Physiological impacts and bioaccumulation of dietary Cu and Cd in a model teleost: The Amazonian tambaqui (Colossoma macropomum)

Detalhes bibliográficos
Autor(a) principal: Giacomin, Marina
Data de Publicação: 2018
Outros Autores: Vilarinho, Gisele C., Castro, Katia F., Ferreira, Márcio, Duarte, Rafael M. [UNESP], Wood, Chris M., Val, Adalberto L.
Tipo de documento: Artigo
Idioma: eng
Título da fonte: Repositório Institucional da UNESP
Texto Completo: http://dx.doi.org/10.1016/j.aquatox.2018.03.021
http://hdl.handle.net/11449/170831
Resumo: Increasing anthropogenic activities in the Amazon have led to elevated metals in the aquatic environment. Since fish are the main source of animal protein for the Amazonian population, understanding metal bioaccumulation patterns and physiological impacts is of critical importance. Juvenile tambaqui, a local model species, were exposed to chronic dietary Cu (essential, 500 μg Cu/g food) and Cd (non-essential, 500 μg Cd/g food). Fish were sampled at 10–14, 18–20 and 33–36 days of exposure and the following parameters were analyzed: growth, voluntary food consumption, conversion efficiency, tissue-specific metal bioaccumulation, ammonia and urea-N excretion, O2 consumption, Pcrit, hypoxia tolerance, nitrogen quotient, major blood plasma ions and metabolites, gill and gut enzyme activities, and in vitro gut fluid transport. The results indicate no ionoregulatory impacts of either of the metal-contaminated diets at gill, gut, or plasma levels, and no differences in plasma cortisol or lactate. The Cd diet appeared to have suppressed feeding, though overall tank growth was not affected. Bioaccumulation of both metals was observed. Distinct tissue-specific and time-specific patterns were seen. Metal burdens in the edible white muscle remained low. Overall, physiological impacts of the Cu diet were minimal. However dietary Cd increased hypoxia tolerance, as evidenced by decreased Pcrit, increased time to loss of equilibrium, a lack of plasma glucose elevation, decreased plasma ethanol, and decreased NQ during hypoxia. Blood O2 transport characteristics (P50, Bohr coefficient, hemoglobin, hematocrit) were unaffected, suggesting that tissue level changes in metabolism accounted for the greater hypoxia tolerance in tambaqui fed with a Cd-contaminated diet.
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spelling Physiological impacts and bioaccumulation of dietary Cu and Cd in a model teleost: The Amazonian tambaqui (Colossoma macropomum)Dietary metalsHypoxiaPcritTissue accumulationTropical teleostIncreasing anthropogenic activities in the Amazon have led to elevated metals in the aquatic environment. Since fish are the main source of animal protein for the Amazonian population, understanding metal bioaccumulation patterns and physiological impacts is of critical importance. Juvenile tambaqui, a local model species, were exposed to chronic dietary Cu (essential, 500 μg Cu/g food) and Cd (non-essential, 500 μg Cd/g food). Fish were sampled at 10–14, 18–20 and 33–36 days of exposure and the following parameters were analyzed: growth, voluntary food consumption, conversion efficiency, tissue-specific metal bioaccumulation, ammonia and urea-N excretion, O2 consumption, Pcrit, hypoxia tolerance, nitrogen quotient, major blood plasma ions and metabolites, gill and gut enzyme activities, and in vitro gut fluid transport. The results indicate no ionoregulatory impacts of either of the metal-contaminated diets at gill, gut, or plasma levels, and no differences in plasma cortisol or lactate. The Cd diet appeared to have suppressed feeding, though overall tank growth was not affected. Bioaccumulation of both metals was observed. Distinct tissue-specific