complex I activity with 60–71% decreased striatum mitochondrial NOS activity, determined both as biochemical activity and as functional activity (by the NO inhibition of active respiration); (d) 34–40% increased rates of mitochondrial O 2 •- and H 2 O 2 productions and 36–46% increased contents of the products of phospholipid peroxidation and of protein oxidation; and (e) 24% decreased striatum mitochondrial content, likely associated to decreased NO-dependent mitochondrial biogenesis. Intermediate values were observed after 30 days of rotenone treatment. Frontal cortex tissue and mitochondria showed similar but less marked changes. Rotenone-treated rats showed mitochondrial complex I syndrome associated with cellular oxidative stress in the dopaminergic brain areas of striatum and frontal cortex, a fact that describes the high sensitivity of mitochondrial complex I to inactivation by oxidative reactions.
Fil: Valdez, Laura Batriz. 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: Zaobornyj, Tamara. 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: Bández, Manuel J.. Universidad de Cádiz; España
Fil: López Cepero, José María. Universidad de Cádiz; España
Fil: Boveris, Alberto Antonio. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay; Argentina. Universidad de Buenos Aires; Argentina
Fil: Navarro, Ana. Universidad de Cádiz; España
Materia
BRAIN MITOCHONDRIA
COMPLEX I
MITOCHONDRIAL NOS ACTIVITY
NO PRODUCTION
ROTENONE
Nivel de accesibilidad
acceso abierto
Condiciones de uso
https://creativecommons.org/licenses/by-nc-nd/2.5/ar/
Repositorio
CONICET Digital (CONICET)
Institución
Consejo Nacional de Investigaciones Científicas y Técnicas
OAI Identificador
oai:ri.conicet.gov.ar:11336/125938
Acceder
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oai_identifier_str oai:ri.conicet.gov.ar:11336/125938
network_acronym_str CONICETDig
repository_id_str 3498
network_name_str CONICET Digital (CONICET)
spelling Complex I syndrome in striatum and frontal cortex in a rat model of Parkinson diseaseValdez, Laura BatrizZaobornyj, TamaraBández, Manuel J.López Cepero, José MaríaBoveris, Alberto AntonioNavarro, AnaBRAIN MITOCHONDRIACOMPLEX IMITOCHONDRIAL NOS ACTIVITYNO PRODUCTIONROTENONEhttps://purl.org/becyt/ford/1.6https://purl.org/becyt/ford/1Mitochondrial dysfunction named complex I syndrome was observed in striatum mitochondria of rotenone treated rats (2 mg rotenone/kg, i. p., for 30 or 60 days) in an animal model of Parkinson disease. After 60 days of rotenone treatment, the animals showed: (a) 6-fold increased bradykinesia and 60% decreased locomotor activity; (b) 35-34% decreases in striatum O 2 uptake and in state 3 mitochondrial respiration with malate-glutamate as substrate; (c) 43–57% diminished striatum complex I activity with 60–71% decreased striatum mitochondrial NOS activity, determined both as biochemical activity and as functional activity (by the NO inhibition of active respiration); (d) 34–40% increased rates of mitochondrial O 2 •- and H 2 O 2 productions and 36–46% increased contents of the products of phospholipid peroxidation and of protein oxidation; and (e) 24% decreased striatum mitochondrial content, likely associated to decreased NO-dependent mitochondrial biogenesis. Intermediate values were observed after 30 days of rotenone treatment. Frontal cortex tissue and mitochondria showed similar but less marked changes. Rotenone-treated rats showed mitochondrial complex I syndrome associated with cellular oxidative stress in the dopaminergic brain areas of striatum and frontal cortex, a fact that describes the high sensitivity of mitochondrial complex I to inactivation by oxidative reactions.Fil: Valdez, Laura Batriz. 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: Zaobornyj, Tamara. 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: Bández, Manuel J.. Universidad de Cádiz; EspañaFil: López Cepero, José María. Universidad de Cádiz; EspañaFil: Boveris, Alberto Antonio. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay; Argentina. Universidad de Buenos Aires; ArgentinaFil: Navarro, Ana. Universidad de Cádiz; EspañaElsevier Science Inc2019-03info: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/11336/125938Valdez, Laura Batriz; Zaobornyj, Tamara; Bández, Manuel J.; López Cepero, José María; Boveris, Alberto Antonio; et al.; Complex I syndrome in striatum and frontal cortex in a rat model of Parkinson disease; Elsevier Science Inc; Free Radical Biology and Medicine; 135; 3-2019; 274-2820891-5849CONICET DigitalCONICETenginfo:eu-repo/semantics/altIdentifier/url/https://linkinghub.elsevier.com/retrieve/pii/S0891584919300802info:eu-repo/semantics/altIdentifier/doi/10.1016/j.freeradbiomed.2019.03.001info:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-nd/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-09-03T10:01:02Zoai:ri.conicet.gov.ar:11336/125938instacron: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:34982025-09-03 10:01:02.354CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse
dc.title.none.fl_str_mv Complex I syndrome in striatum and frontal cortex in a rat model of Parkinson disease
title Complex I syndrome in striatum and frontal cortex in a rat model of Parkinson disease
spellingShingle Complex I syndrome in striatum and frontal cortex in a rat model of Parkinson disease
Valdez, Laura Batriz
BRAIN MITOCHONDRIA
COMPLEX I
MITOCHONDRIAL NOS ACTIVITY
NO PRODUCTION
ROTENONE
title_short Complex I syndrome in striatum and frontal cortex in a rat model of Parkinson disease
title_full Complex I syndrome in striatum and frontal cortex in a rat model of Parkinson disease
title_fullStr Complex I syndrome in striatum and frontal cortex in a rat model of Parkinson disease
title_full_unstemmed Complex I syndrome in striatum and frontal cortex in a rat model of Parkinson disease
title_sort Complex I syndrome in striatum and frontal cortex in a rat model of Parkinson disease
dc.creator.none.fl_str_mv Valdez, Laura Batriz
Zaobornyj, Tamara
Bández, Manuel J.
