Involvement of glutamate and reactive oxygen species in methylmercury neurotoxicity

Detalhes bibliográficos
Autor(a) principal: Aschner,M.
Data de Publicação: 2007
Outros Autores: Syversen,T., Souza,D.O., Rocha,J.B.T., Farina,M.
Tipo de documento: Artigo
Idioma: eng
Título da fonte: Brazilian Journal of Medical and Biological Research
Texto Completo: http://old.scielo.br/scielo.php?script=sci_arttext&pid=S0100-879X2007000300001
Resumo: This review addresses the mechanisms of methylmercury (MeHg)-induced neurotoxicity, specifically examining the role of oxidative stress in mediating neuronal damage. A number of critical findings point to a central role for astrocytes in mediating MeHg-induced neurotoxicity as evidenced by the following observations: a) MeHg preferentially accumulates in astrocytes; b) MeHg specifically inhibits glutamate uptake in astrocytes; c) neuronal dysfunction is secondary to disturbances in astrocytes. The generation of reactive oxygen species (ROS) by MeHg has been observed in various experimental paradigms. For example, MeHg enhances ROS formation both in vivo (rodent cerebellum) and in vitro (isolated rat brain synaptosomes), as well as in neuronal and mixed reaggregating cell cultures. Antioxidants, including selenocompounds, can rescue astrocytes from MeHg-induced cytotoxicity by reducing ROS formation. We emphasize that oxidative stress plays a significant role in mediating MeHg-induced neurotoxic damage with active involvement of the mitochondria in this process. Furthermore, we provide a mechanistic overview on oxidative stress induced by MeHg that is triggered by a series of molecular events such as activation of various kinases, stress proteins and other immediate early genes culminating in cell damage.
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spelling Involvement of glutamate and reactive oxygen species in methylmercury neurotoxicityMethylmercury neurotoxicityOxidative stressGlutamate and selenocompoundsReactive oxygen speciesAstrocytesThis review addresses the mechanisms of methylmercury (MeHg)-induced neurotoxicity, specifically examining the role of oxidative stress in mediating neuronal damage. A number of critical findings point to a central role for astrocytes in mediating MeHg-induced neurotoxicity as evidenced by the following observations: a) MeHg preferentially accumulates in astrocytes; b) MeHg specifically inhibits glutamate uptake in astrocytes; c) neuronal dysfunction is secondary to disturbances in astrocytes. The generation of reactive oxygen species (ROS) by MeHg has been observed in various experimental paradigms. For example, MeHg enhances ROS formation both in vivo (rodent cerebellum) and in vitro (isolated rat brain synaptosomes), as well as in neuronal and mixed reaggregating cell cultures. Antioxidants, including selenocompounds, can rescue astrocytes from MeHg-induced cytotoxicity by reducing ROS formation. We emphasize that oxidative stress plays a significant role in mediating MeHg-induced neurotoxic damage with active involvement of the mitochondria in this process. Furthermore, we provide a mechanistic overview on oxidative stress induced by MeHg that is triggered by a series of molecular events such as activation of various kinases, stress proteins and other immediate early genes culminating in cell damage.Associação Brasileira de Divulgação Científica2007-03-01info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersiontext/htmlhttp://old.scielo.br/scielo.php?script=sci_arttext&pid=S0100-879X2007000300001Brazilian Journal of Medical and Biological Research v.40 n.3 2007reponame:Brazilian Journal of Medical and Biological Researchinstname:Associação Brasileira de Divulgação Científica (ABDC)instacron:ABDC10.1590/S0100-879X2007000300001info:eu-repo/semantics/openAccessAschner,M.Syversen,T.Souza,D.O.Rocha,J.B.T.Farina,M.eng2008-02-12T00:00:00Zoai:scielo:S0100-879X2007000300001Revistahttps://www.bjournal.org/https://old.scielo.br/oai/scielo-oai.phpbjournal@terra.com.br||bjournal@terra.com.br1414-431X0100-879Xopendoar:2008-02-12T00:00Brazilian Journal of Medical and Biological Research - Associação Brasileira de Divulgação Científica (ABDC)false
dc.title.none.fl_str_mv Involvement of glutamate and reactive oxygen species in methylmercury neurotoxicity
title Involvement of glutamate and reactive oxygen species in methylmercury neurotoxicity
spellingShingle Involvement of glutamate and reactive oxygen species in methylmercury neurotoxicity
Aschner,M.
