Melatonin and mitochondrial dysfunction in the central nervous system

Autores
Cardinali, Daniel Pedro; Pagano, Eleonora S.; Scacchi Bernasconi, Pablo A.; Reynoso, Roxana; Scacchi, Pablo
Año de publicación
2012
Idioma
inglés
Tipo de recurso
artículo
Estado
versión enviada
Descripción
Fil: Cardinali, Daniel P. Pontificia Universidad Católica Argentina. Facultad de Ciencias Médicas; Argentina
Fil: Pagano, Eleonora S. Pontificia Universidad Católica Argentina. Facultad de Ciencias Médicas; Argentina
Fil: Scacchi Bernasconi, Pablo A. Pontificia Universidad Católica Argentina. Facultad de Ciencias Médicas; Argentina
Fil: Reynoso, Roxana. Pontificia Universidad Católica Argentina. Facultad de Ciencias Médicas; Argentina
Fil: Scacchi, Pablo. Pontificia Universidad Católica Argentina. Facultad de Ciencias Médicas; Argentina
Abstract: Cell death and survival are critical events for neurodegeneration, mitochondria being increasingly seen as important determinants of both. Mitochondrial dysfunction is considered a major causative factor in Alzheimer’s disease (AD), Parkinson’s disease (PD) and Huntington’s disease (HD). Increased free radical generation, enhanced mitochondrial inducible nitric oxide (NO) synthase activity and NO production, and disrupted electron transport system and mitochondrial permeability transition, have all been involved in impaired mitochondrial function. Melatonin, the major secretory product of the pineal gland, is an antioxidant and an effective protector of mitochondrial bioenergetic function. Both in vitro and in vivo, melatonin was effective to prevent oxidative stress/nitrosative stress-induced mitochondrial dysfunction seen in experimental models of AD, PD and HD. These effects are seen at doses 2-3 orders of magnitude higher than those required to affect sleep and circadian rhythms, both conspicuous targets of melatonin action. Melatonin is selectively taken up by mitochondria, a function not shared by other antioxidants. A limited number of clinical studies indicate that melatonin can improve sleep and circadian rhythm disruption in PD and AD patients. More recently, attention has been focused on the development of potent melatonin analogs with prolonged effects which were employed in clinical trials in sleep-disturbed or depressed patients in doses considerably higher than those employed for melatonin. In view that the relative potencies of the analogs are higher than that of the natural compound, clinical trials employing melatonin in the range of 50-100 mg/day are needed to assess its therapeutic validity in neurodegenerative disorders.
Fuente
Hormones and Behavior. 2013, 63 (2)
Materia
MELATONINA
MITOCONDRIAS
SISTEMA NERVIOSO CENTRAL
RADICALES LIBRES
ENVEJECIMIENTO
STRESS
ENFERMEDAD DE ALZHEIMER
ENFERMEDAD DE HUNTINGTON
ENFERMEDAD DE PARKINSON
Nivel de accesibilidad
acceso abierto
Condiciones de uso
https://creativecommons.org/licenses/by-nc-sa/4.0/
Repositorio
Repositorio Institucional (UCA)
Institución
Pontificia Universidad Católica Argentina
OAI Identificador
oai:ucacris:123456789/1632

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oai_identifier_str oai:ucacris:123456789/1632
network_acronym_str RIUCA
repository_id_str 2585
network_name_str Repositorio Institucional (UCA)
spelling Melatonin and mitochondrial dysfunction in the central nervous systemCardinali, Daniel PedroPagano, Eleonora S.Scacchi Bernasconi, Pablo A.Reynoso, RoxanaScacchi, PabloMELATONINAMITOCONDRIASSISTEMA NERVIOSO CENTRALRADICALES LIBRESENVEJECIMIENTOSTRESSENFERMEDAD DE ALZHEIMERENFERMEDAD DE HUNTINGTONENFERMEDAD DE PARKINSONFil: Cardinali, Daniel P. Pontificia Universidad Católica Argentina. Facultad de Ciencias Médicas; ArgentinaFil: Pagano, Eleonora S. Pontificia Universidad Católica Argentina. Facultad de Ciencias Médicas; ArgentinaFil: Scacchi Bernasconi, Pablo A. Pontificia Universidad Católica Argentina. Facultad de Ciencias Médicas; ArgentinaFil: Reynoso, Roxana. Pontificia Universidad Católica Argentina. Facultad de Ciencias Médicas; ArgentinaFil: Scacchi, Pablo. Pontificia Universidad