2,3,7,8-Tetrachlorodibenzo- p -dioxin induces apoptotic cell death and cytochrome P4501A expression in developing Fundulus heteroclitus embryos
Identifieur interne : 000463 ( Istex/Corpus ); précédent : 000462; suivant : 0004642,3,7,8-Tetrachlorodibenzo- p -dioxin induces apoptotic cell death and cytochrome P4501A expression in developing Fundulus heteroclitus embryos
Auteurs : Barbara Holland Toomey ; Susan Bello ; Mark E. Hahn ; Susannah Cantrell ; Peggy Wright ; Donald E. Tillitt ; Richard T. Di GiulioSource :
- Aquatic Toxicology [ 0166-445X ] ; 2000.
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- KwdEn :
Abstract
Fundulus heteroclitus embryos were exposed to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) during early development using nanoinjection or water bath exposure. TCDD caused developmental abnormalities that included hemorrhaging, loss of vascular integrity, edema, stunted development and death. The LC50 and LD50 of TCDD for Fundulus embryos were ∼19.7±9.5 pg TCDD/μl (water bath) and 0.25±0.09 ng TCDD/g embryo (nanoinjection). To identify a possible cause for these developmental abnormalities we analyzed the effects of TCDD on apoptotic cell death and cytochrome P4501A (CYP1A) expression in the embryos. TCDD exposure increased apoptotic cell death in several tissues including brain, eye, gill, kidney, tail, intestine, heart, and vascular tissue. CYP1A expression was also increased in the TCDD-exposed embryos predominantly in liver, kidney, gill, heart, intestine, and in vascular tissues throughout the embryo. There was co-occurrence of TCDD-induced apoptosis and CYP1A expression in some, but not all, cell types. In addition the dose response relationships for apoptosis and mortality were similar, while CYP1A expression appeared more sensitive to TCDD induction.
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DOI: 10.1016/S0166-445X(00)00161-2
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<record><TEI wicri:istexFullTextTei="biblStruct"><teiHeader><fileDesc><titleStmt><title xml:lang="en">2,3,7,8-Tetrachlorodibenzo- p -dioxin induces apoptotic cell death and cytochrome P4501A expression in developing Fundulus heteroclitus embryos</title><author><name sortKey="Toomey, Barbara Holland" sort="Toomey, Barbara Holland" uniqKey="Toomey B" first="Barbara Holland" last="Toomey">Barbara Holland Toomey</name><affiliation><mods:affiliation>Nicholas School of the Environment, Duke University, Durham, NC 27709, USA</mods:affiliation></affiliation><affiliation><mods:affiliation>Corresponding author. Present address: 411 Millbrook Road, Middletown, CT 06457-5543, USA. Tel.: +1-860-3449634</mods:affiliation></affiliation><affiliation><mods:affiliation>E-mail: btoomey@dellnet.com</mods:affiliation></affiliation></author><author><name sortKey="Bello, Susan" sort="Bello, Susan" uniqKey="Bello S" first="Susan" last="Bello">Susan Bello</name><affiliation><mods:affiliation>Woods Hole Oceanographic Institute, Woods Hole, MA 02543, USA</mods:affiliation></affiliation></author><author><name sortKey="Hahn, Mark E" sort="Hahn, Mark E" uniqKey="Hahn M" first="Mark E." last="Hahn">Mark E. 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Tel.: +1-919-6138024; fax: +1-919-6848741.</mods:affiliation></affiliation><affiliation><mods:affiliation>E-mail: richd@acpub.duke.edu</mods:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">ISTEX</idno><idno type="RBID">ISTEX:DAF6218914F5191CEE4942071E5602A7D7D0C403</idno><date when="2001" year="2001">2001</date><idno type="doi">10.1016/S0166-445X(00)00161-2</idno><idno type="url">https://api.istex.fr/document/DAF6218914F5191CEE4942071E5602A7D7D0C403/fulltext/pdf</idno><idno type="wicri:Area/Istex/Corpus">000463</idno></publicationStmt><sourceDesc><biblStruct><analytic><title level="a" type="main" xml:lang="en">2,3,7,8-Tetrachlorodibenzo- p -dioxin induces apoptotic cell death and cytochrome P4501A expression in developing Fundulus heteroclitus embryos</title><author><name sortKey="Toomey, Barbara Holland" sort="Toomey, Barbara Holland" uniqKey="Toomey B" first="Barbara Holland" last="Toomey">Barbara Holland Toomey</name><affiliation><mods:affiliation>Nicholas School of the Environment, Duke University, Durham, NC 27709, USA</mods:affiliation></affiliation><affiliation><mods:affiliation>Corresponding author. Present address: 411 Millbrook Road, Middletown, CT 06457-5543, USA. Tel.: +1-860-3449634</mods:affiliation></affiliation><affiliation><mods:affiliation>E-mail: btoomey@dellnet.com</mods:affiliation></affiliation></author><author><name sortKey="Bello, Susan" sort="Bello, Susan" uniqKey="Bello S" first="Susan" last="Bello">Susan Bello</name><affiliation><mods:affiliation>Woods Hole Oceanographic Institute, Woods Hole, MA 02543, USA</mods:affiliation></affiliation></author><author><name sortKey="Hahn, Mark E" sort="Hahn, Mark E" uniqKey="Hahn M" first="Mark E." last="Hahn">Mark E. Hahn</name><affiliation><mods:affiliation>Woods Hole Oceanographic Institute, Woods Hole, MA 02543, USA</mods:affiliation></affiliation></author><author><name sortKey="Cantrell, Susannah" sort="Cantrell, Susannah" uniqKey="Cantrell S" first="Susannah" last="Cantrell">Susannah Cantrell</name><affiliation><mods:affiliation>Columbia Environmental Research Center, USGS, Columbia, MO 65201, USA</mods:affiliation></affiliation><affiliation><mods:affiliation>Department of Biochemistry, University of Missouri, Columbia, MO 65202, USA</mods:affiliation></affiliation></author><author><name sortKey="Wright, Peggy" sort="Wright, Peggy" uniqKey="Wright P" first="Peggy" last="Wright">Peggy Wright</name><affiliation><mods:affiliation>Columbia Environmental Research Center, USGS, Columbia, MO 65201, USA</mods:affiliation></affiliation><affiliation><mods:affiliation>Department of Fisheries and Wildlife Sciences, University of Missouri, Columbia, MO 65202, USA</mods:affiliation></affiliation></author><author><name sortKey="Tillitt, Donald E" sort="Tillitt, Donald E" uniqKey="Tillitt D" first="Donald E." last="Tillitt">Donald E. Tillitt</name><affiliation><mods:affiliation>Columbia Environmental Research Center, USGS, Columbia, MO 65201, USA</mods:affiliation></affiliation></author><author><name sortKey="Di Giulio, Richard T" sort="Di Giulio, Richard T" uniqKey="Di Giulio R" first="Richard T." last="Di Giulio">Richard T. Di Giulio</name><affiliation><mods:affiliation>Nicholas School of the Environment, Duke University, Durham, NC 27709, USA</mods:affiliation></affiliation><affiliation><mods:affiliation>1 Also corresponding author. Tel.: +1-919-6138024; fax: +1-919-6848741.</mods:affiliation></affiliation><affiliation><mods:affiliation>E-mail: richd@acpub.duke.edu</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">Aquatic Toxicology</title><title level="j" type="abbrev">AQTOX</title><idno type="ISSN">0166-445X</idno><imprint><publisher>ELSEVIER</publisher><date type="published" when="2000">2000</date><biblScope unit="volume">53</biblScope><biblScope unit="issue">2</biblScope><biblScope unit="page" from="127">127</biblScope><biblScope unit="page" to="138">138</biblScope></imprint><idno type="ISSN">0166-445X</idno></series><idno type="istex">DAF6218914F5191CEE4942071E5602A7D7D0C403</idno><idno type="DOI">10.1016/S0166-445X(00)00161-2</idno><idno type="PII">S0166-445X(00)00161-2</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0166-445X</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Apoptosis</term><term>Cell death</term><term>Cytochrome P450</term><term>Embryo</term><term>Fundulus</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Fundulus heteroclitus embryos were exposed to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) during early development using nanoinjection or water bath exposure. TCDD caused developmental abnormalities that included hemorrhaging, loss of vascular integrity, edema, stunted development and death. The LC50 and LD50 of TCDD for Fundulus embryos were ∼19.7±9.5 pg TCDD/μl (water bath) and 0.25±0.09 ng TCDD/g embryo (nanoinjection). To identify a possible cause for these developmental abnormalities we analyzed the effects of TCDD on apoptotic cell death and cytochrome P4501A (CYP1A) expression in the embryos. TCDD exposure increased apoptotic cell death in several tissues including brain, eye, gill, kidney, tail, intestine, heart, and vascular tissue. CYP1A expression was also increased in the TCDD-exposed embryos predominantly in liver, kidney, gill, heart, intestine, and in vascular tissues throughout the embryo. There was co-occurrence of TCDD-induced apoptosis and CYP1A expression in some, but not all, cell types. In addition the dose response relationships for apoptosis and mortality were similar, while CYP1A expression appeared more sensitive to TCDD induction.