A comparison of the dose and time response of CYP1A1 mRNA induction in chemically treated Atlantic tomcod from two populations
Identifieur interne : 001319 ( Istex/Corpus ); précédent : 001318; suivant : 001320A comparison of the dose and time response of CYP1A1 mRNA induction in chemically treated Atlantic tomcod from two populations
Auteurs : Simon C. Courtenay ; Cheryl M. Grunwald ; Guat-Lian Kreamer ; Wayne L. Fairchild ; Jacqueline T. Arsenault ; Michael Ikonomou ; Isaac I. WirginSource :
- Aquatic Toxicology [ 0166-445X ] ; 1999.
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Abstract
Quantification of cytochrome P4501A1 (CYP1A1) mRNA levels in environmentally exposed Atlantic tomcod (Microgadus tomcod) has revealed significantly induced gene expression in fish from contaminated locales including the Hudson River, New York, and the Miramichi River, New Brunswick. In order to calibrate this response, determine its sensitivity and dose-responsiveness, levels of hepatic CYP1A1 mRNA were quantified in depurated Atlantic tomcod intraperitoneally (i.p.) injected with various concentrations of: β-naphthoflavone (β-NF), the PAH benzo[a]pyrene (B[a]P), the non-ortho coplanar PCB congener-3,3′,4,4′- tetrachlorobiphenyl (IUPAC: PCB-77), and the dioxin 2,3,7,8-tetrachlorodibenzo-p-dioxin (2,3,7,8-TCDD). Additionally, the rates of CYP1A1 mRNA induction and disappearance were quantified in depurated Atlantic tomcod i.p. injected with single doses of these chemicals and sacrificed at times ranging up to 72 days. Levels of CYP1A1 mRNA were dose-responsive for all four chemicals with maximum induction ranging from 50- to 460-fold and first significant induction being observed in the low mg per kg fish (wet weight) range for β-NF and B[a]P, μg/kg range for PCB-77 and ng/kg range for 2,3,7,8-TCDD. However, while tomcod from the Miramichi River responded to both PAHs and halogenated aromatic hydrocarbons (HAHs), Hudson River tomcod responded only to PAHs indicating population level differences in CYP1A1 mRNA inducibility in tomcod. Furthermore, differences in the responsiveness to PAHs and HAHs suggest that more than one molecular mechanism mediates CYP1A1 transcription in Atlantic tomcod. Kinetic profiles of CYP1A1 mRNA induction differed greatly between tomcod treated with HAHs and PAHs. Initial induction occurred within hours of treatment with PAHs and peaked after 1–3 days, compared to initial induction 4–7 days after treatment with HAHs, and maximum induction not occurring for up to 72 days after exposure. Quantification of halogenated aromatic hydrocarbons (HAH) in the livers of tomcod caught in the Hudson and Miramichi Rivers confirmed exposure and accumulation of known CYP1A1 inducing chemicals including 2,3,7,8-TCDD at concentrations as high as 1.5 μg/kg lipid (554 ng/kg w.w.) and PCB-77 at concentrations as high as 108 μg/kg lipid (15 μg/kg w.w.). These results suggest that hepatic CYP1A1 mRNA concentration can be a useful bioindicator of exposure to some aromatic hydrocarbon compounds in the aquatic environment and that profiles of gene induction and disappearance may help identify environmental inducers provided that gene responsiveness is also evaluated under controlled laboratory conditions.