Methylmercury neurotoxicity
Oxidative stress
Glutamate and selenocompounds
Reactive oxygen species
Astrocytes
title_short Involvement of glutamate and reactive oxygen species in methylmercury neurotoxicity
title_full Involvement of glutamate and reactive oxygen species in methylmercury neurotoxicity
title_fullStr Involvement of glutamate and reactive oxygen species in methylmercury neurotoxicity
title_full_unstemmed Involvement of glutamate and reactive oxygen species in methylmercury neurotoxicity
title_sort Involvement of glutamate and reactive oxygen species in methylmercury neurotoxicity
author Aschner,M.
author_facet Aschner,M.
Syversen,T.
Souza,D.O.
Rocha,J.B.T.
Farina,M.
author_role author
author2 Syversen,T.
Souza,D.O.
Rocha,J.B.T.
Farina,M.
author2_role author
author
author
author
dc.contributor.author.fl_str_mv Aschner,M.
Syversen,T.
Souza,D.O.
Rocha,J.B.T.
Farina,M.
dc.subject.por.fl_str_mv Methylmercury neurotoxicity
Oxidative stress
Glutamate and selenocompounds
Reactive oxygen species
Astrocytes
topic Methylmercury neurotoxicity
Oxidative stress
Glutamate and selenocompounds
Reactive oxygen species
Astrocytes
description This review addresses the mechanisms of methylmercury (MeHg)-induced neurotoxicity, specifically examining the role of oxidative stress in mediating neuronal damage. A number of critical findings point to a central role for astrocytes in mediating MeHg-induced neurotoxicity as evidenced by the following observations: a) MeHg preferentially accumulates in astrocytes; b) MeHg specifically inhibits glutamate uptake in astrocytes; c) neuronal dysfunction is secondary to disturbances in astrocytes. The generation of reactive oxygen species (ROS) by MeHg has been observed in various experimental paradigms. For example, MeHg enhances ROS formation both in vivo (rodent cerebellum) and in vitro (isolated rat brain synaptosomes), as well as in neuronal and mixed reaggregating cell cultures. Antioxidants, including selenocompounds, can rescue astrocytes from MeHg-induced cytotoxicity by reducing ROS formation. We emphasize that oxidative stress plays a significant role in mediating MeHg-induced neurotoxic damage with active involvement of the mitochondria in this process. Furthermore, we provide a mechanistic overview on oxidative stress induced by MeHg that is triggered by a series of molecular events such as activation of various kinases, stress proteins and other immediate early genes culminating in cell damage.
publishDate 2007
dc.date.none.fl_str_mv 2007-03-01
dc.type.driver.fl_str_mv info:eu-repo/semantics/article
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dc.identifier.uri.fl_str_mv http://old.scielo.br/scielo.php?script=sci_arttext&pid=S0100-879X2007000300001
url http://old.scielo.br/scielo.php?script=sci_arttext&pid=S0100-879X2007000300001
dc.language.iso.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv 10.1590/S0100-879X2007000300001
dc.rights.driver.fl_str_mv info:eu-repo/semantics/openAccess
eu_rights_str_mv openAccess
dc.format.none.fl_str_mv text/html
dc.publisher.none.fl_str_mv Associação Brasileira de Divulgação Científica
publisher.none.fl_str_mv Associação Brasileira de Divulgação Científica
dc.source.none.fl_str_mv Brazilian Journal of Medical and Biological Research v.40 n.3 2007
reponame:Brazilian Journal of Medical and Biological Research
instname:Associação Brasileira de Divulgação Científica (ABDC)
instacron:ABDC
instname_str Associação Brasileira de Divulgação Científica (ABDC)
instacron_str ABDC
institution ABDC
reponame_str Brazilian Journal of Medical and Biological Research
collection Brazilian Journal of Medical and Biological Research
repository.name.fl_str_mv Brazilian Journal of Medical and Biological Research - Associação Brasileira de Divulgação Científica (ABDC)
repository.mail.fl_str_mv bjournal@terra.com.br||bjournal@terra.com.br
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