and time-specific patterns were seen. Metal burdens in the edible white muscle remained low. Overall, physiological impacts of the Cu diet were minimal. However dietary Cd increased hypoxia tolerance, as evidenced by decreased Pcrit, increased time to loss of equilibrium, a lack of plasma glucose elevation, decreased plasma ethanol, and decreased NQ during hypoxia. Blood O2 transport characteristics (P50, Bohr coefficient, hemoglobin, hematocrit) were unaffected, suggesting that tissue level changes in metabolism accounted for the greater hypoxia tolerance in tambaqui fed with a Cd-contaminated diet.Instituto Nacional de Ciência e Tecnologia Centro de Estudos das Adaptações da Biota Aquática da AmazôniaNatural Sciences and Engineering Research Council of CanadaDepartment of Zoology The University of British ColumbiaLaboratory of Ecophysiology and Molecular Evolution Instituto Nacional de Pesquisas da Amazônia (INPA)São Paulo State University (UNESP) Institute of BiosciencesDepartment of Biology McMaster UniversityRosenstiel School of Marine and Atmospheric Science University of MiamiSão Paulo State University (UNESP) Institute of BiosciencesThe University of British ColumbiaInstituto Nacional de Pesquisas da Amazônia (INPA)Universidade Estadual Paulista (Unesp)McMaster UniversityUniversity of MiamiGiacomin, MarinaVilarinho, Gisele C.Castro, Katia F.Ferreira, MárcioDuarte, Rafael M. [UNESP]Wood, Chris M.Val, Adalberto L.2018-12-11T16:52:36Z2018-12-11T16:52:36Z2018-06-01info:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/article30-45application/pdfhttp://dx.doi.org/10.1016/j.aquatox.2018.03.021Aquatic Toxicology, v. 199, p. 30-45.1879-15140166-445Xhttp://hdl.handle.net/11449/17083110.1016/j.aquatox.2018.03.0212-s2.0-850445026422-s2.0-85044502642.pdf30557957777876120000-0001-5649-0692Scopusreponame:Repositório Institucional da UNESPinstname:Universidade Estadual Paulista (UNESP)instacron:UNESPengAquatic Toxicology1,456info:eu-repo/semantics/openAccess2024-01-13T06:31:40Zoai:repositorio.unesp.br:11449/170831Repositório InstitucionalPUBhttp://repositorio.unesp.br/oai/requestopendoar:29462024-01-13T06:31:40Repositório Institucional da UNESP - Universidade Estadual Paulista (UNESP)false
dc.title.none.fl_str_mv Physiological impacts and bioaccumulation of dietary Cu and Cd in a model teleost: The Amazonian tambaqui (Colossoma macropomum)
title Physiological impacts and bioaccumulation of dietary Cu and Cd in a model teleost: The Amazonian tambaqui (Colossoma macropomum)
spellingShingle Physiological impacts and bioaccumulation of dietary Cu and Cd in a model teleost: The Amazonian tambaqui (Colossoma macropomum)
Giacomin, Marina
Dietary metals
Hypoxia
Pcrit
Tissue accumulation
Tropical teleost
title_short Physiological impacts and bioaccumulation of dietary Cu and Cd in a model teleost: The Amazonian tambaqui (Colossoma macropomum)
title_full Physiological impacts and bioaccumulation of dietary Cu and Cd in a model teleost: The Amazonian tambaqui (Colossoma macropomum)
title_fullStr Physiological impacts and bioaccumulation of dietary Cu and Cd in a model teleost: The Amazonian tambaqui (Colossoma macropomum)
title_full_unstemmed Physiological impacts and bioaccumulation of dietary Cu and Cd in a model teleost: The Amazonian tambaqui (Colossoma macropomum)
title_sort Physiological impacts and bioaccumulation of dietary Cu and Cd in a model teleost: The Amazonian tambaqui (Colossoma macropomum)
author Giacomin, Marina
author_facet Giacomin, Marina
Vilarinho, Gisele C.
Castro, Katia F.
Ferreira, Márcio
Duarte, Rafael M. [UNESP]
Wood, Chris M.
Val, Adalberto L.
author_role author
author2 Vilarinho, Gisele C.
Castro, Katia F.
Ferreira, Márcio
Duarte, Rafael M. [UNESP]
Wood, Chris M.
