Diphenyl diselenide dietary supplementation alleviates behavior impairment and brain damage in grass carp (Ctenopharyngodon idella) exposed to methylmercury chloride

Bibliographic Details
Main Author: Baldissera M.D.
Publication Date: 2020
Other Authors: Souza C.F., da Silva A.S.*, Henn A.S., Flores E.M.M., Baldisserotto B.
Format: Article
Language: eng
Source: Repositório Institucional da Udesc
dARK ID: ark:/33523/0013000007t77
Download full: https://repositorio.udesc.br/handle/UDESC/4758
Summary: © 2019 Elsevier Inc.Mercury (Hg) induces neurobehavioral disorders through reactive oxygen species (ROS) elevation and impairment of brain key enzyme activities. Nevertheless, the therapeutic and toxic selenium concentrations for fish are very close; diphenyl diselenide (Ph2Se2), an organoselenium compound with neuroprotective effects, may be an alternative to elemental Se. Therefore, the aim of this study was to determine whether dietary supplementation with Ph2Se2 prevented or reduced the neurobehavioral alterations and oxidative damage elicited by CH3HgCl in grass carp Ctenopharyngodon idella. Fish exposed to CH3HgCl exhibited significantly reduced distance travelled and swimming speed compared to the control group, as well as augmented cortisol and ROS levels and xanthine oxidase (XO) activities. CH3HgCl exposure significantly increased lipid peroxidation (LOOH) and protein carbonylation (PC) levels compared to those of the control group, while acetylcholinesterase (AChE) and sodium-potassium pump (Na+, K+-ATPase) activities were inhibited. Dietary supplementation with 3 mg/kg Ph2Se2 ameliorated locomotor activity impairment and prevented the augmented brain cortisol and ROS levels as well as XO activity. The supplement reduced lipid and protein damage elicited by CH3HgCl and exerted protective effects on brain AChE and Na+, K+-ATPase activities. Exposure to an environmental concentration of CH3HgCl elicited neurobehavioral alterations linked to reduced locomotor activity, a finding that can be explained by oxidative damage and reduced activity of AChE and Na+, K+-ATPase in telencephalon and mesencephalon structures. Dietary supplementation with Ph2Se2 prevented CH3HgCl-induced locomotor impairment. This effect appeared to be mediated by antioxidant action. Ph2Se2 may be a viable approach to prevention or reduction CH3HgCl-mediated neurotoxic effects.
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spelling Diphenyl diselenide dietary supplementation alleviates behavior impairment and brain damage in grass carp (Ctenopharyngodon idella) exposed to methylmercury chloride© 2019 Elsevier Inc.Mercury (Hg) induces neurobehavioral disorders through reactive oxygen species (ROS) elevation and impairment of brain key enzyme activities. Nevertheless, the therapeutic and toxic selenium concentrations for fish are very close; diphenyl diselenide (Ph2Se2), an organoselenium compound with neuroprotective effects, may be an alternative to elemental Se. Therefore, the aim of this study was to determine whether dietary supplementation with Ph2Se2 prevented or reduced the neurobehavioral alterations and oxidative damage elicited by CH3HgCl in grass carp Ctenopharyngodon idella. Fish exposed to CH3HgCl exhibited significantly reduced distance travelled and swimming speed compared to the control group, as well as augmented cortisol and ROS levels and xanthine oxidase (XO) activities. CH3HgCl exposure significantly increased lipid peroxidation (LOOH) and protein carbonylation (PC) levels compared to those of the control group, while acetylcholinesterase (AChE) and sodium-potassium pump (Na+, K+-ATPase) activities were inhibited. Dietary supplementation with 3 mg/kg Ph2Se2 ameliorated locomotor activity impairment and prevented the augmented brain cortisol and ROS levels as well as XO activity. The supplement reduced lipid and protein damage elicited by CH3HgCl and exerted protective effects on brain AChE and Na+, K+-ATPase activities. Exposure to an environmental concentration of CH3HgCl elicited neurobehavioral alterations linked to reduced locomotor activity, a finding that can be explained by oxidative damage and reduced activity of AChE and Na+, K+-ATPase in telencephalon and mesencephalon structures. Dietary supplementation with Ph2Se2 prevented CH3HgCl-induced locomotor impairment. This effect appeared to be mediated by antioxidant action. Ph2Se2 may be a viable approach to prevention or reduction CH3HgCl-mediated neurotoxic effects.2024-12-06T12:00:38Z2020info:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/article1878-165910.1016/j.cbpc.2019.108674https://repositorio.udesc.br/handle/UDESC/4758ark:/33523/0013000007t77Comparative Biochemistry and Physiology Part - C: Toxicology and Pharmacology229Baldissera M.D.Souza C.F.da Silva A.S.*Henn A.S.Flores E.M.M.Baldisserotto B.engreponame:Repositório Institucional da Udescinstname:Universidade do Estado de Santa Catarina (UDESC)instacron:UDESCinfo:eu-repo/semantics/openAccess2024-12-07T20:45:36Zoai:repositorio.udesc.br:UDESC/4758Biblioteca Digital de Teses e Dissertaçõeshttps://pergamumweb.udesc.br/biblioteca/index.phpPRIhttps://repositorio-api.udesc.br/server/oai/requestri@udesc.bropendoar:63912024-12-07T20:45:36Repositório Institucional da Udesc - Universidade do Estado de Santa Catarina (UDESC)false
dc.title.none.fl_str_mv Diphenyl diselenide dietary supplementation alleviates behavior impairment and brain damage in grass carp (Ctenopharyngodon idella) exposed to methylmercury chloride
title Diphenyl diselenide dietary supplementation alleviates behavior impairment and brain damage in grass carp (Ctenopharyngodon idella) exposed to methylmercury chloride
spellingShingle Diphenyl diselenide dietary supplementation alleviates behavior impairment and brain damage in grass carp (Ctenopharyngodon idella) exposed to methylmercury chloride
Baldissera M.D.
