Diphenyl diselenide administration enhances cortical mitochondrial number and activity by increasing hemeoxygenase type 1 content in a methylmercury-induced neurotoxicity mouse mod...

Autores: Glaser, Viviane; de Paula Martins, Roberta; Hoffmann Vieira, Ana Julia; de Medeiros Oliveira, Eliana; Straliotto, Marcos Raniel; Mukdsi, Jorge Humberto; Torres, Alicia Ines; Fabro de Bem, Andreza; Farina, Marcelo; Teixeira da Rocha, Joao Batista; de Paul, Ana Lucia; Latini, Alexandra
Año de publicación: 2014
Idioma: inglés
Tipo de recurso: artículo
Estado: versión publicada
Descripción: Interest in biochemistry of organoselenium compound has increased in the last decades, mainly due to their chemical and biological activities. Here, we investigated the protective effect of diphenyl diselenide (PhSe)2 (5 μmol/kg), in a mouse model of methylmercury (MeHg)-induced brain toxicity. Swiss male mice were divided into four experimental groups: control, (PhSe)2 (5 μmol/kg, subcutaneous administration), MeHg (40 mg/L, in tap water), and MeHg + (PhSe)2. After the treatment (21 days), the animals were killed and the cerebral cortex was analyzed. Electron microscopy indicated an enlarged and fused mitochondria leading to a reduced number of organelles, in the MeHg-exposed mice. Furthermore, cortical creatine kinase activity, a sensitive mitochondrial oxidative stress sensor, was almost abolished by MeHg. Subcutaneous (PhSe)2 co-treatment rescued from MeHg-induced mitochondrial alterations. (PhSe)2 also behaved as an enhancer of mitochondrial biogenesis, by increasing cortical mitochondria content in mouse-receiving (PhSe)2 alone. Mechanistically, (PhSe)2 (1 μM; 24 h) would trigger the cytoprotective Nrf-2 pathway for activating target genes, since astroglial cells exposed to the chalcogen showed increased content of hemeoxygenase type 1, a sensitive marker of the activation of this via. Thus, it is proposed that the (PhSe)2-neuroprotective effect might be linked to its mitoprotective activity.
Fil: Glaser, Viviane. Universidade Federal de Santa Catarina; Brasil
Fil: de Paula Martins, Roberta. Universidade Federal de Santa Catarina; Brasil
Fil: Hoffmann Vieira, Ana Julia. Universidade Federal de Santa Catarina; Brasil
Fil: de Medeiros Oliveira, Eliana. Universidade Federal de Santa Catarina; Brasil
Fil: Straliotto, Marcos Raniel. Universidade Federal de Santa Catarina; Brasil
Fil: Mukdsi, Jorge Humberto. Universidad Nacional de Córdoba. Facultad de Medicina. Centro de Microscopia Electronica; Argentina
Fil: Torres, Alicia Ines. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Universidad Nacional de Córdoba. Facultad de Medicina. Centro de Microscopia Electronica; Argentina
Fil: Fabro de Bem, Andreza. Universidade Federal de Santa Catarina; Brasil
Fil: Farina, Marcelo. Universidade Federal de Santa Catarina; Brasil
Fil: Teixeira da Rocha, Joao Batista. Universidade Federal de Santa Maria. Santa Maria; Brasil
Fil: de Paul, Ana Lucia. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Universidad Nacional de Córdoba. Facultad de Medicina. Centro de Microscopia Electronica; Argentina
Fil: Latini, Alexandra. Universidade Federal de Santa Catarina; Brasil
Materia: Diphenyl Diselenide
Methylmercury
Mitochondrial Morphology
Creatine Kinase
Hemeoxygenase Type 1
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:11336/33427

Acceder

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repository_id_str	3498
network_name_str	CONICET Digital (CONICET)
spelling	Diphenyl diselenide administration enhances cortical mitochondrial number and activity by increasing hemeoxygenase type 1 content in a methylmercury-induced neurotoxicity mouse modelGlaser, Vivianede Paula Martins, RobertaHoffmann Vieira, Ana Juliade Medeiros Oliveira, ElianaStraliotto, Marcos RanielMukdsi, Jorge HumbertoTorres, Alicia InesFabro de Bem, AndrezaFarina, MarceloTeixeira da Rocha, Joao Batistade Paul, Ana LuciaLatini, AlexandraDiphenyl DiselenideMethylmercuryMitochondrial MorphologyCreatine KinaseHemeoxygenase Type 1https://purl.org/becyt/ford/3.1https://purl.org/becyt/ford/3Interest in biochemistry