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DOI: 10.1016/S0166-445X(99)00006-5
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<record><TEI wicri:istexFullTextTei="biblStruct"><teiHeader><fileDesc><titleStmt><title xml:lang="en">A comparison of the dose and time response of CYP1A1 mRNA induction in chemically treated Atlantic tomcod from two populations</title><author><name sortKey="Courtenay, Simon C" sort="Courtenay, Simon C" uniqKey="Courtenay S" first="Simon C" last="Courtenay">Simon C. Courtenay</name><affiliation><mods:affiliation>E-mail: courtenays@mar.dfo-mpo.gc.ca</mods:affiliation></affiliation><affiliation><mods:affiliation>Fisheries and Oceans Canada, Gulf Fisheries Centre, P.O. Box 5030, Moncton, NB E1C 9B6, Canada</mods:affiliation></affiliation></author><author><name sortKey="Grunwald, Cheryl M" sort="Grunwald, Cheryl M" uniqKey="Grunwald C" first="Cheryl M" last="Grunwald">Cheryl M. Grunwald</name><affiliation><mods:affiliation>Nelson Institute of Environmental Medicine, New York University Medical Center, Long Meadow Road, Tuxedo, NY 10987, USA</mods:affiliation></affiliation></author><author><name sortKey="Kreamer, Guat Lian" sort="Kreamer, Guat Lian" uniqKey="Kreamer G" first="Guat-Lian" last="Kreamer">Guat-Lian Kreamer</name><affiliation><mods:affiliation>Nelson Institute of Environmental Medicine, New York University Medical Center, Long Meadow Road, Tuxedo, NY 10987, USA</mods:affiliation></affiliation></author><author><name sortKey="Fairchild, Wayne L" sort="Fairchild, Wayne L" uniqKey="Fairchild W" first="Wayne L" last="Fairchild">Wayne L. Fairchild</name><affiliation><mods:affiliation>Fisheries and Oceans Canada, Gulf Fisheries Centre, P.O. Box 5030, Moncton, NB E1C 9B6, Canada</mods:affiliation></affiliation></author><author><name sortKey="Arsenault, Jacqueline T" sort="Arsenault, Jacqueline T" uniqKey="Arsenault J" first="Jacqueline T" last="Arsenault">Jacqueline T. Arsenault</name><affiliation><mods:affiliation>Fisheries and Oceans Canada, Gulf Fisheries Centre, P.O. Box 5030, Moncton, NB E1C 9B6, Canada</mods:affiliation></affiliation></author><author><name sortKey="Ikonomou, Michael" sort="Ikonomou, Michael" uniqKey="Ikonomou M" first="Michael" last="Ikonomou">Michael Ikonomou</name><affiliation><mods:affiliation>Fisheries and Oceans Canada, Institute of Ocean Science, P.O. Box 9860, Sidney, BC V8L 4B2, Canada</mods:affiliation></affiliation></author><author><name sortKey="Wirgin, Isaac I" sort="Wirgin, Isaac I" uniqKey="Wirgin I" first="Isaac I" last="Wirgin">Isaac I. 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Courtenay</name><affiliation><mods:affiliation>E-mail: courtenays@mar.dfo-mpo.gc.ca</mods:affiliation></affiliation><affiliation><mods:affiliation>Fisheries and Oceans Canada, Gulf Fisheries Centre, P.O. Box 5030, Moncton, NB E1C 9B6, Canada</mods:affiliation></affiliation></author><author><name sortKey="Grunwald, Cheryl M" sort="Grunwald, Cheryl M" uniqKey="Grunwald C" first="Cheryl M" last="Grunwald">Cheryl M. Grunwald</name><affiliation><mods:affiliation>Nelson Institute of Environmental Medicine, New York University Medical Center, Long Meadow Road, Tuxedo, NY 10987, USA</mods:affiliation></affiliation></author><author><name sortKey="Kreamer, Guat Lian" sort="Kreamer, Guat Lian" uniqKey="Kreamer G" first="Guat-Lian" last="Kreamer">Guat-Lian Kreamer</name><affiliation><mods:affiliation>Nelson Institute of Environmental Medicine, New York University Medical Center, Long Meadow Road, Tuxedo, NY 10987, USA</mods:affiliation></affiliation></author><author><name sortKey="Fairchild, Wayne L" sort="Fairchild, Wayne L" uniqKey="Fairchild W" first="Wayne L" last="Fairchild">Wayne L. Fairchild</name><affiliation><mods:affiliation>Fisheries and Oceans Canada, Gulf Fisheries Centre, P.O. Box 5030, Moncton, NB E1C 9B6, Canada</mods:affiliation></affiliation></author><author><name sortKey="Arsenault, Jacqueline T" sort="Arsenault, Jacqueline T" uniqKey="Arsenault J" first="Jacqueline T" last="Arsenault">Jacqueline T. Arsenault</name><affiliation><mods:affiliation>Fisheries and Oceans Canada, Gulf Fisheries Centre, P.O. Box 5030, Moncton, NB E1C 9B6, Canada</mods:affiliation></affiliation></author><author><name sortKey="Ikonomou, Michael" sort="Ikonomou, Michael" uniqKey="Ikonomou