Is hepatic oxidative stress a main driver of dietary selenium toxicity in white sturgeon (Acipenser transmontanus)?
Identifieur interne : 000029 ( PubMed/Corpus ); précédent : 000028; suivant : 000030Is hepatic oxidative stress a main driver of dietary selenium toxicity in white sturgeon (Acipenser transmontanus)?
Auteurs : Jenna Zee ; Sarah Patterson ; Steve Wiseman ; Markus HeckerSource :
- Ecotoxicology and environmental safety [ 1090-2414 ] ; 2016.
English descriptors
- KwdEn :
- Animal Feed (analysis), Animals, Chemical and Drug Induced Liver Injury (veterinary), Diet, Dioxins (toxicity), Fish Diseases (chemically induced), Fishes, Glutathione Transferase (metabolism), Oxidative Stress, Selenium (metabolism), Selenium (toxicity), Selenium Compounds, Selenomethionine (administration & dosage), Selenomethionine (analysis), Selenomethionine (toxicity), Water Pollutants, Chemical (toxicity).
- MESH :
- chemical , administration & dosage : Selenomethionine.
- chemical , analysis : Selenomethionine.
- chemical , metabolism : Glutathione Transferase, Selenium.
- chemical , toxicity : Dioxins, Selenium, Selenomethionine, Water Pollutants, Chemical.
- analysis : Animal Feed.
- chemically induced : Fish Diseases.
- veterinary : Chemical and Drug Induced Liver Injury.
- Animals, Diet, Fishes, Oxidative Stress, Selenium Compounds.
Abstract
Most species of sturgeon have experienced significant population declines and poor recruitment over the past decades, leading many, including white sturgeon (Acipenser transmontanus), to be listed as endangered. Reasons for these declines are not yet fully understood but benthic lifestyle, longevity, and delayed sexual maturation likely render sturgeon particularly susceptible to factors such as habitat alteration and contaminant exposures. One contaminant of particular concern to white sturgeon is selenium (Se), especially in its more bioavailable form selenomethionine (SeMet), as it is known to efficiently bioaccumulate in prey items of this species. Studies have shown white sturgeon to be among the most sensitive species of fish to dietary SeMet as well as other pollutants such as metals, dioxin-like chemicals and endocrine disrupters. One of the primary hypothesized mechanisms of toxicity of SeMet in fish is oxidative stress; however, little is know about the specific mode by which SeMet affects the health of white sturgeon. Therefore, the aim of this study was to characterize oxidative stress and associated antioxidant responses as a molecular event of toxicity, and to link it with the pathological effects observed previously. Specifically, three-year-old white sturgeon were exposed for 72 days via their diet to 1.4, 5.6, 22.4 or 104.4µg Se per g feed (dm). Doses were chosen to range over a necessary Se intake level, current environmentally relevant intakes and an intake representing predicted increases of Se release. Lipid hydroperoxides, which are end products of lipid oxidation, were quantified as a marker of oxidative stress. Changes in gene expression of glutathione peroxidase (GPx), superoxide dismutase, catalase, glutathione S-transferase, apoptosis inducing factor and caspase 3 were quantified as markers of the response to oxidative stress. Concentrations of lipid hydroperoxides were highly variable within dose groups and no dose response was observed. GPx expression was significantly increased in the low dose group indicating an induced antioxidant response. Expression of other genes were not significantly induced or suppressed. Overall, there was very little evidence of oxidative stress, and therefore, in contrast to previous reports on other species of teleost fishes, oxidative stress is not believed to be a main driver of toxicity in white sturgeon exposed to SeMet.