</div></front></TEI><istex><corpusName>elsevier</corpusName><author><json:item><name>Barbara Holland Toomey</name><affiliations><json:string>Nicholas School of the Environment, Duke University, Durham, NC 27709, USA</json:string><json:string>Corresponding author. Present address: 411 Millbrook Road, Middletown, CT 06457-5543, USA. Tel.: +1-860-3449634</json:string><json:string>E-mail: btoomey@dellnet.com</json:string></affiliations></json:item><json:item><name>Susan Bello</name><affiliations><json:string>Woods Hole Oceanographic Institute, Woods Hole, MA 02543, USA</json:string></affiliations></json:item><json:item><name>Mark E. Hahn</name><affiliations><json:string>Woods Hole Oceanographic Institute, Woods Hole, MA 02543, USA</json:string></affiliations></json:item><json:item><name>Susannah Cantrell</name><affiliations><json:string>Columbia Environmental Research Center, USGS, Columbia, MO 65201, USA</json:string><json:string>Department of Biochemistry, University of Missouri, Columbia, MO 65202, USA</json:string></affiliations></json:item><json:item><name>Peggy Wright</name><affiliations><json:string>Columbia Environmental Research Center, USGS, Columbia, MO 65201, USA</json:string><json:string>Department of Fisheries and Wildlife Sciences, University of Missouri, Columbia, MO 65202, USA</json:string></affiliations></json:item><json:item><name>Donald E. Tillitt</name><affiliations><json:string>Columbia Environmental Research Center, USGS, Columbia, MO 65201, USA</json:string></affiliations></json:item><json:item><name>Richard T. Di Giulio</name><affiliations><json:string>Nicholas School of the Environment, Duke University, Durham, NC 27709, USA</json:string><json:string>1 Also corresponding author. Tel.: +1-919-6138024; fax: +1-919-6848741.</json:string><json:string>E-mail: richd@acpub.duke.edu</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>Apoptosis</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Cell death</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Cytochrome P450</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Embryo</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Fundulus</value></json:item></subject><language><json:string>eng</json:string></language><abstract>Fundulus heteroclitus embryos were exposed to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) during early development using nanoinjection or water bath exposure. TCDD caused developmental abnormalities that included hemorrhaging, loss of vascular integrity, edema, stunted development and death. The LC50 and LD50 of TCDD for Fundulus embryos were ∼19.7±9.5 pg TCDD/μl (water bath) and 0.25±0.09 ng TCDD/g embryo (nanoinjection). To identify a possible cause for these developmental abnormalities we analyzed the effects of TCDD on apoptotic cell death and cytochrome P4501A (CYP1A) expression in the embryos. TCDD exposure increased apoptotic cell death in several tissues including brain, eye, gill, kidney, tail, intestine, heart, and vascular tissue. CYP1A expression was also increased in the TCDD-exposed embryos predominantly in liver, kidney, gill, heart, intestine, and in vascular tissues throughout the embryo. There was co-occurrence of TCDD-induced apoptosis and CYP1A expression in some, but not all, cell types. In addition the dose response relationships for apoptosis and mortality were similar, while CYP1A expression appeared more sensitive to TCDD induction.</abstract><qualityIndicators><score>6.932</score><pdfVersion>1.2</pdfVersion><pdfPageSize>536 x 674 pts</pdfPageSize><refBibsNative>true</refBibsNative><keywordCount>5</keywordCount><abstractCharCount>1174</abstractCharCount><pdfWordCount>5570</pdfWordCount><pdfCharCount>34812</pdfCharCount><pdfPageCount>12</pdfPageCount><abstractWordCount>161</abstractWordCount></qualityIndicators><title>2,3,7,8-Tetrachlorodibenzo- p -dioxin induces apoptotic cell death and cytochrome P4501A expression in developing Fundulus heteroclitus embryos</title><pii><json:string>S0166-445X(00)00161-2</json:string></pii><genre><json:string>research-article</json:string></genre><host><volume>53</volume><pii><json:string>S0166-445X(00)X0070-7</json:string></pii><pages><last>138</last><first>127</first></pages><issn><json:string>0166-445X</json:string></issn><issue>2</issue><genre></genre><language><json:string>unknown</json:string></language><title>Aquatic Toxicology</title><publicationDate>2001</publicationDate></host><categories><wos><json:string>MARINE & FRESHWATER