High doses of vitamin E improve mitochondrial dysfunction in rat hippocampus and frontal cortex upon aging

Autores
Navarro, Ana; Bández, Manuel J.; López Cepero, José M.; Gómez, Carmen; Boveris, Alejandro D.; Cadenas, Enrique; Boveris, Alberto Antonio
Año de publicación
2011
Idioma
inglés
Tipo de recurso
artículo
Estado
versión publicada
Descripción
Rat aging from 4 to 12 mo was accompanied by hippocampus and frontal cortex mitochondrial dysfunction, with decreases of 23 to 53% in tissue and mitochondrial respiration and in the activities of complexes I and IV and of mitochondrial nitric oxide synthase (mtNOS) (P < 0.02). In aged rats, the two brain areas showed mitochondria with higher content (35–78%) of oxidation products of phospholipids and proteins and with higher (59–95%) rates of O2− and H2O2 production (P < 0.02). Dietary supplementation with vitamin E (2.0 or 5.0 g/kg of food) from 9 to 12 mo of rat age, restored in a dose-dependent manner, the decreases in tissue and mitochondrial respiration (to 90–96%) and complexes I and IV and mtNOS activities (to 86–88%) of the values of 4-mo-old rats (P < 0.02). Vitamin E prevented, by 73–80%, the increases in oxidation products, and by 62–68%, the increases in O2− and H2O2 production (P < 0.05). High resolution histochemistry of cytochrome oxidase in the hippocampal CA1 region showed higher staining in vitamin E-treated rats than in control animals. Aging decreased (19%) hippocampus mitochondrial mass, an effect that was restored by vitamin E. High doses of vitamin E seem to sustain mitochondrial biogenesis in synaptic areas.
Fil: Navarro, Ana. Universidad de Cádiz; España
Fil: Bández, Manuel J.. Universidad de Cádiz; España
Fil: López Cepero, José M.. Universidad de Cádiz; España
Fil: Gómez, Carmen. Universidad de Cádiz; España
Fil: Boveris, Alejandro D.. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica; Argentina
Fil: Cadenas, Enrique. University Of Southern California; Estados Unidos
Fil: Boveris, Alberto Antonio. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
Materia
Brain Aging
Complex I Syndrome
Hippocampal Aging
Frontal Cortex Aging
Antioxidant Protection
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:11336/16327
Acceder
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network_acronym_str CONICETDig
repository_id_str 3498
network_name_str CONICET Digital (CONICET)
spelling High doses of vitamin E improve mitochondrial dysfunction in rat hippocampus and frontal cortex upon agingNavarro, AnaBández, Manuel J.López Cepero, José M.Gómez, CarmenBoveris, Alejandro D.Cadenas, EnriqueBoveris, Alberto AntonioBrain AgingComplex I SyndromeHippocampal AgingFrontal Cortex AgingAntioxidant Protectionhttps://purl.org/becyt/ford/1.6https://purl.org/becyt/ford/1Rat aging from 4 to 12 mo was accompanied by hippocampus and frontal cortex mitochondrial dysfunction, with decreases of 23 to 53% in tissue and mitochondrial respiration and in the activities of complexes I and IV and of mitochondrial nitric oxide synthase (mtNOS) (P < 0.02). In aged rats, the two brain areas showed mitochondria with higher content (35–78%) of oxidation products of phospholipids and proteins and with higher (59–95%) rates of O2− and H2O2 production (P < 0.02). Dietary supplementation with vitamin E (2.0 or 5.0 g/kg of food) from 9 to 12 mo of rat age, restored in a dose-dependent manner, the decreases in tissue and mitochondrial respiration (to 90–96%) and complexes I and IV and mtNOS activities (to 86–88%) of