Melatonin in mitochondrial dysfunction and related disorders
- Autores
- Srinivasan, Venkatramanujam; Spence, David Warren; Pandi Perumal, Seithikurippu R.; Brown, Gregory M.; Cardinali, Daniel Pedro
- Año de publicación
- 2011
- Idioma
- inglés
- Tipo de recurso
- artículo
- Estado
- versión publicada
- Descripción
- Mitochondrial dysfunction is considered one of the major causative factors in the aging process, ischemia/reperfusion (I/R), septic shock, and neurodegenerative disorders like Parkinson's disease (PD), Alzheimer's disease (AD), and Huntington's disease (HD). Increased free radical generation, enhanced mitochondrial inducible nitric oxide (NO) synthase activity, enhanced NO production, decreased respiratory complex activity, impaired electron transport system, and opening of mitochondrial permeability transition pore all have been suggested as factors responsible for impaired mitochondrial function. Melatonin, the major hormone of the pineal gland, also acts as an antioxidant and as a regulator of mitochondrial bioenergetic function. Both in vitro and in vivo, melatonin was effective for preventing oxidative stress/nitrosative stress-induced mitochondrial dysfunction seen in experimental models of PD, AD, and HD. In addition, melatonin is known to retard aging and to inhibit the lethal effects of septic shock or I/R lesions by maintaining respiratory complex activities, electron transport chain, and ATP production in mitochondria. Melatonin is selectively taken up by mitochondrial membranes, a function not shared by other antioxidants. Melatonin has thus emerged as a major potential therapeutic tool for treating neurodegenerative disorders such as PD or AD, and for preventing the lethal effects of septic shock or I/R.
Fil: Srinivasan, Venkatramanujam. No especifíca;
Fil: Spence, David Warren. No especifíca;
Fil: Pandi Perumal, Seithikurippu R.. No especifíca;
Fil: Brown, Gregory M.. No especifíca;
Fil: Cardinali, Daniel Pedro. Universidad de Buenos Aires; Argentina. Pontificia Universidad Católica Argentina "Santa María de los Buenos Aires"; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina - Materia
-
MITOCHONDRIAL DYSFUNCTION
AGING
ALZHEIMER´S DISEASE
MELATONIN - Nivel de accesibilidad
- acceso abierto
- Condiciones de uso
- https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
- Repositorio
- Institución
- Consejo Nacional de Investigaciones Científicas y Técnicas
- OAI Identificador
- oai:ri.conicet.gov.ar:11336/192058
Ver los metadatos del registro completo
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Melatonin in mitochondrial dysfunction and related disordersSrinivasan, VenkatramanujamSpence, David WarrenPandi Perumal, Seithikurippu R.Brown, Gregory M.Cardinali, Daniel PedroMITOCHONDRIAL DYSFUNCTIONAGINGALZHEIMER´S DISEASEMELATONINhttps://purl.org/becyt/ford/3.1https://purl.org/becyt/ford/3Mitochondrial dysfunction is considered one of the major causative factors in the aging process, ischemia/reperfusion (I/R), septic shock, and neurodegenerative disorders like Parkinson's disease (PD), Alzheimer's disease (AD), and Huntington's disease (HD). Increased free radical generation, enhanced mitochondrial inducible nitric oxide (NO) synthase activity, enhanced NO production, decreased respiratory complex activity, impaired electron transport system, and opening of mitochondrial permeability transition pore all have been suggested as factors responsible for impaired mitochondrial function. Melatonin, the major hormone of the pineal gland, also acts as an antioxidant and as a regulator of mitochondrial bioenergetic function. Both in vitro and in vivo, melatonin was effective for preventing oxidative stress/nitrosative stress-induced mitochondrial dysfunction seen in experimental models of PD, AD, and HD. In addition, melatonin is known to retard aging and to inhibit the lethal effects of septic shock or I/R lesions by maintaining respiratory complex activities, electron transport chain, and ATP production in mitochondria. Melatonin is selectively taken up by mitochondrial membranes, a function not shared by other antioxidants. Melatonin has thus emerged as a major potential therapeutic tool for treating neurodegenerative disorders such as PD or AD, and for preventing the lethal effects of septic shock or I/R.Fil: Srinivasan, Venkatramanujam. No especifíca;Fil: Spence, David Warren. No especifíca;Fil: Pandi Perumal, Seithikurippu R.. No especifíca;Fil: Brown, Gregory M.. No especifíca;Fil: Cardinali, Daniel Pedro. Universidad de Buenos Aires; Argentina. Pontificia Universidad Católica Argentina "Santa María de los Buenos Aires"; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaHindawi Publishing Corporation2011-03info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/192058Srinivasan, Venkatramanujam; Spence, David Warren; Pandi Perumal, Seithikurippu R.; Brown, Gregory M.; Cardinali, Daniel Pedro; Melatonin in mitochondrial dysfunction and related disorders; Hindawi Publishing Corporation; International Journal of Alzheimer's Disease; 2011; 3-2011; 1-162090-0252CONICET DigitalCONICETenginfo:eu-repo/semantics/altIdentifier/doi/10.4061/2011/326320info:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-sa/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-09-10T13:02:42Zoai:ri.conicet.gov.ar:11336/192058instacron: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 13:02:42.961CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse |
dc.title.none.fl_str_mv |
Melatonin in mitochondrial dysfunction and related disorders |
title |
Melatonin in mitochondrial dysfunction and related disorders |
spellingShingle |
Melatonin in mitochondrial dysfunction and related disorders Srinivasan, Venkatramanujam MITOCHONDRIAL DYSFUNCTION AGING ALZHEIMER´S DISEASE MELATONIN |