M" first="Michael" last="Ikonomou">Michael Ikonomou</name><affiliation><mods:affiliation>Fisheries and Oceans Canada, Institute of Ocean Science, P.O. Box 9860, Sidney, BC V8L 4B2, Canada</mods:affiliation></affiliation></author><author><name sortKey="Wirgin, Isaac I" sort="Wirgin, Isaac I" uniqKey="Wirgin I" first="Isaac I" last="Wirgin">Isaac I. Wirgin</name><affiliation><mods:affiliation>Nelson Institute of Environmental Medicine, New York University Medical Center, Long Meadow Road, Tuxedo, NY 10987, USA</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="1999">1999</date><biblScope unit="volume">47</biblScope><biblScope unit="issue">1</biblScope><biblScope unit="page" from="43">43</biblScope><biblScope unit="page" to="69">69</biblScope></imprint><idno type="ISSN">0166-445X</idno></series><idno type="istex">06FA3FC513F76E119B4020DF552EB599F1563C37</idno><idno type="DOI">10.1016/S0166-445X(99)00006-5</idno><idno type="PII">S0166-445X(99)00006-5</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0166-445X</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>2,3,7,8-TCDD</term><term>Atlantic tomcod</term><term>B[a]P</term><term>CYP1A1 mRNA</term><term>Dose–response</term><term>PCB-77</term><term>Time–response</term><term>β-NF</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Quantification of cytochrome P4501A1 (CYP1A1) mRNA levels in environmentally exposed Atlantic tomcod (Microgadus tomcod) has revealed significantly induced gene expression in fish from contaminated locales including the Hudson River, New York, and the Miramichi River, New Brunswick. In order to calibrate this response, determine its sensitivity and dose-responsiveness, levels of hepatic CYP1A1 mRNA were quantified in depurated Atlantic tomcod intraperitoneally (i.p.) injected with various concentrations of: β-naphthoflavone (β-NF), the PAH benzo[a]pyrene (B[a]P), the non-ortho coplanar PCB congener-3,3′,4,4′- tetrachlorobiphenyl (IUPAC: PCB-77), and the dioxin 2,3,7,8-tetrachlorodibenzo-p-dioxin (2,3,7,8-TCDD). Additionally, the rates of CYP1A1 mRNA induction and disappearance were quantified in depurated Atlantic tomcod i.p. injected with single doses of these chemicals and sacrificed at times ranging up to 72 days. Levels of CYP1A1 mRNA were dose-responsive for all four chemicals with maximum induction ranging from 50- to 460-fold and first significant induction being observed in the low mg per kg fish (wet weight) range for β-NF and B[a]P, μg/kg range for PCB-77 and ng/kg range for 2,3,7,8-TCDD. However, while tomcod from the Miramichi River responded to both PAHs and halogenated aromatic hydrocarbons (HAHs), Hudson River tomcod responded only to PAHs indicating population level differences in CYP1A1 mRNA inducibility in tomcod. Furthermore, differences in the responsiveness to PAHs and HAHs suggest that more than one molecular mechanism mediates CYP1A1 transcription in Atlantic tomcod. Kinetic profiles of CYP1A1 mRNA induction differed greatly between tomcod treated with HAHs and PAHs. Initial induction occurred within hours of treatment with PAHs and peaked after 1–3 days, compared to initial induction 4–7 days after treatment with HAHs, and maximum induction not occurring for up to 72 days after exposure. Quantification of halogenated aromatic hydrocarbons (HAH) in the livers of tomcod caught in the Hudson and Miramichi Rivers confirmed exposure and accumulation of known CYP1A1 inducing chemicals including 2,3,7,8-TCDD at concentrations as high as 1.5 μg/kg lipid (554 ng/kg w.w.) and PCB-77 at concentrations as high as 108 μg/kg lipid (15 μg/kg w.w.). These results suggest that hepatic CYP1A1 mRNA concentration can be a useful bioindicator of exposure to some aromatic hydrocarbon compounds in the aquatic environment and that profiles of gene induction and disappearance may help identify environmental inducers provided that gene responsiveness is also evaluated under controlled laboratory conditions.