the values of 4-mo-old rats (P < 0.02). Vitamin E prevented, by 73–80%, the increases in oxidation products, and by 62–68%, the increases in O2− and H2O2 production (P < 0.05). High resolution histochemistry of cytochrome oxidase in the hippocampal CA1 region showed higher staining in vitamin E-treated rats than in control animals. Aging decreased (19%) hippocampus mitochondrial mass, an effect that was restored by vitamin E. High doses of vitamin E seem to sustain mitochondrial biogenesis in synaptic areas.Fil: Navarro, Ana. Universidad de Cádiz; EspañaFil: Bández, Manuel J.. Universidad de Cádiz; EspañaFil: López Cepero, José M.. Universidad de Cádiz; EspañaFil: Gómez, Carmen. Universidad de Cádiz; EspañaFil: Boveris, Alejandro D.. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica; ArgentinaFil: Cadenas, Enrique. University Of Southern California; Estados UnidosFil: Boveris, Alberto Antonio. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaAmerican Physiological Society2011-04info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/16327Navarro, Ana; Bández, Manuel J.; López Cepero, José M.; Gómez, Carmen; Boveris, Alejandro D.; et al.; High doses of vitamin E improve mitochondrial dysfunction in rat hippocampus and frontal cortex upon aging; American Physiological Society; American Journal Of Physiology-regulatory, Integrative And Comparative Physiology; 300; 4; 4-2011; 827-8340363-6119enginfo:eu-repo/semantics/altIdentifier/doi/10.1152/ajpregu.00525.2010info:eu-repo/semantics/altIdentifier/url/http://ajpregu.physiology.org/content/300/4/R827.longinfo:eu-repo/semantics/altIdentifier/url/https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3075077/info:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-sa/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-09-10T13:04:17Zoai:ri.conicet.gov.ar:11336/16327instacron: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:34982025-09-10 13:04:17.485CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse
dc.title.none.fl_str_mv High doses of vitamin E improve mitochondrial dysfunction in rat hippocampus and frontal cortex upon aging
title High doses of vitamin E improve mitochondrial dysfunction in rat hippocampus and frontal cortex upon aging
spellingShingle High doses of vitamin E improve mitochondrial dysfunction in rat hippocampus and frontal cortex upon aging
Navarro, Ana
Brain Aging
Complex I Syndrome
Hippocampal Aging
Frontal Cortex Aging
Antioxidant Protection
title_short High doses of vitamin E improve mitochondrial dysfunction in rat hippocampus and frontal cortex upon aging
title_full High doses of vitamin E improve mitochondrial dysfunction in rat hippocampus and frontal cortex upon aging
title_fullStr High doses of vitamin E improve mitochondrial dysfunction in rat hippocampus and frontal cortex upon aging
title_full_unstemmed High doses of vitamin E improve mitochondrial dysfunction in rat hippocampus and frontal cortex upon aging
title_sort High doses of vitamin E improve mitochondrial dysfunction in rat hippocampus and frontal cortex upon aging
dc.creator.none.fl_str_mv Navarro, Ana
Bández, Manuel J.
López Cepero, José M.
Gómez, Carmen
Boveris, Alejandro D.
Cadenas, Enrique
Boveris, Alberto Antonio
author Navarro, Ana
author_facet Navarro, Ana
Bández, Manuel J.
López Cepero, José M.
Gómez, Carmen
Boveris, Alejandro D.
Cadenas, Enrique
Boveris, Alberto Antonio
author_role author
author2 Bández, Manuel J.
López Cepero, José M.
Gómez, Carmen
Boveris, Alejandro D.