of organoselenium compound has increased in the last decades, mainly due to their chemical and biological activities. Here, we investigated the protective effect of diphenyl diselenide (PhSe)2 (5 μmol/kg), in a mouse model of methylmercury (MeHg)-induced brain toxicity. Swiss male mice were divided into four experimental groups: control, (PhSe)2 (5 μmol/kg, subcutaneous administration), MeHg (40 mg/L, in tap water), and MeHg + (PhSe)2. After the treatment (21 days), the animals were killed and the cerebral cortex was analyzed. Electron microscopy indicated an enlarged and fused mitochondria leading to a reduced number of organelles, in the MeHg-exposed mice. Furthermore, cortical creatine kinase activity, a sensitive mitochondrial oxidative stress sensor, was almost abolished by MeHg. Subcutaneous (PhSe)2 co-treatment rescued from MeHg-induced mitochondrial alterations. (PhSe)2 also behaved as an enhancer of mitochondrial biogenesis, by increasing cortical mitochondria content in mouse-receiving (PhSe)2 alone. Mechanistically, (PhSe)2 (1 μM; 24 h) would trigger the cytoprotective Nrf-2 pathway for activating target genes, since astroglial cells exposed to the chalcogen showed increased content of hemeoxygenase type 1, a sensitive marker of the activation of this via. Thus, it is proposed that the (PhSe)2-neuroprotective effect might be linked to its mitoprotective activity.Fil: Glaser, Viviane. Universidade Federal de Santa Catarina; BrasilFil: de Paula Martins, Roberta. Universidade Federal de Santa Catarina; BrasilFil: Hoffmann Vieira, Ana Julia. Universidade Federal de Santa Catarina; BrasilFil: de Medeiros Oliveira, Eliana. Universidade Federal de Santa Catarina; BrasilFil: Straliotto, Marcos Raniel. Universidade Federal de Santa Catarina; BrasilFil: Mukdsi, Jorge Humberto. Universidad Nacional de Córdoba. Facultad de Medicina. Centro de Microscopia Electronica; ArgentinaFil: Torres, Alicia Ines. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Universidad Nacional de Córdoba. Facultad de Medicina. Centro de Microscopia Electronica; ArgentinaFil: Fabro de Bem, Andreza. Universidade Federal de Santa Catarina; BrasilFil: Farina, Marcelo. Universidade Federal de Santa Catarina; BrasilFil: Teixeira da Rocha, Joao Batista. Universidade Federal de Santa Maria. Santa Maria; BrasilFil: de Paul, Ana Lucia. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Universidad Nacional de Córdoba. Facultad de Medicina. Centro de Microscopia Electronica; ArgentinaFil: Latini, Alexandra. Universidade Federal de Santa Catarina; BrasilSpringer2014-03info: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/11336/33427Glaser, Viviane; de Paula Martins, Roberta; Hoffmann Vieira, Ana Julia; de Medeiros Oliveira, Eliana; Straliotto, Marcos Raniel; et al.; Diphenyl diselenide administration enhances cortical mitochondrial number and activity by increasing hemeoxygenase type 1 content in a methylmercury-induced neurotoxicity mouse model; Springer; Molecular and Cellular Biochemistry; 390; 1-2; 3-2014; 1-80300-81771573-4919CONICET DigitalCONICETenginfo:eu-repo/semantics/altIdentifier/doi/10.1007/s11010-013-1870-9info:eu-repo/semantics/altIdentifier/url/https://link.springer.com/article/10.1007%2Fs11010-013-1870-9info:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-sa/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-09-29T10:17:00Zoai:ri.conicet.gov.ar:11336/33427instacron: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:34982025-09-29 10:17:00.917CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse
dc.title.none.fl_str_mv	Diphenyl diselenide administration enhances cortical mitochondrial number and activity by increasing hemeoxygenase type 1 content in a methylmercury-induced neurotoxicity mouse model
title	Diphenyl diselenide administration enhances cortical mitochondrial number and activity by increasing hemeoxygenase type 1 content in a methylmercury-induced neurotoxicity mouse model