BIOLOGY</json:string><json:string>TOXICOLOGY</json:string><json:string>TRANSPLANTATION</json:string></wos></categories><publicationDate>2000</publicationDate><copyrightDate>2001</copyrightDate><doi><json:string>10.1016/S0166-445X(00)00161-2</json:string></doi><id>DAF6218914F5191CEE4942071E5602A7D7D0C403</id><fulltext><json:item><original>true</original><mimetype>application/pdf</mimetype><extension>pdf</extension><uri>https://api.istex.fr/document/DAF6218914F5191CEE4942071E5602A7D7D0C403/fulltext/pdf</uri></json:item><json:item><original>false</original><mimetype>application/zip</mimetype><extension>zip</extension><uri>https://api.istex.fr/document/DAF6218914F5191CEE4942071E5602A7D7D0C403/fulltext/zip</uri></json:item><istex:fulltextTEI uri="https://api.istex.fr/document/DAF6218914F5191CEE4942071E5602A7D7D0C403/fulltext/tei"><teiHeader><fileDesc><titleStmt><title level="a" type="main" xml:lang="en">2,3,7,8-Tetrachlorodibenzo- p -dioxin induces apoptotic cell death and cytochrome P4501A expression in developing Fundulus heteroclitus embryos</title></titleStmt><publicationStmt><authority>ISTEX</authority><publisher>ELSEVIER</publisher><availability><p>ELSEVIER</p></availability><date>2001</date></publicationStmt><notesStmt><note type="content">Fig. 1: Mortality of Fundulus embryos exposed to TCDD via microinjection (A) or water bath exposure (B). Embryos were exposed to TCDD during early development and viability was assessed through hatching. The percent of dead embryos (those lacking a heartbeat, pericardial sac, or circulating blood) vs. dose of TCDD are graphed with values representing the average of three experiments for (A) and six experiments for (B). Error bars represent S.E.M.</note><note type="content">Fig. 2: Graphs of cell death in tissues of Fundulus embryos exposed to TCDD. Embryos were exposed to TCDD for 2 h in early development and were allowed to develop to three different stages [early (A), mid (B), and late (C)] before analysis of cell death. The bars represent the number of TUNEL-positive cells in several tissues of embryos exposed to increasing concentrations of TCDD (Unt.=0 pg/μl TCDD; 6.1 pg/μl TCDD, 12.5 pg/μl TCDD, and 50 pg/μl TCDD). Error bars represent S.E.M. ***P<0.001, **P<0.01, *P<0.1.</note><note type="content">Fig. 3: Photomicrographs of late stage Fundulus embryos after the TUNEL assay. Control embryos (A) show background autoflourescence but very little bright, punctate staining that is apparent in TCDD-exposed embryos (B–D). Embryos exposed to 12.5 (B) and 50 (C) pg/μl TCDD have an increase in the number of TUNEL-positive cells (arrows) in several tissue including gill, brain, eye and intestine. The photomicrograph in (D) is a higher magnification of (B) showing the bright, punctate and scattered nature of the TUNEL-positive cells.</note><note type="content">Fig. 4: Graphs of the CYP1A staining index in tissues of Fundulus embryos exposed to TCDD. Embryos were exposed to TCDD for 2 h in early development and were allowed to develop to three different stages early (A), mid (B), and late (C) before analysis of CYP1A expression. The bars represent the average staining index in several tissues of embryos exposed to increasing concentrations of TCDD (Unt.=0 pg/μl TCDD; 6.1 pg/μl TCDD, 12.5 pg/μl TCDD, and 50 pg/μl TCDD). Error bars represent S.E.M. ***P<0.001, **P<0.01, *P<0.1.</note><note type="content">Fig. 5: Photomicrographs of Late stage Fundulus embryos after immunostaining for CYP1A. The control embryo (A) has no reddish brown CYP1A labeling. Embryos exposed to 6.1 pg/μl TCDD (B) have increased CYP1A staining in the kidney and vascular cells in the gill and intestine.The embryo exposed to 12.5 pg/μl TCDD also has a large increase in staining in the liver and vasculature, and the embryo exposed to 50 pg/μl TCDD has very dark CYP1A staining in the embryonic vasculature, kidney, liver, intestine and gill.</note></notesStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a" type="main" xml:lang="en">2,3,7,8-Tetrachlorodibenzo- p -dioxin induces apoptotic cell death and cytochrome P4501A expression in developing Fundulus heteroclitus embryos</title><author><persName><forename type="first">Barbara Holland</forename><surname>Toomey</surname></persName><email>btoomey@dellnet.com</email><affiliation>Nicholas School of the Environment, Duke University, Durham, NC 27709, USA</affiliation><affiliation>Corresponding author. Present address: 411 Millbrook Road, Middletown, CT 06457-5543, USA. Tel.: +1-860-3449634</affiliation></author><author><persName><forename type="first">Susan</forename><surname>Bello</surname></persName><affiliation>Woods Hole Oceanographic Institute, Woods Hole, MA 02543, USA</affiliation></author><author><persName><forename type="first">Mark E.