DOI: 10.1016/j.ecoenv.2016.07.004
PubMed: 27494256
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pubmed:27494256Le document en format XML
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Electronic address: sep662@mail.usask.ca.</nlm:affiliation></affiliation></author><author><name sortKey="Wiseman, Steve" sort="Wiseman, Steve" uniqKey="Wiseman S" first="Steve" last="Wiseman">Steve Wiseman</name><affiliation><nlm:affiliation>Toxicology Centre, University of Saskatchewan, 44 Campus Drive, Saskatoon, Saskatchewan, Canada S7N 5B3. Electronic address: steve.wiseman@uleth.ca.</nlm:affiliation></affiliation></author><author><name sortKey="Hecker, Markus" sort="Hecker, Markus" uniqKey="Hecker M" first="Markus" last="Hecker">Markus Hecker</name><affiliation><nlm:affiliation>School of Environment and Sustainability, University of Saskatchewan, Room 323, Kirk Hall, 117 Science Place, Saskatoon, Saskatchewan, Canada S7N 5C8; Toxicology Centre, University of Saskatchewan, 44 Campus Drive, Saskatoon, Saskatchewan, Canada S7N 5B3. 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Electronic address: jmz584@mail.usask.ca.</nlm:affiliation></affiliation></author><author><name sortKey="Patterson, Sarah" sort="Patterson, Sarah" uniqKey="Patterson S" first="Sarah" last="Patterson">Sarah Patterson</name><affiliation><nlm:affiliation>Toxicology Centre, University of Saskatchewan, 44 Campus Drive, Saskatoon, Saskatchewan, Canada S7N 5B3. Electronic address: sep662@mail.usask.ca.</nlm:affiliation></affiliation></author><author><name sortKey="Wiseman, Steve" sort="Wiseman, Steve" uniqKey="Wiseman S" first="Steve" last="Wiseman">Steve Wiseman</name><affiliation><nlm:affiliation>Toxicology Centre, University of Saskatchewan, 44 Campus Drive, Saskatoon, Saskatchewan, Canada S7N 5B3. Electronic address: steve.wiseman@uleth.ca.</nlm:affiliation></affiliation></author><author><name sortKey="Hecker, Markus" sort="Hecker, Markus" uniqKey="Hecker M" first="Markus" last="Hecker">Markus Hecker</name><affiliation><nlm:affiliation>School of Environment and Sustainability, University of Saskatchewan, Room 323, Kirk Hall, 117 Science Place, Saskatoon, Saskatchewan, Canada S7N 5C8; Toxicology Centre, University of Saskatchewan, 44 Campus Drive, Saskatoon, Saskatchewan, Canada S7N 5B3. Electronic address: markus.hecker@usask.ca.</nlm:affiliation></affiliation></author></analytic><series><title level="j">Ecotoxicology and environmental safety</title><idno type="eISSN">1090-2414</idno><imprint><date when="2016" type="published">2016</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animal Feed (analysis)</term><term>Animals</term><term>Chemical and Drug Induced Liver Injury (veterinary)</term><term>Diet</term><term>Dioxins (toxicity)</term><term>Fish Diseases (chemically induced)</term><term>Fishes</term><term>Glutathione Transferase (metabolism)</term><term>Oxidative Stress</term><term>Selenium (metabolism)</term><term>Selenium (toxicity)</term><term>Selenium Compounds</term><term>Selenomethionine (administration & dosage)</term><term>Selenomethionine (analysis)</term><term>Selenomethionine (toxicity)</term><term>Water Pollutants, Chemical (toxicity)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="administration & dosage" xml:lang="en"><term>Selenomethionine</term></keywords><keywords scheme="MESH" type="chemical" qualifier="analysis" xml:lang="en"><term>Selenomethionine</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Glutathione Transferase</term><term>Selenium</term></keywords><keywords scheme="MESH" type="chemical" qualifier="toxicity" xml:lang="en"><term>Dioxins</term><term>Selenium</term><term>Selenomethionine</term><term>Water Pollutants, Chemical</term></keywords><keywords scheme="MESH" qualifier="analysis" xml:lang="en"><term>Animal Feed</term></keywords><keywords scheme="MESH" qualifier="chemically induced" xml:lang="en"><term>Fish Diseases</term></keywords><keywords scheme="MESH" qualifier="veterinary" xml:lang="en"><term>Chemical and Drug Induced Liver Injury</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Diet</term><term>Fishes</term><term>Oxidative Stress</term><term>Selenium Compounds</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Most species of sturgeon have experienced significant population declines and poor recruitment over the past decades, leading many, including white sturgeon (Acipenser transmontanus), to be listed as endangered. Reasons for these declines are not yet fully understood but benthic lifestyle, longevity, and delayed sexual maturation likely render sturgeon particularly susceptible to factors such as habitat alteration and contaminant exposures. One contaminant of particular concern to white sturgeon is selenium (Se), especially in its more bioavailable form selenomethionine (SeMet), as it is known to efficiently bioaccumulate in prey items of this species. Studies have shown white sturgeon to be among the most sensitive species of fish to dietary SeMet as well as other pollutants such as metals, dioxin-like chemicals and endocrine disrupters. One of the primary hypothesized mechanisms of toxicity of