title_short |
Melatonin in mitochondrial dysfunction and related disorders |
title_full |
Melatonin in mitochondrial dysfunction and related disorders |
title_fullStr |
Melatonin in mitochondrial dysfunction and related disorders |
title_full_unstemmed |
Melatonin in mitochondrial dysfunction and related disorders |
title_sort |
Melatonin in mitochondrial dysfunction and related disorders |
dc.creator.none.fl_str_mv |
Srinivasan, Venkatramanujam Spence, David Warren Pandi Perumal, Seithikurippu R. Brown, Gregory M. Cardinali, Daniel Pedro |
author |
Srinivasan, Venkatramanujam |
author_facet |
Srinivasan, Venkatramanujam Spence, David Warren Pandi Perumal, Seithikurippu R. Brown, Gregory M. Cardinali, Daniel Pedro |
author_role |
author |
author2 |
Spence, David Warren Pandi Perumal, Seithikurippu R. Brown, Gregory M. Cardinali, Daniel Pedro |
author2_role |
author author author author |
dc.subject.none.fl_str_mv |
MITOCHONDRIAL DYSFUNCTION AGING ALZHEIMER´S DISEASE MELATONIN |
topic |
MITOCHONDRIAL DYSFUNCTION AGING ALZHEIMER´S DISEASE MELATONIN |
purl_subject.fl_str_mv |
https://purl.org/becyt/ford/3.1 https://purl.org/becyt/ford/3 |
dc.description.none.fl_txt_mv |
Mitochondrial dysfunction is considered one of the major causative factors in the aging process, ischemia/reperfusion (I/R), septic shock, and neurodegenerative disorders like Parkinson's disease (PD), Alzheimer's disease (AD), and Huntington's disease (HD). Increased free radical generation, enhanced mitochondrial inducible nitric oxide (NO) synthase activity, enhanced NO production, decreased respiratory complex activity, impaired electron transport system, and opening of mitochondrial permeability transition pore all have been suggested as factors responsible for impaired mitochondrial function. Melatonin, the major hormone of the pineal gland, also acts as an antioxidant and as a regulator of mitochondrial bioenergetic function. Both in vitro and in vivo, melatonin was effective for preventing oxidative stress/nitrosative stress-induced mitochondrial dysfunction seen in experimental models of PD, AD, and HD. In addition, melatonin is known to retard aging and to inhibit the lethal effects of septic shock or I/R lesions by maintaining respiratory complex activities, electron transport chain, and ATP production in mitochondria. Melatonin is selectively taken up by mitochondrial membranes, a function not shared by other antioxidants. Melatonin has thus emerged as a major potential therapeutic tool for treating neurodegenerative disorders such as PD or AD, and for preventing the lethal effects of septic shock or I/R. Fil: Srinivasan, Venkatramanujam. No especifíca; Fil: Spence, David Warren. No especifíca; Fil: Pandi Perumal, Seithikurippu R.. No especifíca; Fil: Brown, Gregory M.. No especifíca; Fil: Cardinali, Daniel Pedro. Universidad de Buenos Aires; Argentina. Pontificia Universidad Católica Argentina "Santa María de los Buenos Aires"; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina |
description |
Mitochondrial dysfunction is considered one of the major causative factors in the aging process, ischemia/reperfusion (I/R), septic shock, and neurodegenerative disorders like Parkinson's disease (PD), Alzheimer's disease (AD), and Huntington's disease (HD). Increased free radical generation, enhanced mitochondrial inducible nitric oxide (NO) synthase activity, enhanced NO production, decreased respiratory complex activity, impaired electron transport system, and opening of mitochondrial permeability transition pore all have been suggested as factors responsible for impaired mitochondrial function. Melatonin, the major hormone of the pineal gland, also acts as an antioxidant and as a regulator of mitochondrial bioenergetic function. Both in vitro and in vivo, melatonin was effective for preventing oxidative stress/nitrosative stress-induced mitochondrial dysfunction seen in experimental models of PD, AD, and HD. In addition, melatonin is known to retard aging and to inhibit the lethal effects of septic shock or I/R lesions by maintaining respiratory complex activities, electron transport chain, and ATP production in mitochondria. Melatonin is selectively taken up by mitochondrial membranes, a function not shared by other antioxidants. Melatonin has thus emerged as a major potential therapeutic tool for treating neurodegenerative disorders such as PD or AD, and for preventing the lethal effects of septic shock or I/R. |
publishDate |
2011 |
dc.date.none.fl_str_mv |
2011-03 |
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/11336/192058 Srinivasan, Venkatramanujam; Spence, David Warren; Pandi Perumal, Seithikurippu R.; Brown, Gregory M.; Cardinali, Daniel Pedro; Melatonin in mitochondrial dysfunction and related disorders; Hindawi Publishing Corporation; International Journal of Alzheimer's Disease; 2011; 3-2011; 1-16 2090-0252 CONICET Digital CONICET |
url |
http://hdl.handle.net/11336/192058 |
identifier_str_mv |
Srinivasan, Venkatramanujam; Spence, David Warren; Pandi Perumal, Seithikurippu R.; Brown, Gregory M.; Cardinali, Daniel Pedro; Melatonin in mitochondrial dysfunction and related disorders; Hindawi Publishing Corporation; International Journal of Alzheimer's Disease; 2011; 3-2011; 1-16 2090-0252 CONICET Digital CONICET |
dc.language.none.fl_str_mv |
eng |
language |
eng |
dc.relation.none.fl_str_mv |
info:eu-repo/semantics/altIdentifier/doi/10.4061/2011/326320 |
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 |
Hindawi Publishing Corporation |
publisher.none.fl_str_mv |
Hindawi Publishing Corporation |
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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1842980034559606784 |
score |
12.993085 |