</div></front></TEI><istex><corpusName>elsevier</corpusName><author><json:item><name>Simon C Courtenay</name><affiliations><json:string>E-mail: courtenays@mar.dfo-mpo.gc.ca</json:string><json:string>Fisheries and Oceans Canada, Gulf Fisheries Centre, P.O. Box 5030, Moncton, NB E1C 9B6, Canada</json:string></affiliations></json:item><json:item><name>Cheryl M Grunwald</name><affiliations><json:string>Nelson Institute of Environmental Medicine, New York University Medical Center, Long Meadow Road, Tuxedo, NY 10987, USA</json:string></affiliations></json:item><json:item><name>Guat-Lian Kreamer</name><affiliations><json:string>Nelson Institute of Environmental Medicine, New York University Medical Center, Long Meadow Road, Tuxedo, NY 10987, USA</json:string></affiliations></json:item><json:item><name>Wayne L Fairchild</name><affiliations><json:string>Fisheries and Oceans Canada, Gulf Fisheries Centre, P.O. Box 5030, Moncton, NB E1C 9B6, Canada</json:string></affiliations></json:item><json:item><name>Jacqueline T Arsenault</name><affiliations><json:string>Fisheries and Oceans Canada, Gulf Fisheries Centre, P.O. Box 5030, Moncton, NB E1C 9B6, Canada</json:string></affiliations></json:item><json:item><name>Michael Ikonomou</name><affiliations><json:string>Fisheries and Oceans Canada, Institute of Ocean Science, P.O. Box 9860, Sidney, BC V8L 4B2, Canada</json:string></affiliations></json:item><json:item><name>Isaac I Wirgin</name><affiliations><json:string>Nelson Institute of Environmental Medicine, New York University Medical Center, Long Meadow Road, Tuxedo, NY 10987, USA</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>Atlantic tomcod</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>CYP1A1 mRNA</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>β-NF</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>B[a]P</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Dose–response</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>PCB-77</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>2,3,7,8-TCDD</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Time–response</value></json:item></subject><language><json:string>eng</json:string></language><originalGenre><json:string>Full-length article</json:string></originalGenre><abstract>Quantification of cytochrome P4501A1 (CYP1A1) mRNA levels in environmentally exposed Atlantic tomcod (Microgadus tomcod) has revealed significantly induced gene expression in fish from contaminated locales including the Hudson River, New York, and the Miramichi River, New Brunswick. In order to calibrate this response, determine its sensitivity and dose-responsiveness, levels of hepatic CYP1A1 mRNA were quantified in depurated Atlantic tomcod intraperitoneally (i.p.) injected with various concentrations of: β-naphthoflavone (β-NF), the PAH benzo[a]pyrene (B[a]P), the non-ortho coplanar PCB congener-3,3′,4,4′- tetrachlorobiphenyl (IUPAC: PCB-77), and the dioxin 2,3,7,8-tetrachlorodibenzo-p-dioxin (2,3,7,8-TCDD). Additionally, the rates of CYP1A1 mRNA induction and disappearance were quantified in depurated Atlantic tomcod i.p. injected with single doses of these chemicals and sacrificed at times ranging up to 72 days. Levels of CYP1A1 mRNA were dose-responsive for all four chemicals with maximum induction ranging from 50- to 460-fold and first significant induction being observed in the low mg per kg fish (wet weight) range for β-NF and B[a]P, μg/kg range for PCB-77 and ng/kg range for 2,3,7,8-TCDD. However, while tomcod from the Miramichi River responded to both PAHs and halogenated aromatic hydrocarbons (HAHs), Hudson River tomcod responded only to PAHs indicating population level differences in CYP1A1 mRNA inducibility in tomcod. Furthermore, differences in the responsiveness to PAHs and HAHs suggest that more than one molecular mechanism mediates CYP1A1 transcription in Atlantic tomcod. Kinetic profiles of CYP1A1 mRNA induction differed greatly between tomcod treated with HAHs and PAHs. Initial induction occurred within hours of treatment with PAHs and peaked after 1–3 days, compared to initial induction 4–7 days after treatment with HAHs, and maximum induction not occurring for up to 72 days after exposure. Quantification of halogenated aromatic hydrocarbons (HAH) in the livers of tomcod caught in the Hudson and Miramichi Rivers confirmed exposure and accumulation of known CYP1A1 inducing chemicals including 2,3,7,8-TCDD at concentrations as high as 1.5 μg/kg lipid (554 ng/kg w.w.) and PCB-77 at concentrations as high as 108 μg/kg lipid (15 μg/kg w.w.). These results suggest that hepatic CYP1A1 mRNA concentration can be a useful bioindicator of exposure to some aromatic hydrocarbon compounds in the aquatic environment and that profiles of gene induction and disappearance may help identify environmental inducers provided that gene responsiveness is also evaluated under controlled laboratory conditions.