</forename><surname>Hahn</surname></persName><affiliation>Woods Hole Oceanographic Institute, Woods Hole, MA 02543, USA</affiliation></author><author><persName><forename type="first">Susannah</forename><surname>Cantrell</surname></persName><affiliation>Columbia Environmental Research Center, USGS, Columbia, MO 65201, USA</affiliation><affiliation>Department of Biochemistry, University of Missouri, Columbia, MO 65202, USA</affiliation></author><author><persName><forename type="first">Peggy</forename><surname>Wright</surname></persName><affiliation>Columbia Environmental Research Center, USGS, Columbia, MO 65201, USA</affiliation><affiliation>Department of Fisheries and Wildlife Sciences, University of Missouri, Columbia, MO 65202, USA</affiliation></author><author><persName><forename type="first">Donald E.</forename><surname>Tillitt</surname></persName><affiliation>Columbia Environmental Research Center, USGS, Columbia, MO 65201, USA</affiliation></author><author><persName><forename type="first">Richard T.</forename><surname>Di Giulio</surname></persName><email>richd@acpub.duke.edu</email><affiliation>Nicholas School of the Environment, Duke University, Durham, NC 27709, USA</affiliation><affiliation>1 Also corresponding author. Tel.: +1-919-6138024; fax: +1-919-6848741.</affiliation></author></analytic><monogr><title level="j">Aquatic Toxicology</title><title level="j" type="abbrev">AQTOX</title><idno type="pISSN">0166-445X</idno><idno type="PII">S0166-445X(00)X0070-7</idno><imprint><publisher>ELSEVIER</publisher><date type="published" when="2000"></date><biblScope unit="volume">53</biblScope><biblScope unit="issue">2</biblScope><biblScope unit="page" from="127">127</biblScope><biblScope unit="page" to="138">138</biblScope></imprint></monogr><idno type="istex">DAF6218914F5191CEE4942071E5602A7D7D0C403</idno><idno type="DOI">10.1016/S0166-445X(00)00161-2</idno><idno type="PII">S0166-445X(00)00161-2</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>2001</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>Fundulus heteroclitus embryos were exposed to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) during early development using nanoinjection or water bath exposure. TCDD caused developmental abnormalities that included hemorrhaging, loss of vascular integrity, edema, stunted development and death. The LC50 and LD50 of TCDD for Fundulus embryos were ∼19.7±9.5 pg TCDD/μl (water bath) and 0.25±0.09 ng TCDD/g embryo (nanoinjection). To identify a possible cause for these developmental abnormalities we analyzed the effects of TCDD on apoptotic cell death and cytochrome P4501A (CYP1A) expression in the embryos. TCDD exposure increased apoptotic cell death in several tissues including brain, eye, gill, kidney, tail, intestine, heart, and vascular tissue. CYP1A expression was also increased in the TCDD-exposed embryos predominantly in liver, kidney, gill, heart, intestine, and in vascular tissues throughout the embryo. There was co-occurrence of TCDD-induced apoptosis and CYP1A expression in some, but not all, cell types. In addition the dose response relationships for apoptosis and mortality were similar, while CYP1A expression appeared more sensitive to TCDD induction.</p></abstract><textClass xml:lang="en"><keywords scheme="keyword"><list><head>Keywords</head><item><term>Apoptosis</term></item><item><term>Cell death</term></item><item><term>Cytochrome P450</term></item><item><term>Embryo</term></item><item><term>Fundulus</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="2000-08-08">Registration</change><change when="2000-08-01">Modified</change><change when="2000">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><original>false</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/DAF6218914F5191CEE4942071E5602A7D7D0C403/fulltext/txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="Elsevier, elements deleted: ce:floats; body; tail"><istex:xmlDeclaration>version="1.0" encoding="utf-8"</istex:xmlDeclaration><istex:docType PUBLIC="-//ES//DTD journal article DTD version 4.5.2//EN//XML" URI="art452.dtd" name="istex:docType"><istex:entity SYSTEM="gr1" NDATA="IMAGE" name="gr1"></istex:entity><istex:entity SYSTEM="gr2" NDATA="IMAGE" name="gr2"></istex:entity><istex:entity SYSTEM="gr3" NDATA="IMAGE" name="gr3"></istex:entity><istex:entity SYSTEM="gr4" NDATA="IMAGE" name="gr4"></istex:entity><istex:entity SYSTEM="gr5" NDATA="IMAGE" name="gr5"></istex:entity></istex:docType><istex:document><converted-article version="4.5.2" docsubtype="fla" xml:lang="en"><item-info><jid>AQTOX</jid><aid>1217</aid><ce:pii>S0166-445X(00)00161-2</ce:pii><ce:doi>10.1016/S0166-445X(00)00161-2</ce:doi><ce:copyright type="full-transfer" year="2001">Elsevier Science B.V.