Católica Argentina. Facultad de Ciencias Médicas; ArgentinaAbstract: Cell death and survival are critical events for neurodegeneration, mitochondria being increasingly seen as important determinants of both. Mitochondrial dysfunction is considered a major causative factor in Alzheimer’s disease (AD), Parkinson’s disease (PD) and Huntington’s disease (HD). Increased free radical generation, enhanced mitochondrial inducible nitric oxide (NO) synthase activity and NO production, and disrupted electron transport system and mitochondrial permeability transition, have all been involved in impaired mitochondrial function. Melatonin, the major secretory product of the pineal gland, is an antioxidant and an effective protector of mitochondrial bioenergetic function. Both in vitro and in vivo, melatonin was effective to prevent oxidative stress/nitrosative stress-induced mitochondrial dysfunction seen in experimental models of AD, PD and HD. These effects are seen at doses 2-3 orders of magnitude higher than those required to affect sleep and circadian rhythms, both conspicuous targets of melatonin action. Melatonin is selectively taken up by mitochondria, a function not shared by other antioxidants. A limited number of clinical studies indicate that melatonin can improve sleep and circadian rhythm disruption in PD and AD patients. More recently, attention has been focused on the development of potent melatonin analogs with prolonged effects which were employed in clinical trials in sleep-disturbed or depressed patients in doses considerably higher than those employed for melatonin. In view that the relative potencies of the analogs are higher than that of the natural compound, clinical trials employing melatonin in the range of 50-100 mg/day are needed to assess its therapeutic validity in neurodegenerative disorders.Elsevier2012info:eu-repo/semantics/articleinfo:eu-repo/semantics/submittedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfhttps://repositorio.uca.edu.ar/handle/123456789/16320018-506X10.1016/j.yhbeh.2012.02.020Cardinali D. P., et al. Melatonin and mitochondrial dysfunction in the central nervous system [en línea]. Hormones and Behavior. 2013, 63 (2). doi:10.1016/j.yhbeh.2012.02.020. Disponible en: https://repositorio.uca.edu.ar/handle/123456789/1632Hormones and Behavior. 2013, 63 (2)reponame:Repositorio Institucional (UCA)instname:Pontificia Universidad Católica Argentinaengenginfo:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-sa/4.0/2025-07-03T10:55:19Zoai:ucacris:123456789/1632instacron:UCAInstitucionalhttps://repositorio.uca.edu.ar/Universidad privadaNo correspondehttps://repositorio.uca.edu.ar/oaiclaudia_fernandez@uca.edu.arArgentinaNo correspondeNo correspondeNo correspondeopendoar:25852025-07-03 10:55:20.024Repositorio Institucional (UCA) - Pontificia Universidad Católica Argentinafalse
dc.title.none.fl_str_mv Melatonin and mitochondrial dysfunction in the central nervous system
title Melatonin and mitochondrial dysfunction in the central nervous system
spellingShingle Melatonin and mitochondrial dysfunction in the central nervous system
Cardinali, Daniel Pedro
MELATONINA
MITOCONDRIAS
SISTEMA NERVIOSO CENTRAL
RADICALES LIBRES
ENVEJECIMIENTO
STRESS
ENFERMEDAD DE ALZHEIMER
ENFERMEDAD DE HUNTINGTON
ENFERMEDAD DE PARKINSON
title_short Melatonin and mitochondrial dysfunction in the central nervous system
title_full Melatonin and mitochondrial dysfunction in the central nervous system
title_fullStr Melatonin and mitochondrial dysfunction in the central nervous system
title_full_unstemmed Melatonin and mitochondrial dysfunction in the central nervous system
title_sort Melatonin and mitochondrial dysfunction in the central nervous system
dc.creator.none.fl_str_mv Cardinali, Daniel Pedro
Pagano, Eleonora S.
Scacchi Bernasconi, Pablo A.
Reynoso, Roxana
Scacchi, Pablo
author Cardinali, Daniel Pedro
author_facet Cardinali, Daniel Pedro
Pagano, Eleonora S.
Scacchi Bernasconi, Pablo A.
Reynoso, Roxana
Scacchi, Pablo
author_role author
author2 Pagano, Eleonora S.
Scacchi Bernasconi, Pablo A.