Val, Adalberto L.
author2_role author
author
author
author
author
author
dc.contributor.none.fl_str_mv The University of British Columbia
Instituto Nacional de Pesquisas da Amazônia (INPA)
Universidade Estadual Paulista (Unesp)
McMaster University
University of Miami
dc.contributor.author.fl_str_mv Giacomin, Marina
Vilarinho, Gisele C.
Castro, Katia F.
Ferreira, Márcio
Duarte, Rafael M. [UNESP]
Wood, Chris M.
Val, Adalberto L.
dc.subject.por.fl_str_mv Dietary metals
Hypoxia
Pcrit
Tissue accumulation
Tropical teleost
topic Dietary metals
Hypoxia
Pcrit
Tissue accumulation
Tropical teleost
description Increasing anthropogenic activities in the Amazon have led to elevated metals in the aquatic environment. Since fish are the main source of animal protein for the Amazonian population, understanding metal bioaccumulation patterns and physiological impacts is of critical importance. Juvenile tambaqui, a local model species, were exposed to chronic dietary Cu (essential, 500 μg Cu/g food) and Cd (non-essential, 500 μg Cd/g food). Fish were sampled at 10–14, 18–20 and 33–36 days of exposure and the following parameters were analyzed: growth, voluntary food consumption, conversion efficiency, tissue-specific metal bioaccumulation, ammonia and urea-N excretion, O2 consumption, Pcrit, hypoxia tolerance, nitrogen quotient, major blood plasma ions and metabolites, gill and gut enzyme activities, and in vitro gut fluid transport. The results indicate no ionoregulatory impacts of either of the metal-contaminated diets at gill, gut, or plasma levels, and no differences in plasma cortisol or lactate. The Cd diet appeared to have suppressed feeding, though overall tank growth was not affected. Bioaccumulation of both metals was observed. Distinct tissue-specific and time-specific patterns were seen. Metal burdens in the edible white muscle remained low. Overall, physiological impacts of the Cu diet were minimal. However dietary Cd increased hypoxia tolerance, as evidenced by decreased Pcrit, increased time to loss of equilibrium, a lack of plasma glucose elevation, decreased plasma ethanol, and decreased NQ during hypoxia. Blood O2 transport characteristics (P50, Bohr coefficient, hemoglobin, hematocrit) were unaffected, suggesting that tissue level changes in metabolism accounted for the greater hypoxia tolerance in tambaqui fed with a Cd-contaminated diet.
publishDate 2018
dc.date.none.fl_str_mv 2018-12-11T16:52:36Z
2018-12-11T16:52:36Z
2018-06-01
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 http://dx.doi.org/10.1016/j.aquatox.2018.03.021
Aquatic Toxicology, v. 199, p. 30-45.
1879-1514
0166-445X
http://hdl.handle.net/11449/170831
10.1016/j.aquatox.2018.03.021
2-s2.0-85044502642
2-s2.0-85044502642.pdf
3055795777787612
0000-0001-5649-0692
url http://dx.doi.org/10.1016/j.aquatox.2018.03.021
http://hdl.handle.net/11449/170831
identifier_str_mv Aquatic Toxicology, v. 199, p. 30-45.
1879-1514
0166-445X
10.1016/j.aquatox.2018.03.021
2-s2.0-85044502642
2-s2.0-85044502642.pdf
3055795777787612
0000-0001-5649-0692
dc.language.iso.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv Aquatic Toxicology
1,456
dc.rights.driver.fl_str_mv info:eu-repo/semantics/openAccess
eu_rights_str_mv openAccess
dc.format.none.fl_str_mv 30-45
application/pdf
dc.source.none.fl_str_mv Scopus
reponame:Repositório Institucional da UNESP
instname:Universidade Estadual Paulista (UNESP)
instacron:UNESP
instname_str Universidade Estadual Paulista (UNESP)
instacron_str UNESP
institution UNESP
reponame_str Repositório Institucional da UNESP
collection Repositório Institucional da UNESP
repository.name.fl_str_mv Repositório Institucional da UNESP - Universidade Estadual Paulista (UNESP)
repository.mail.fl_str_mv
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