</ce:copyright></item-info><head><ce:title>2,3,7,8-Tetrachlorodibenzo-<ce:italic>p</ce:italic>-dioxin induces apoptotic cell death and cytochrome P4501A expression in developing <ce:italic>Fundulus heteroclitus</ce:italic> embryos</ce:title><ce:author-group><ce:author><ce:given-name>Barbara Holland</ce:given-name><ce:surname>Toomey</ce:surname><ce:cross-ref refid="AFF1"><ce:sup>a</ce:sup></ce:cross-ref><ce:cross-ref refid="CORR1">*</ce:cross-ref><ce:e-address>btoomey@dellnet.com</ce:e-address></ce:author><ce:author><ce:given-name>Susan</ce:given-name><ce:surname>Bello</ce:surname><ce:cross-ref refid="AFF2"><ce:sup>b</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>Mark E.</ce:given-name><ce:surname>Hahn</ce:surname><ce:cross-ref refid="AFF2"><ce:sup>b</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>Susannah</ce:given-name><ce:surname>Cantrell</ce:surname><ce:cross-ref refid="AFF3"><ce:sup>c</ce:sup></ce:cross-ref><ce:cross-ref refid="AFF4"><ce:sup>d</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>Peggy</ce:given-name><ce:surname>Wright</ce:surname><ce:cross-ref refid="AFF3"><ce:sup>c</ce:sup></ce:cross-ref><ce:cross-ref refid="AFF5"><ce:sup>e</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>Donald E.</ce:given-name><ce:surname>Tillitt</ce:surname><ce:cross-ref refid="AFF3"><ce:sup>c</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>Richard T.</ce:given-name><ce:surname>Di Giulio</ce:surname><ce:cross-ref refid="FN1"><ce:sup>1</ce:sup></ce:cross-ref><ce:cross-ref refid="AFF1"><ce:sup>a</ce:sup></ce:cross-ref><ce:e-address>richd@acpub.duke.edu</ce:e-address></ce:author><ce:affiliation id="AFF1"><ce:label>a</ce:label><ce:textfn>Nicholas School of the Environment, Duke University, Durham, NC 27709, USA</ce:textfn></ce:affiliation><ce:affiliation id="AFF2"><ce:label>b</ce:label><ce:textfn>Woods Hole Oceanographic Institute, Woods Hole, MA 02543, USA</ce:textfn></ce:affiliation><ce:affiliation id="AFF3"><ce:label>c</ce:label><ce:textfn>Columbia Environmental Research Center, USGS, Columbia, MO 65201, USA</ce:textfn></ce:affiliation><ce:affiliation id="AFF4"><ce:label>d</ce:label><ce:textfn>Department of Biochemistry, University of Missouri, Columbia, MO 65202, USA</ce:textfn></ce:affiliation><ce:affiliation id="AFF5"><ce:label>e</ce:label><ce:textfn>Department of Fisheries and Wildlife Sciences, University of Missouri, Columbia, MO 65202, USA</ce:textfn></ce:affiliation><ce:correspondence id="CORR1"><ce:label>*</ce:label><ce:text>Corresponding author. Present address: 411 Millbrook Road, Middletown, CT 06457-5543, USA. Tel.: +1-860-3449634</ce:text></ce:correspondence><ce:footnote id="FN1"><ce:label>1</ce:label><ce:note-para>Also corresponding author. Tel.: +1-919-6138024; fax: +1-919-6848741.</ce:note-para></ce:footnote></ce:author-group><ce:date-received day="25" month="2" year="2000"></ce:date-received><ce:date-revised day="1" month="8" year="2000"></ce:date-revised><ce:date-accepted day="8" month="8" year="2000"></ce:date-accepted><ce:abstract><ce:section-title>Abstract</ce:section-title><ce:abstract-sec><ce:simple-para><ce:italic>Fundulus heteroclitus</ce:italic> embryos were exposed to 2,3,7,8-tetrachlorodibenzo-<ce:italic>p</ce:italic>-dioxin (TCDD) during early development using nanoinjection or water bath exposure. TCDD caused developmental abnormalities that included hemorrhaging, loss of vascular integrity, edema, stunted development and death. The LC<ce:inf>50</ce:inf> and LD<ce:inf>50</ce:inf> of TCDD for <ce:italic>Fundulus</ce:italic> embryos were ∼19.7±9.5 pg TCDD/μl (water bath) and 0.25±0.09 ng TCDD/g embryo (nanoinjection). To identify a possible cause for these developmental abnormalities we analyzed the effects of TCDD on apoptotic cell death and cytochrome P4501A (CYP1A) expression in the embryos. TCDD exposure increased apoptotic cell death in several tissues including brain, eye, gill, kidney, tail, intestine, heart, and vascular tissue. CYP1A expression was also increased in the TCDD-exposed embryos predominantly in liver, kidney, gill, heart, intestine, and in vascular tissues throughout the embryo. There was co-occurrence of TCDD-induced apoptosis and CYP1A expression in some, but not all, cell types. In addition the dose response relationships for apoptosis and mortality were similar, while CYP1A expression appeared more sensitive to TCDD induction.