Cadenas, Enrique
Boveris, Alberto Antonio
author2_role author
author
author
author
author
author
dc.subject.none.fl_str_mv Brain Aging
Complex I Syndrome
Hippocampal Aging
Frontal Cortex Aging
Antioxidant Protection
topic Brain Aging
Complex I Syndrome
Hippocampal Aging
Frontal Cortex Aging
Antioxidant Protection
purl_subject.fl_str_mv https://purl.org/becyt/ford/1.6
https://purl.org/becyt/ford/1
dc.description.none.fl_txt_mv Rat aging from 4 to 12 mo was accompanied by hippocampus and frontal cortex mitochondrial dysfunction, with decreases of 23 to 53% in tissue and mitochondrial respiration and in the activities of complexes I and IV and of mitochondrial nitric oxide synthase (mtNOS) (P < 0.02). In aged rats, the two brain areas showed mitochondria with higher content (35–78%) of oxidation products of phospholipids and proteins and with higher (59–95%) rates of O2− and H2O2 production (P < 0.02). Dietary supplementation with vitamin E (2.0 or 5.0 g/kg of food) from 9 to 12 mo of rat age, restored in a dose-dependent manner, the decreases in tissue and mitochondrial respiration (to 90–96%) and complexes I and IV and mtNOS activities (to 86–88%) of the values of 4-mo-old rats (P < 0.02). Vitamin E prevented, by 73–80%, the increases in oxidation products, and by 62–68%, the increases in O2− and H2O2 production (P < 0.05). High resolution histochemistry of cytochrome oxidase in the hippocampal CA1 region showed higher staining in vitamin E-treated rats than in control animals. Aging decreased (19%) hippocampus mitochondrial mass, an effect that was restored by vitamin E. High doses of vitamin E seem to sustain mitochondrial biogenesis in synaptic areas.
Fil: Navarro, Ana. Universidad de Cádiz; España
Fil: Bández, Manuel J.. Universidad de Cádiz; España
Fil: López Cepero, José M.. Universidad de Cádiz; España
Fil: Gómez, Carmen. Universidad de Cádiz; España
Fil: Boveris, Alejandro D.. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica; Argentina
Fil: Cadenas, Enrique. University Of Southern California; Estados Unidos
Fil: Boveris, Alberto Antonio. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
description Rat aging from 4 to 12 mo was accompanied by hippocampus and frontal cortex mitochondrial dysfunction, with decreases of 23 to 53% in tissue and mitochondrial respiration and in the activities of complexes I and IV and of mitochondrial nitric oxide synthase (mtNOS) (P < 0.02). In aged rats, the two brain areas showed mitochondria with higher content (35–78%) of oxidation products of phospholipids and proteins and with higher (59–95%) rates of O2− and H2O2 production (P < 0.02). Dietary supplementation with vitamin E (2.0 or 5.0 g/kg of food) from 9 to 12 mo of rat age, restored in a dose-dependent manner, the decreases in tissue and mitochondrial respiration (to 90–96%) and complexes I and IV and mtNOS activities (to 86–88%) of the values of 4-mo-old rats (P < 0.02). Vitamin E prevented, by 73–80%, the increases in oxidation products, and by 62–68%, the increases in O2− and H2O2 production (P < 0.05). High resolution histochemistry of cytochrome oxidase in the hippocampal CA1 region showed higher staining in vitamin E-treated rats than in control animals. Aging decreased (19%) hippocampus mitochondrial mass, an effect that was restored by vitamin E. High doses of vitamin E seem to sustain mitochondrial biogenesis in synaptic areas.
publishDate 2011
dc.date.none.fl_str_mv 2011-04
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/11336/16327
Navarro, Ana; Bández, Manuel J.; López Cepero, José M.; Gómez, Carmen; Boveris, Alejandro D.; et al.; High doses of vitamin E improve mitochondrial dysfunction in rat hippocampus and frontal cortex upon aging; American Physiological Society; American Journal Of Physiology-regulatory, Integrative And Comparative Physiology; 300; 4; 4-2011; 827-834
0363-6119
url http://hdl.handle.net/11336/16327
identifier_str_mv Navarro, Ana; Bández, Manuel J.; López Cepero, José M.; Gómez, Carmen; Boveris, Alejandro D.; et al.; High doses of vitamin E improve mitochondrial dysfunction in rat hippocampus and frontal cortex upon aging; American Physiological Society; American Journal Of Physiology-regulatory, Integrative And Comparative Physiology; 300; 4; 4-2011; 827-834
0363-6119
dc.language.none.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv info:eu-repo/semantics/altIdentifier/doi/10.1152/ajpregu.00525.2010
info:eu-repo/semantics/altIdentifier/url/http://ajpregu.physiology.org/content/300/4/R827.long
info:eu-repo/semantics/altIdentifier/url/https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3075077/
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 American Physiological Society
publisher.none.fl_str_mv American Physiological Society
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 12.993085

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