</abstract><qualityIndicators><score>8</score><pdfVersion>1.2</pdfVersion><pdfPageSize>536 x 674 pts</pdfPageSize><refBibsNative>true</refBibsNative><keywordCount>8</keywordCount><abstractCharCount>2652</abstractCharCount><pdfWordCount>14464</pdfWordCount><pdfCharCount>92528</pdfCharCount><pdfPageCount>27</pdfPageCount><abstractWordCount>371</abstractWordCount></qualityIndicators><title>A comparison of the dose and time response of CYP1A1 mRNA induction in chemically treated Atlantic tomcod from two populations</title><pii><json:string>S0166-445X(99)00006-5</json:string></pii><genre><json:string>research-article</json:string></genre><serie><volume>90</volume><editor><json:item><name>E. Arinc</name></json:item><json:item><name>J.B. Schenkman</name></json:item><json:item><name>E. Hodgson</name></json:item></editor><pages><last>603</last><first>591</first></pages><language><json:string>unknown</json:string></language><title>Molecular aspects of oxidative drug metabolizing enzymes: their significance in environmental toxicology, chemical carcinogenesis and health, NATO ASI Series H: Cell Biology</title></serie><host><volume>47</volume><pii><json:string>S0166-445X(00)X0050-1</json:string></pii><pages><last>69</last><first>43</first></pages><issn><json:string>0166-445X</json:string></issn><issue>1</issue><genre><json:string>journal</json:string></genre><language><json:string>unknown</json:string></language><title>Aquatic Toxicology</title><publicationDate>1999</publicationDate></host><categories><wos><json:string>science</json:string><json:string>toxicology</json:string><json:string>marine & freshwater biology</json:string></wos><scienceMetrix><json:string>health sciences</json:string><json:string>biomedical research</json:string><json:string>toxicology</json:string></scienceMetrix></categories><publicationDate>1999</publicationDate><copyrightDate>1999</copyrightDate><doi><json:string>10.1016/S0166-445X(99)00006-5</json:string></doi><id>06FA3FC513F76E119B4020DF552EB599F1563C37</id><score>0.014426637</score><fulltext><json:item><extension>pdf</extension><original>true</original><mimetype>application/pdf</mimetype><uri>https://api.istex.fr/document/06FA3FC513F76E119B4020DF552EB599F1563C37/fulltext/pdf</uri></json:item><json:item><extension>zip</extension><original>false</original><mimetype>application/zip</mimetype><uri>https://api.istex.fr/document/06FA3FC513F76E119B4020DF552EB599F1563C37/fulltext/zip</uri></json:item><istex:fulltextTEI uri="https://api.istex.fr/document/06FA3FC513F76E119B4020DF552EB599F1563C37/fulltext/tei"><teiHeader><fileDesc><titleStmt><title level="a" type="main" xml:lang="en">A comparison of the dose and time response of CYP1A1 mRNA induction in chemically treated Atlantic tomcod from two populations</title></titleStmt><publicationStmt><authority>ISTEX</authority><publisher>ELSEVIER</publisher><availability><p>©1999 Elsevier Science B.V.</p></availability><date>1999</date></publicationStmt><notesStmt><note type="content">Fig. 1: A northern gel and hybridizations with total RNAs from Atlantic tomcod from the Miramichi River that were depurated for 75 days in clean laboratory water and treated with graded doses of 2,3,7,8-TCDD (1–500 ng/kg) as described in the text or corn oil vehicle. Gel contains five tiers of samples with up to 25 samples per tier. In Panel 1, the gel was stained with ethidium bromide and 28S and 18S rRNAs are visible. In Panel 2, RNAs were transferred to a nylon hybridization membrane and hybridized to a 32P-radiolabeled Atlantic tomcod CYP1A1 cDNA probe. In Panel 3, membrane was stripped of the CYP1A1 probe and rehybridized to a 32P-radiolabeled rat 18S rRNA probe which served as a housekeeping gene.</note><note type="content">Fig. 2: Relative mean (±1 SEM) levels of hepatic CYP1A1 mRNA (integrated optical density units) in Hudson River tomcod i.p. injected with different doses of β-naphthoflavone (β-NF) dissolved in corn oil and sacrificed 70 h later. Doses are represented on a log scale. Controls (0 mg/kg fish) were injected with corn oil and sacrificed 7 days later. *Significantly different than control at P<0.05. Numbers above bars represent sample size.