spellingShingle	Diphenyl diselenide administration enhances cortical mitochondrial number and activity by increasing hemeoxygenase type 1 content in a methylmercury-induced neurotoxicity mouse model Glaser, Viviane Diphenyl Diselenide Methylmercury Mitochondrial Morphology Creatine Kinase Hemeoxygenase Type 1
title_short	Diphenyl diselenide administration enhances cortical mitochondrial number and activity by increasing hemeoxygenase type 1 content in a methylmercury-induced neurotoxicity mouse model
title_full	Diphenyl diselenide administration enhances cortical mitochondrial number and activity by increasing hemeoxygenase type 1 content in a methylmercury-induced neurotoxicity mouse model
title_fullStr	Diphenyl diselenide administration enhances cortical mitochondrial number and activity by increasing hemeoxygenase type 1 content in a methylmercury-induced neurotoxicity mouse model
title_full_unstemmed	Diphenyl diselenide administration enhances cortical mitochondrial number and activity by increasing hemeoxygenase type 1 content in a methylmercury-induced neurotoxicity mouse model
title_sort	Diphenyl diselenide administration enhances cortical mitochondrial number and activity by increasing hemeoxygenase type 1 content in a methylmercury-induced neurotoxicity mouse model
dc.creator.none.fl_str_mv	Glaser, Viviane de Paula Martins, Roberta Hoffmann Vieira, Ana Julia de Medeiros Oliveira, Eliana Straliotto, Marcos Raniel Mukdsi, Jorge Humberto Torres, Alicia Ines Fabro de Bem, Andreza Farina, Marcelo Teixeira da Rocha, Joao Batista de Paul, Ana Lucia Latini, Alexandra
author	Glaser, Viviane
author_facet	Glaser, Viviane de Paula Martins, Roberta Hoffmann Vieira, Ana Julia de Medeiros Oliveira, Eliana Straliotto, Marcos Raniel Mukdsi, Jorge Humberto Torres, Alicia Ines Fabro de Bem, Andreza Farina, Marcelo Teixeira da Rocha, Joao Batista de Paul, Ana Lucia Latini, Alexandra
author_role	author
author2	de Paula Martins, Roberta Hoffmann Vieira, Ana Julia de Medeiros Oliveira, Eliana Straliotto, Marcos Raniel Mukdsi, Jorge Humberto Torres, Alicia Ines Fabro de Bem, Andreza Farina, Marcelo Teixeira da Rocha, Joao Batista de Paul, Ana Lucia Latini, Alexandra
author2_role	author author author author author author author author author author author
dc.subject.none.fl_str_mv	Diphenyl Diselenide Methylmercury Mitochondrial Morphology Creatine Kinase Hemeoxygenase Type 1
topic	Diphenyl Diselenide Methylmercury Mitochondrial Morphology Creatine Kinase Hemeoxygenase Type 1
purl_subject.fl_str_mv	https://purl.org/becyt/ford/3.1 https://purl.org/becyt/ford/3
dc.description.none.fl_txt_mv	Interest in biochemistry of organoselenium compound has increased in the last decades, mainly due to their chemical and biological activities. Here, we investigated the protective effect of diphenyl diselenide (PhSe)2 (5 μmol/kg), in a mouse model of methylmercury (MeHg)-induced brain toxicity. Swiss male mice were divided into four experimental groups: control, (PhSe)2 (5 μmol/kg, subcutaneous administration), MeHg (40 mg/L, in tap water), and MeHg + (PhSe)2. After the treatment (21 days), the animals were killed and the cerebral cortex was analyzed. Electron microscopy indicated an enlarged and fused mitochondria leading to a reduced number of organelles, in the MeHg-exposed mice. Furthermore, cortical creatine kinase activity, a sensitive mitochondrial oxidative stress sensor, was almost abolished by MeHg. Subcutaneous (PhSe)2 co-treatment rescued from MeHg-induced mitochondrial alterations. (PhSe)2 also behaved as an enhancer of mitochondrial biogenesis, by increasing cortical mitochondria content in mouse-receiving (PhSe)2 alone. Mechanistically, (PhSe)2 (1 μM; 24 h) would trigger the cytoprotective Nrf-2 pathway for activating target genes, since astroglial cells exposed to the chalcogen showed increased content of hemeoxygenase type 1, a sensitive marker of the activation of this via. Thus, it is proposed that the (PhSe)2-neuroprotective effect might be linked to its mitoprotective activity. Fil: Glaser, Viviane. Universidade Federal de Santa Catarina; Brasil Fil: de Paula Martins, Roberta. Universidade Federal de Santa Catarina; Brasil Fil: Hoffmann Vieira, Ana Julia. Universidade Federal de Santa Catarina; Brasil Fil: de Medeiros Oliveira, Eliana. Universidade Federal de Santa Catarina; Brasil Fil: Straliotto, Marcos Raniel. Universidade Federal de Santa Catarina; Brasil Fil: Mukdsi, Jorge Humberto. Universidad Nacional de Córdoba. Facultad de Medicina. Centro de Microscopia Electronica; Argentina Fil: Torres, Alicia Ines. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Universidad Nacional de Córdoba. Facultad de Medicina. Centro de Microscopia Electronica; Argentina Fil: Fabro de Bem, Andreza. Universidade Federal de Santa Catarina; Brasil Fil: Farina, Marcelo. Universidade Federal de Santa Catarina; Brasil Fil: Teixeira da Rocha, Joao Batista. Universidade Federal de Santa Maria. Santa Maria; Brasil Fil: de Paul, Ana Lucia. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Universidad Nacional de Córdoba. Facultad de Medicina. Centro de Microscopia Electronica; Argentina Fil: Latini, Alexandra. Universidade Federal de Santa Catarina; Brasil
description	Interest in biochemistry of organoselenium compound has increased in the last decades, mainly due to their chemical and biological activities. Here, we investigated the protective effect of diphenyl diselenide (PhSe)2 (5 μmol/kg), in a mouse model of methylmercury (MeHg)-induced brain toxicity. Swiss male mice were divided into four experimental groups: control, (PhSe)2 (5 μmol/kg, subcutaneous administration), MeHg (40 mg/L, in tap water), and MeHg + (PhSe)2. After the treatment (21 days), the animals were killed and the cerebral cortex was analyzed. Electron microscopy indicated an enlarged and fused mitochondria leading to a reduced number of organelles, in the MeHg-exposed mice. Furthermore, cortical creatine kinase activity, a sensitive mitochondrial oxidative stress sensor, was almost abolished by MeHg. Subcutaneous (PhSe)2 co-treatment rescued from MeHg-induced mitochondrial alterations. (PhSe)2 also behaved as an enhancer of mitochondrial biogenesis, by increasing cortical mitochondria content in mouse-receiving (PhSe)2 alone. Mechanistically, (PhSe)2 (1 μM; 24 h) would trigger the cytoprotective Nrf-2 pathway for activating target genes, since astroglial cells exposed to the chalcogen showed increased content of hemeoxygenase type 1, a sensitive marker of the activation of this via. Thus, it is proposed that the (PhSe)2-neuroprotective effect might be linked to its mitoprotective activity.
publishDate	2014
dc.date.none.fl_str_mv	2014-03
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/11336/33427 Glaser, Viviane; de Paula Martins, Roberta; Hoffmann Vieira, Ana Julia; de Medeiros Oliveira, Eliana; Straliotto, Marcos Raniel; et al.; Diphenyl diselenide administration enhances cortical mitochondrial number and activity by increasing hemeoxygenase type 1 content in a methylmercury-induced neurotoxicity mouse model; Springer; Molecular and Cellular Biochemistry; 390; 1-2; 3-2014; 1-8 0300-8177 1573-4919 CONICET Digital CONICET
url	http://hdl.handle.net/11336/33427
identifier_str_mv	Glaser, Viviane; de Paula Martins, Roberta; Hoffmann Vieira, Ana Julia; de Medeiros Oliveira, Eliana; Straliotto, Marcos Raniel; et al.; Diphenyl diselenide administration enhances cortical mitochondrial number and activity by increasing hemeoxygenase type 1 content in a methylmercury-induced neurotoxicity mouse model; Springer; Molecular and Cellular Biochemistry; 390; 1-2; 3-2014; 1-8 0300-8177 1573-4919 CONICET Digital CONICET
dc.language.none.fl_str_mv	eng
language	eng
dc.relation.none.fl_str_mv	info:eu-repo/semantics/altIdentifier/doi/10.1007/s11010-013-1870-9 info:eu-repo/semantics/altIdentifier/url/https://link.springer.com/article/10.1007%2Fs11010-013-1870-9
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 application/pdf
dc.publisher.none.fl_str_mv	Springer
publisher.none.fl_str_mv	Springer
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	13.070432

Diphenyl diselenide administration enhances cortical mitochondrial number and activity by increasing hemeoxygenase type 1 content in a methylmercury-induced neurotoxicity mouse mod...

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