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
- Institución
- Pontificia Universidad Católica Argentina
- OAI Identificador
- oai:ucacris:123456789/1632
Ver los metadatos del registro completo
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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 |
_version_ |
1836638330574340096 |
score |
13.13397 |