</note><note type="content">Fig. 3: Relative mean (±1 SEM) levels of hepatic CYP1A1 mRNA (integrated optical density units) in Hudson River tomcod i.p. injected with different doses of benzo[a]pyrene (B[a]P) dissolved in 1:1 emulphor:acetone and sacrificed 24 h later. Doses are represented on a log scale. Controls (0 mg/kg fish) injected with 1:1 emulphor:acetone and sacrificed 24 or 48 h later (four per group) did not differ significantly and were pooled for comparison with B[a]P exposed fish. *Significantly different than control at P<0.05. Numbers above bars represent sample size.</note><note type="content">Fig. 4: Relative mean (±1 SEM) levels of hepatic CYP1A1 mRNA (integrated optical density units) in Miramichi River tomcod i.p. injected with different doses of 3,3′,4,4′- tetrachlorobiphenyl (PCB-77) dissolved in corn oil and sacrificed 7 days later. Doses are represented on a log scale. Controls (0 mg/kg fish) were injected with corn oil and sacrificed 7 days later. *Significantly different than control at P<0.05. Numbers above bars represent sample size.</note><note type="content">Fig. 5: Relative mean (±1 SEM) levels of hepatic CYP1A1 mRNA (integrated optical density units) in Miramichi River tomcod i.p. injected with different doses of 2,3,7,8-tetrachlorodibenzo-p-dioxin (2,3,7,8-TCDD) dissolved in corn oil and sacrificed 10 days later. Doses are represented on a log scale. Controls (0 mg/kg fish) were injected with corn oil and sacrificed 10 days later. *Significantly different than control at P<0.05. Numbers above bars represent sample size.</note><note type="content">Table 1: Relative mean (±1 SEM) levels of hepatic CYP1A1 mRNA in Hudson River tomcod treated with a single i.p. injection of β-naphthoflavone (β-NF) (100 mg/kg fish) dissolved in corn oil and sacrificed 4, 8, 26, 72, 120 or 168 h after treatmenta</note><note type="content">Table 2: Relative mean (±1 SEM) levels of hepatic CYP1A1 mRNA in Miramichi River tomcod treated with a single i.p. injection of β-naphthoflavone (β-NF) (100 mg/kg fish) dissolved in corn oil and sacrificed 72 h after treatmenta</note><note type="content">Table 3: Relative mean (±1 SEM) levels of hepatic CYP1A1 mRNA in Hudson River tomcod i.p. injected with benzo[a]pyrene (B[a]P) (10 mg/kg fish) dissolved in 1:1 emulphor:acetone and sacrificed 8, 24, 48, 80, 120 or 168 h after treatmenta</note><note type="content">Table 4: Relative mean (±1 SEM) levels of hepatic CYP1A1 mRNA in Hudson River tomcod i.p. injected with 3,3′,4,4′-tetrachlorobiphenyl (PCB-77) dissolved in corn oil and sacrificed 4 or 7 days latera</note><note type="content">Table 5: Relative mean (±1 SEM) levels of hepatic CYP1A1 mRNA in Miramichi River tomcod i.p. injected with 3,3′,4,4′-tetrachlorobiphenyl (PCB-77) (1 mg/kg fish) dissolved in corn oila</note><note type="content">Table 6: Relative mean (±1 SEM) levels of hepatic CYP1A1 mRNA in Hudson River tomcod i.p. injected with 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) (0.5 μg/kg fish) dissolved in corn oila</note><note type="content">Table 7: Relative mean (±1 SEM) levels of hepatic CYP1A1 mRNA in Miramichi River tomcod treated with a single i.p. injection of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) (0.5 μg/kg fish) dissolved in corn oila</note><note type="content">Table 8: Concentrations of chlorinated hydrocarbons that have been shown to induce CYP1A in fish (Stegeman and Hahn 1994) found in livers of Atlantic tomcod from the relatively undeveloped Margaree River (Nova Scotia, Canada; 13 October 1993), the moderately industrialized Miramichi River (New Brunswick, Canada; 8 September 1993) and from two sites in the heavily industrialized Hudson River estuary (New York, USA): Garrison, NY, on the main Hudson River at River Mile 50 (22 December 1997), and the Hackensack River approximately 2–5 km upstream from Newark Bay (17 December 1996)a</note></notesStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a" type="main" xml:lang="en">A comparison of the dose and time response of CYP1A1 mRNA induction in chemically treated Atlantic tomcod from two populations</title><author