</ce:simple-para></ce:abstract-sec></ce:abstract><ce:keywords class="keyword"><ce:section-title>Keywords</ce:section-title><ce:keyword><ce:text>Apoptosis</ce:text></ce:keyword><ce:keyword><ce:text>Cell death</ce:text></ce:keyword><ce:keyword><ce:text>Cytochrome P450</ce:text></ce:keyword><ce:keyword><ce:text>Embryo</ce:text></ce:keyword><ce:keyword><ce:text><ce:italic>Fundulus</ce:italic></ce:text></ce:keyword></ce:keywords></head></converted-article></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>2,3,7,8-Tetrachlorodibenzo- p -dioxin induces apoptotic cell death and cytochrome P4501A expression in developing Fundulus heteroclitus embryos</title></titleInfo><titleInfo type="alternative" lang="en" contentType="CDATA"><title>2,3,7,8-Tetrachlorodibenzo-</title></titleInfo><name type="personal"><namePart type="given">Barbara Holland</namePart><namePart type="family">Toomey</namePart><affiliation>Nicholas School of the Environment, Duke University, Durham, NC 27709, USA</affiliation><affiliation>Corresponding author. Present address: 411 Millbrook Road, Middletown, CT 06457-5543, USA. Tel.: +1-860-3449634</affiliation><affiliation>E-mail: btoomey@dellnet.com</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Susan</namePart><namePart type="family">Bello</namePart><affiliation>Woods Hole Oceanographic Institute, Woods Hole, MA 02543, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Mark E.</namePart><namePart type="family">Hahn</namePart><affiliation>Woods Hole Oceanographic Institute, Woods Hole, MA 02543, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Susannah</namePart><namePart type="family">Cantrell</namePart><affiliation>Columbia Environmental Research Center, USGS, Columbia, MO 65201, USA</affiliation><affiliation>Department of Biochemistry, University of Missouri, Columbia, MO 65202, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Peggy</namePart><namePart type="family">Wright</namePart><affiliation>Columbia Environmental Research Center, USGS, Columbia, MO 65201, USA</affiliation><affiliation>Department of Fisheries and Wildlife Sciences, University of Missouri, Columbia, MO 65202, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Donald E.</namePart><namePart type="family">Tillitt</namePart><affiliation>Columbia Environmental Research Center, USGS, Columbia, MO 65201, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Richard T.</namePart><namePart type="family">Di Giulio</namePart><affiliation>Nicholas School of the Environment, Duke University, Durham, NC 27709, USA</affiliation><affiliation>1 Also corresponding author. Tel.: +1-919-6138024; fax: +1-919-6848741.</affiliation><affiliation>E-mail: richd@acpub.duke.edu</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="research-article" displayLabel="Full-length article"></genre><originInfo><publisher>ELSEVIER</publisher><dateIssued encoding="w3cdtf">2000</dateIssued><dateValid encoding="w3cdtf">2000-08-08</dateValid><dateModified encoding="w3cdtf">2000-08-01</dateModified><copyrightDate encoding="w3cdtf">2001</copyrightDate></originInfo><language><languageTerm type="code" authority="iso639-2b">eng</languageTerm><languageTerm type="code" authority="rfc3066">en</languageTerm></language><physicalDescription><internetMediaType>text/html</internetMediaType></physicalDescription><abstract lang="en">Fundulus heteroclitus embryos were exposed to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) during early development using nanoinjection or water bath exposure. TCDD caused developmental abnormalities that included hemorrhaging, loss of vascular integrity, edema, stunted development and death. The LC50 and LD50 of TCDD for Fundulus embryos were ∼19.7±9.5 pg TCDD/μl (water bath) and 0.25±0.09 ng TCDD/g embryo (nanoinjection). To identify a possible cause for these developmental abnormalities we analyzed the effects of TCDD on apoptotic cell death and cytochrome P4501A (CYP1A) expression in the embryos. TCDD exposure increased apoptotic cell death in several tissues including brain, eye, gill, kidney, tail, intestine, heart, and vascular tissue. CYP1A expression was also increased in the TCDD-exposed embryos predominantly in liver, kidney, gill, heart, intestine, and in vascular tissues throughout the embryo. There was co-occurrence of TCDD-induced apoptosis and CYP1A expression in some, but not all, cell types. In addition the dose response relationships for apoptosis and mortality were similar, while CYP1A expression appeared more sensitive to TCDD induction.