SeMet in fish is oxidative stress; however, little is know about the specific mode by which SeMet affects the health of white sturgeon. Therefore, the aim of this study was to characterize oxidative stress and associated antioxidant responses as a molecular event of toxicity, and to link it with the pathological effects observed previously. Specifically, three-year-old white sturgeon were exposed for 72 days via their diet to 1.4, 5.6, 22.4 or 104.4µg Se per g feed (dm). Doses were chosen to range over a necessary Se intake level, current environmentally relevant intakes and an intake representing predicted increases of Se release. Lipid hydroperoxides, which are end products of lipid oxidation, were quantified as a marker of oxidative stress. Changes in gene expression of glutathione peroxidase (GPx), superoxide dismutase, catalase, glutathione S-transferase, apoptosis inducing factor and caspase 3 were quantified as markers of the response to oxidative stress. Concentrations of lipid hydroperoxides were highly variable within dose groups and no dose response was observed. GPx expression was significantly increased in the low dose group indicating an induced antioxidant response. Expression of other genes were not significantly induced or suppressed. Overall, there was very little evidence of oxidative stress, and therefore, in contrast to previous reports on other species of teleost fishes, oxidative stress is not believed to be a main driver of toxicity in white sturgeon exposed to SeMet.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">27494256</PMID><DateCreated><Year>2016</Year><Month>09</Month><Day>10</Day></DateCreated><DateCompleted><Year>2017</Year><Month>01</Month><Day>13</Day></DateCompleted><DateRevised><Year>2017</Year><Month>01</Month><Day>13</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1090-2414</ISSN><JournalIssue CitedMedium="Internet"><Volume>133</Volume><PubDate><Year>2016</Year><Month>Nov</Month></PubDate></JournalIssue><Title>Ecotoxicology and environmental safety</Title><ISOAbbreviation>Ecotoxicol. Environ. Saf.</ISOAbbreviation></Journal><ArticleTitle>Is hepatic oxidative stress a main driver of dietary selenium toxicity in white sturgeon (Acipenser transmontanus)?</ArticleTitle><Pagination><MedlinePgn>334-40</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1016/j.ecoenv.2016.07.004</ELocationID><ELocationID EIdType="pii" ValidYN="Y">S0147-6513(16)30258-5</ELocationID><Abstract><AbstractText>Most species of sturgeon have experienced significant population declines and poor recruitment over the past decades, leading many, including white sturgeon (Acipenser transmontanus), to be listed as endangered. Reasons for these declines are not yet fully understood but benthic lifestyle, longevity, and delayed sexual maturation likely render sturgeon particularly susceptible to factors such as habitat alteration and contaminant exposures. One contaminant of particular concern to white sturgeon is selenium (Se), especially in its more bioavailable form selenomethionine (SeMet), as it is known to efficiently bioaccumulate in prey items of this species. Studies have shown white sturgeon to be among the most sensitive species of fish to dietary SeMet as well as other pollutants such as metals, dioxin-like chemicals and endocrine disrupters. One of the primary hypothesized mechanisms of toxicity of SeMet in fish is oxidative stress; however, little is know about the specific mode by which SeMet affects the health of white sturgeon. Therefore, the aim of this study was to characterize oxidative stress and associated antioxidant responses as a molecular event of toxicity, and to link it with the pathological effects observed previously. Specifically, three-year-old white sturgeon were exposed for 72 days via their diet to 1.4, 5.6, 22.4 or 104.4µg Se per g feed (dm). Doses were chosen to range over a necessary Se intake level, current environmentally relevant intakes and an intake representing predicted increases of Se release. Lipid hydroperoxides, which are end products of lipid oxidation, were quantified as a marker of oxidative stress. Changes in gene expression of glutathione peroxidase (GPx), superoxide dismutase, catalase, glutathione S-transferase, apoptosis inducing factor and caspase 3 were quantified as markers of the response to oxidative stress. Concentrations of lipid hydroperoxides were highly variable within dose groups and no dose response was observed. GPx expression was significantly increased in the low dose group indicating an induced antioxidant response. Expression of other genes were not significantly induced or suppressed. Overall, there was very little evidence of oxidative stress, and therefore, in contrast to previous reports on other species of teleost fishes, oxidative stress is not believed to be a main driver of toxicity in white sturgeon exposed to SeMet.</AbstractText><CopyrightInformation>Copyright © 2016 Elsevier Inc. All rights reserved.