López Cepero, José María
Boveris, Alberto Antonio
Navarro, Ana
author Valdez, Laura Batriz
author_facet Valdez, Laura Batriz
Zaobornyj, Tamara
Bández, Manuel J.
López Cepero, José María
Boveris, Alberto Antonio
Navarro, Ana
author_role author
author2 Zaobornyj, Tamara
Bández, Manuel J.
López Cepero, José María
Boveris, Alberto Antonio
Navarro, Ana
author2_role author
author
author
author
author
dc.subject.none.fl_str_mv BRAIN MITOCHONDRIA
COMPLEX I
MITOCHONDRIAL NOS ACTIVITY
NO PRODUCTION
ROTENONE
topic BRAIN MITOCHONDRIA
COMPLEX I
MITOCHONDRIAL NOS ACTIVITY
NO PRODUCTION
ROTENONE
purl_subject.fl_str_mv https://purl.org/becyt/ford/1.6
https://purl.org/becyt/ford/1
dc.description.none.fl_txt_mv Mitochondrial dysfunction named complex I syndrome was observed in striatum mitochondria of rotenone treated rats (2 mg rotenone/kg, i. p., for 30 or 60 days) in an animal model of Parkinson disease. After 60 days of rotenone treatment, the animals showed: (a) 6-fold increased bradykinesia and 60% decreased locomotor activity; (b) 35-34% decreases in striatum O 2 uptake and in state 3 mitochondrial respiration with malate-glutamate as substrate; (c) 43–57% diminished striatum complex I activity with 60–71% decreased striatum mitochondrial NOS activity, determined both as biochemical activity and as functional activity (by the NO inhibition of active respiration); (d) 34–40% increased rates of mitochondrial O 2 •- and H 2 O 2 productions and 36–46% increased contents of the products of phospholipid peroxidation and of protein oxidation; and (e) 24% decreased striatum mitochondrial content, likely associated to decreased NO-dependent mitochondrial biogenesis. Intermediate values were observed after 30 days of rotenone treatment. Frontal cortex tissue and mitochondria showed similar but less marked changes. Rotenone-treated rats showed mitochondrial complex I syndrome associated with cellular oxidative stress in the dopaminergic brain areas of striatum and frontal cortex, a fact that describes the high sensitivity of mitochondrial complex I to inactivation by oxidative reactions.
Fil: Valdez, Laura Batriz. 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: Zaobornyj, Tamara. 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: Bández, Manuel J.. Universidad de Cádiz; España
Fil: López Cepero, José María. Universidad de Cádiz; España
Fil: Boveris, Alberto Antonio. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay; Argentina. Universidad de Buenos Aires; Argentina
Fil: Navarro, Ana. Universidad de Cádiz; España
description Mitochondrial dysfunction named complex I syndrome was observed in striatum mitochondria of rotenone treated rats (2 mg rotenone/kg, i. p., for 30 or 60 days) in an animal model of Parkinson disease. After 60 days of rotenone treatment, the animals showed: (a) 6-fold increased bradykinesia and 60% decreased locomotor activity; (b) 35-34% decreases in striatum O 2 uptake and in state 3 mitochondrial respiration with malate-glutamate as substrate; (c) 43–57% diminished striatum complex I activity with 60–71% decreased striatum mitochondrial NOS activity, determined both as biochemical activity and as functional activity (by the NO inhibition of active respiration); (d) 34–40% increased rates of mitochondrial O 2 •- and H 2 O 2 productions and 36–46% increased contents of the products of phospholipid peroxidation and of protein oxidation; and (e) 24% decreased striatum mitochondrial content, likely associated to decreased NO-dependent mitochondrial biogenesis. Intermediate values were observed after 30 days of rotenone treatment. Frontal cortex tissue and mitochondria showed similar but less marked changes. Rotenone-treated rats showed mitochondrial complex I syndrome associated with cellular oxidative stress in the dopaminergic brain areas of striatum and frontal cortex, a fact that describes the high sensitivity of mitochondrial complex I to inactivation by oxidative reactions.
publishDate 2019
dc.date.none.fl_str_mv 2019-03
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/11336/125938
Valdez, Laura Batriz; Zaobornyj, Tamara; Bández, Manuel J.; López Cepero, José María; Boveris, Alberto Antonio; et al.; Complex I syndrome in striatum and frontal cortex in a rat model of Parkinson disease; Elsevier Science Inc; Free Radical Biology and Medicine; 135; 3-2019; 274-282
0891-5849
CONICET Digital
CONICET
url http://hdl.handle.net/11336/125938
identifier_str_mv Valdez, Laura Batriz; Zaobornyj, Tamara; Bández, Manuel J.; López Cepero, José María; Boveris, Alberto Antonio; et al.; Complex I syndrome in striatum and frontal cortex in a rat model of Parkinson disease; Elsevier Science Inc; Free Radical Biology and Medicine; 135; 3-2019; 274-282
0891-5849
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://linkinghub.elsevier.com/retrieve/pii/S0891584919300802
info:eu-repo/semantics/altIdentifier/doi/10.1016/j.freeradbiomed.2019.03.001
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
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 13.13397

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