</abstract><note type="content">Fig. 1: Mortality of Fundulus embryos exposed to TCDD via microinjection (A) or water bath exposure (B). Embryos were exposed to TCDD during early development and viability was assessed through hatching. The percent of dead embryos (those lacking a heartbeat, pericardial sac, or circulating blood) vs. dose of TCDD are graphed with values representing the average of three experiments for (A) and six experiments for (B). Error bars represent S.E.M.</note><note type="content">Fig. 2: Graphs of cell death in tissues of Fundulus embryos exposed to TCDD. Embryos were exposed to TCDD for 2 h in early development and were allowed to develop to three different stages [early (A), mid (B), and late (C)] before analysis of cell death. The bars represent the number of TUNEL-positive cells in several tissues of embryos exposed to increasing concentrations of TCDD (Unt.=0 pg/μl TCDD; 6.1 pg/μl TCDD, 12.5 pg/μl TCDD, and 50 pg/μl TCDD). Error bars represent S.E.M. ***P<0.001, **P<0.01, *P<0.1.</note><note type="content">Fig. 3: Photomicrographs of late stage Fundulus embryos after the TUNEL assay. Control embryos (A) show background autoflourescence but very little bright, punctate staining that is apparent in TCDD-exposed embryos (B–D). Embryos exposed to 12.5 (B) and 50 (C) pg/μl TCDD have an increase in the number of TUNEL-positive cells (arrows) in several tissue including gill, brain, eye and intestine. The photomicrograph in (D) is a higher magnification of (B) showing the bright, punctate and scattered nature of the TUNEL-positive cells.</note><note type="content">Fig. 4: Graphs of the CYP1A staining index in tissues of Fundulus embryos exposed to TCDD. Embryos were exposed to TCDD for 2 h in early development and were allowed to develop to three different stages early (A), mid (B), and late (C) before analysis of CYP1A expression. The bars represent the average staining index in several tissues of embryos exposed to increasing concentrations of TCDD (Unt.=0 pg/μl TCDD; 6.1 pg/μl TCDD, 12.5 pg/μl TCDD, and 50 pg/μl TCDD). Error bars represent S.E.M. ***P<0.001, **P<0.01, *P<0.1.</note><note type="content">Fig. 5: Photomicrographs of Late stage Fundulus embryos after immunostaining for CYP1A. The control embryo (A) has no reddish brown CYP1A labeling. Embryos exposed to 6.1 pg/μl TCDD (B) have increased CYP1A staining in the kidney and vascular cells in the gill and intestine.The embryo exposed to 12.5 pg/μl TCDD also has a large increase in staining in the liver and vasculature, and the embryo exposed to 50 pg/μl TCDD has very dark CYP1A staining in the embryonic vasculature, kidney, liver, intestine and gill.</note><subject lang="en"><genre>Keywords</genre><topic>Apoptosis</topic><topic>Cell death</topic><topic>Cytochrome P450</topic><topic>Embryo</topic><topic>Fundulus</topic></subject><relatedItem type="host"><titleInfo><title>Aquatic Toxicology</title></titleInfo><titleInfo type="abbreviated"><title>AQTOX</title></titleInfo><genre type="Journal">journal</genre><originInfo><dateIssued encoding="w3cdtf">20010701</dateIssued></originInfo><identifier type="ISSN">0166-445X</identifier><identifier type="PII">S0166-445X(00)X0070-7</identifier><part><date>20010701</date><detail type="volume"><number>53</number><caption>vol.</caption></detail><detail type="issue"><number>2</number><caption>no.</caption></detail><extent unit="issue pages"><start>79</start><end>152</end></extent><extent unit="pages"><start>127</start><end>138</end></extent></part></relatedItem><identifier type="istex">DAF6218914F5191CEE4942071E5602A7D7D0C403</identifier><identifier type="DOI">10.1016/S0166-445X(00)00161-2</identifier><identifier type="PII">S0166-445X(00)00161-2</identifier><accessCondition type="use and reproduction" contentType="">© 2001Elsevier Science B.V.</accessCondition><recordInfo><recordContentSource>ELSEVIER</recordContentSource><recordOrigin>Elsevier Science B.V., ©2001</recordOrigin></recordInfo></mods></metadata><enrichments><istex:catWosTEI uri="https://api.istex.fr/document/DAF6218914F5191CEE4942071E5602A7D7D0C403/enrichments/catWos"><teiHeader><profileDesc><textClass><classCode scheme="WOS">MARINE & FRESHWATER BIOLOGY</classCode><classCode scheme="WOS">TOXICOLOGY</classCode><classCode scheme="WOS">TRANSPLANTATION</classCode></textClass></profileDesc></teiHeader></istex:catWosTEI></enrichments><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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