title_short Diphenyl diselenide dietary supplementation alleviates behavior impairment and brain damage in grass carp (Ctenopharyngodon idella) exposed to methylmercury chloride
title_full Diphenyl diselenide dietary supplementation alleviates behavior impairment and brain damage in grass carp (Ctenopharyngodon idella) exposed to methylmercury chloride
title_fullStr Diphenyl diselenide dietary supplementation alleviates behavior impairment and brain damage in grass carp (Ctenopharyngodon idella) exposed to methylmercury chloride
title_full_unstemmed Diphenyl diselenide dietary supplementation alleviates behavior impairment and brain damage in grass carp (Ctenopharyngodon idella) exposed to methylmercury chloride
title_sort Diphenyl diselenide dietary supplementation alleviates behavior impairment and brain damage in grass carp (Ctenopharyngodon idella) exposed to methylmercury chloride
author Baldissera M.D.
author_facet Baldissera M.D.
Souza C.F.
da Silva A.S.*
Henn A.S.
Flores E.M.M.
Baldisserotto B.
author_role author
author2 Souza C.F.
da Silva A.S.*
Henn A.S.
Flores E.M.M.
Baldisserotto B.
author2_role author
author
author
author
author
dc.contributor.author.fl_str_mv Baldissera M.D.
Souza C.F.
da Silva A.S.*
Henn A.S.
Flores E.M.M.
Baldisserotto B.
description © 2019 Elsevier Inc.Mercury (Hg) induces neurobehavioral disorders through reactive oxygen species (ROS) elevation and impairment of brain key enzyme activities. Nevertheless, the therapeutic and toxic selenium concentrations for fish are very close; diphenyl diselenide (Ph2Se2), an organoselenium compound with neuroprotective effects, may be an alternative to elemental Se. Therefore, the aim of this study was to determine whether dietary supplementation with Ph2Se2 prevented or reduced the neurobehavioral alterations and oxidative damage elicited by CH3HgCl in grass carp Ctenopharyngodon idella. Fish exposed to CH3HgCl exhibited significantly reduced distance travelled and swimming speed compared to the control group, as well as augmented cortisol and ROS levels and xanthine oxidase (XO) activities. CH3HgCl exposure significantly increased lipid peroxidation (LOOH) and protein carbonylation (PC) levels compared to those of the control group, while acetylcholinesterase (AChE) and sodium-potassium pump (Na+, K+-ATPase) activities were inhibited. Dietary supplementation with 3 mg/kg Ph2Se2 ameliorated locomotor activity impairment and prevented the augmented brain cortisol and ROS levels as well as XO activity. The supplement reduced lipid and protein damage elicited by CH3HgCl and exerted protective effects on brain AChE and Na+, K+-ATPase activities. Exposure to an environmental concentration of CH3HgCl elicited neurobehavioral alterations linked to reduced locomotor activity, a finding that can be explained by oxidative damage and reduced activity of AChE and Na+, K+-ATPase in telencephalon and mesencephalon structures. Dietary supplementation with Ph2Se2 prevented CH3HgCl-induced locomotor impairment. This effect appeared to be mediated by antioxidant action. Ph2Se2 may be a viable approach to prevention or reduction CH3HgCl-mediated neurotoxic effects.
publishDate 2020
dc.date.none.fl_str_mv 2020
2024-12-06T12:00:38Z
dc.type.status.fl_str_mv info:eu-repo/semantics/publishedVersion
dc.type.driver.fl_str_mv info:eu-repo/semantics/article
format article
status_str publishedVersion
dc.identifier.uri.fl_str_mv 1878-1659
10.1016/j.cbpc.2019.108674
https://repositorio.udesc.br/handle/UDESC/4758
dc.identifier.dark.fl_str_mv ark:/33523/0013000007t77
identifier_str_mv 1878-1659
10.1016/j.cbpc.2019.108674
ark:/33523/0013000007t77
url https://repositorio.udesc.br/handle/UDESC/4758
dc.language.iso.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv Comparative Biochemistry and Physiology Part - C: Toxicology and Pharmacology
229
dc.rights.driver.fl_str_mv info:eu-repo/semantics/openAccess
eu_rights_str_mv openAccess
dc.source.none.fl_str_mv reponame:Repositório Institucional da Udesc
instname:Universidade do Estado de Santa Catarina (UDESC)
instacron:UDESC
instname_str Universidade do Estado de Santa Catarina (UDESC)
instacron_str UDESC
institution UDESC
reponame_str Repositório Institucional da Udesc
collection Repositório Institucional da Udesc
repository.name.fl_str_mv Repositório Institucional da Udesc - Universidade do Estado de Santa Catarina (UDESC)
repository.mail.fl_str_mv ri@udesc.br
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