Reynoso, Roxana
Scacchi, Pablo
author2_role author
author
author
author
dc.subject.none.fl_str_mv MELATONINA
MITOCONDRIAS
SISTEMA NERVIOSO CENTRAL
RADICALES LIBRES
ENVEJECIMIENTO
STRESS
ENFERMEDAD DE ALZHEIMER
ENFERMEDAD DE HUNTINGTON
ENFERMEDAD DE PARKINSON
topic MELATONINA
MITOCONDRIAS
SISTEMA NERVIOSO CENTRAL
RADICALES LIBRES
ENVEJECIMIENTO
STRESS
ENFERMEDAD DE ALZHEIMER
ENFERMEDAD DE HUNTINGTON
ENFERMEDAD DE PARKINSON
dc.description.none.fl_txt_mv Fil: Cardinali, Daniel P. Pontificia Universidad Católica Argentina. Facultad de Ciencias Médicas; Argentina
Fil: Pagano, Eleonora S. Pontificia Universidad Católica Argentina. Facultad de Ciencias Médicas; Argentina
Fil: Scacchi Bernasconi, Pablo A. Pontificia Universidad Católica Argentina. Facultad de Ciencias Médicas; Argentina
Fil: Reynoso, Roxana. Pontificia Universidad Católica Argentina. Facultad de Ciencias Médicas; Argentina
Fil: Scacchi, Pablo. Pontificia Universidad Católica Argentina. Facultad de Ciencias Médicas; Argentina
Abstract: Cell death and survival are critical events for neurodegeneration, mitochondria being increasingly seen as important determinants of both. Mitochondrial dysfunction is considered a major causative factor in Alzheimer’s disease (AD), Parkinson’s disease (PD) and Huntington’s disease (HD). Increased free radical generation, enhanced mitochondrial inducible nitric oxide (NO) synthase activity and NO production, and disrupted electron transport system and mitochondrial permeability transition, have all been involved in impaired mitochondrial function. Melatonin, the major secretory product of the pineal gland, is an antioxidant and an effective protector of mitochondrial bioenergetic function. Both in vitro and in vivo, melatonin was effective to prevent oxidative stress/nitrosative stress-induced mitochondrial dysfunction seen in experimental models of AD, PD and HD. These effects are seen at doses 2-3 orders of magnitude higher than those required to affect sleep and circadian rhythms, both conspicuous targets of melatonin action. Melatonin is selectively taken up by mitochondria, a function not shared by other antioxidants. A limited number of clinical studies indicate that melatonin can improve sleep and circadian rhythm disruption in PD and AD patients. More recently, attention has been focused on the development of potent melatonin analogs with prolonged effects which were employed in clinical trials in sleep-disturbed or depressed patients in doses considerably higher than those employed for melatonin. In view that the relative potencies of the analogs are higher than that of the natural compound, clinical trials employing melatonin in the range of 50-100 mg/day are needed to assess its therapeutic validity in neurodegenerative disorders.
description Fil: Cardinali, Daniel P. Pontificia Universidad Católica Argentina. Facultad de Ciencias Médicas; Argentina
publishDate 2012
dc.date.none.fl_str_mv 2012
dc.type.none.fl_str_mv info:eu-repo/semantics/article
info:eu-repo/semantics/submittedVersion
http://purl.org/coar/resource_type/c_6501
info:ar-repo/semantics/articulo
format article
status_str submittedVersion
dc.identifier.none.fl_str_mv https://repositorio.uca.edu.ar/handle/123456789/1632
0018-506X
10.1016/j.yhbeh.2012.02.020
Cardinali D. P., et al. Melatonin and mitochondrial dysfunction in the central nervous system [en línea]. Hormones and Behavior. 2013, 63 (2). doi:10.1016/j.yhbeh.2012.02.020. Disponible en: https://repositorio.uca.edu.ar/handle/123456789/1632
url https://repositorio.uca.edu.ar/handle/123456789/1632
identifier_str_mv 0018-506X
10.1016/j.yhbeh.2012.02.020
Cardinali D. P., et al. Melatonin and mitochondrial dysfunction in the central nervous system [en línea]. Hormones and Behavior. 2013, 63 (2). doi:10.1016/j.yhbeh.2012.02.020. Disponible en: https://repositorio.uca.edu.ar/handle/123456789/1632
dc.language.none.fl_str_mv eng
eng
language eng
dc.rights.none.fl_str_mv info:eu-repo/semantics/openAccess
https://creativecommons.org/licenses/by-nc-sa/4.0/
eu_rights_str_mv openAccess
rights_invalid_str_mv https://creativecommons.org/licenses/by-nc-sa/4.0/
dc.format.none.fl_str_mv application/pdf
dc.publisher.none.fl_str_mv Elsevier
publisher.none.fl_str_mv Elsevier
dc.source.none.fl_str_mv Hormones and Behavior. 2013, 63 (2)
reponame:Repositorio Institucional (UCA)
instname:Pontificia Universidad Católica Argentina
reponame_str Repositorio Institucional (UCA)
collection Repositorio Institucional (UCA)
instname_str Pontificia Universidad Católica Argentina
repository.name.fl_str_mv Repositorio Institucional (UCA) - Pontificia Universidad Católica Argentina
repository.mail.fl_str_mv claudia_fernandez@uca.edu.ar
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score 13.13397