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Zee</LastName><ForeName>Jenna</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>School of Environment and Sustainability, University of Saskatchewan, Room 323, Kirk Hall, 117 Science Place, Saskatoon, Saskatchewan, Canada S7N 5C8. Electronic address: jmz584@mail.usask.ca.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Patterson</LastName><ForeName>Sarah</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Toxicology Centre, University of Saskatchewan, 44 Campus Drive, Saskatoon, Saskatchewan, Canada S7N 5B3. Electronic address: sep662@mail.usask.ca.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Wiseman</LastName><ForeName>Steve</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Toxicology Centre, University of Saskatchewan, 44 Campus Drive, Saskatoon, Saskatchewan, Canada S7N 5B3. Electronic address: steve.wiseman@uleth.ca.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Hecker</LastName><ForeName>Markus</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>School of Environment and Sustainability, University of Saskatchewan, Room 323, Kirk Hall, 117 Science Place, Saskatoon, Saskatchewan, Canada S7N 5C8; Toxicology Centre, University of Saskatchewan, 44 Campus Drive, Saskatoon, Saskatchewan, Canada S7N 5B3. Electronic address: markus.hecker@usask.ca.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2016</Year><Month>08</Month><Day>03</Day></ArticleDate></Article><MedlineJournalInfo><Country>Netherlands</Country><MedlineTA>Ecotoxicol Environ Saf</MedlineTA><NlmUniqueID>7805381</NlmUniqueID><ISSNLinking>0147-6513</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D004147">Dioxins</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D018036">Selenium Compounds</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D014874">Water Pollutants, Chemical</NameOfSubstance></Chemical><Chemical><RegistryNumber>964MRK2PEL</RegistryNumber><NameOfSubstance UI="D012645">Selenomethionine</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 2.5.1.18</RegistryNumber><NameOfSubstance UI="D005982">Glutathione Transferase</NameOfSubstance></Chemical><Chemical><RegistryNumber>H6241UJ22B</RegistryNumber><NameOfSubstance UI="D012643">Selenium</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000821" MajorTopicYN="N">Animal Feed</DescriptorName><QualifierName UI="Q000032" MajorTopicYN="N">analysis</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D056486" MajorTopicYN="N">Chemical and Drug Induced Liver Injury</DescriptorName><QualifierName UI="Q000662" MajorTopicYN="Y">veterinary</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D004032" MajorTopicYN="N">Diet</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D004147" MajorTopicYN="N">Dioxins</DescriptorName><QualifierName UI="Q000633" MajorTopicYN="N">toxicity</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005393" MajorTopicYN="N">Fish Diseases</DescriptorName><QualifierName UI="Q000139" MajorTopicYN="Y">chemically induced</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005399" MajorTopicYN="Y">Fishes</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005982" MajorTopicYN="N">Glutathione Transferase</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D018384" MajorTopicYN="N">Oxidative Stress</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D012643" MajorTopicYN="N">Selenium</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000633" MajorTopicYN="Y">toxicity</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D018036" MajorTopicYN="N">Selenium Compounds</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D012645" MajorTopicYN="N">Selenomethionine</DescriptorName><QualifierName UI="Q000008" MajorTopicYN="N">administration & dosage</QualifierName><QualifierName UI="Q000032" MajorTopicYN="N">analysis</QualifierName><QualifierName UI="Q000633" MajorTopicYN="N">toxicity</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D014874" MajorTopicYN="N">Water Pollutants, Chemical</DescriptorName><QualifierName UI="Q000633" MajorTopicYN="Y">toxicity</QualifierName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Antioxidant response</Keyword><Keyword MajorTopicYN="N">Endangered</Keyword><Keyword MajorTopicYN="N">Fish</Keyword><Keyword MajorTopicYN="N">Oxidative stress</Keyword><Keyword MajorTopicYN="N">Selenium toxicity</Keyword><Keyword MajorTopicYN="N">Sturgeon</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2016</Year><Month>02</Month><Day>10</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2016</Year><Month>06</Month><Day>30</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2016</Year><Month>07</Month><Day>05</Day></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2016</Year><Month>8</Month><Day>6</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2016</Year><Month>8</Month><Day>6</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2017</Year><Month>1</Month><Day>14</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">27494256</ArticleId><ArticleId IdType="pii">S0147-6513(16)30258-5</ArticleId><ArticleId IdType="doi">10.1016/j.ecoenv.2016.07.004</ArticleId></ArticleIdList></PubmedData></pubmed></record>Pour manipuler ce document sous Unix (Dilib)
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