xml:id="author-1"><persName><forename type="first">Simon C</forename><surname>Courtenay</surname></persName><email>courtenays@mar.dfo-mpo.gc.ca</email><note type="correspondence"><p>Corresponding author. Tel.: +1-506-851-6709; fax +1-506-851-2079</p></note><affiliation>Fisheries and Oceans Canada, Gulf Fisheries Centre, P.O. Box 5030, Moncton, NB E1C 9B6, Canada</affiliation></author><author xml:id="author-2"><persName><forename type="first">Cheryl M</forename><surname>Grunwald</surname></persName><affiliation>Nelson Institute of Environmental Medicine, New York University Medical Center, Long Meadow Road, Tuxedo, NY 10987, USA</affiliation></author><author xml:id="author-3"><persName><forename type="first">Guat-Lian</forename><surname>Kreamer</surname></persName><affiliation>Nelson Institute of Environmental Medicine, New York University Medical Center, Long Meadow Road, Tuxedo, NY 10987, USA</affiliation></author><author xml:id="author-4"><persName><forename type="first">Wayne L</forename><surname>Fairchild</surname></persName><affiliation>Fisheries and Oceans Canada, Gulf Fisheries Centre, P.O. Box 5030, Moncton, NB E1C 9B6, Canada</affiliation></author><author xml:id="author-5"><persName><forename type="first">Jacqueline T</forename><surname>Arsenault</surname></persName><affiliation>Fisheries and Oceans Canada, Gulf Fisheries Centre, P.O. Box 5030, Moncton, NB E1C 9B6, Canada</affiliation></author><author xml:id="author-6"><persName><forename type="first">Michael</forename><surname>Ikonomou</surname></persName><affiliation>Fisheries and Oceans Canada, Institute of Ocean Science, P.O. Box 9860, Sidney, BC V8L 4B2, Canada</affiliation></author><author xml:id="author-7"><persName><forename type="first">Isaac I</forename><surname>Wirgin</surname></persName><affiliation>Nelson Institute of Environmental Medicine, New York University Medical Center, Long Meadow Road, Tuxedo, NY 10987, USA</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)X0050-1</idno><imprint><publisher>ELSEVIER</publisher><date type="published" when="1999"></date><biblScope unit="volume">47</biblScope><biblScope unit="issue">1</biblScope><biblScope unit="page" from="43">43</biblScope><biblScope unit="page" to="69">69</biblScope></imprint></monogr><idno type="istex">06FA3FC513F76E119B4020DF552EB599F1563C37</idno><idno type="DOI">10.1016/S0166-445X(99)00006-5</idno><idno type="PII">S0166-445X(99)00006-5</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>1999</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>Quantification of cytochrome P4501A1 (CYP1A1) mRNA levels in environmentally exposed Atlantic tomcod (Microgadus tomcod) has revealed significantly induced gene expression in fish from contaminated locales including the Hudson River, New York, and the Miramichi River, New Brunswick. In order to calibrate this response, determine its sensitivity and dose-responsiveness, levels of hepatic CYP1A1 mRNA were quantified in depurated Atlantic tomcod intraperitoneally (i.p.) injected with various concentrations of: β-naphthoflavone (β-NF), the PAH benzo[a]pyrene (B[a]P), the non-ortho coplanar PCB congener-3,3′,4,4′- tetrachlorobiphenyl (IUPAC: PCB-77), and the dioxin 2,3,7,8-tetrachlorodibenzo-p-dioxin (2,3,7,8-TCDD). Additionally, the rates of CYP1A1 mRNA induction and disappearance were quantified in depurated Atlantic tomcod i.p. injected with single doses of these chemicals and sacrificed at times ranging up to 72 days. Levels of CYP1A1 mRNA were dose-responsive for all four chemicals with maximum induction ranging from 50- to 460-fold and first significant induction being observed in the low mg per kg fish (wet weight) range for β-NF and B[a]P, μg/kg range for PCB-77 and ng/kg range for 2,3,7,8-TCDD. However, while tomcod from the Miramichi River responded to both PAHs and halogenated aromatic hydrocarbons (HAHs), Hudson River tomcod responded only to PAHs indicating population level differences in CYP1A1 mRNA inducibility in tomcod. Furthermore, differences in the responsiveness to PAHs and HAHs suggest that more than one molecular mechanism mediates CYP1A1 transcription in Atlantic tomcod. Kinetic profiles of CYP1A1 mRNA induction differed greatly between tomcod treated with HAHs and PAHs. Initial induction occurred within hours of treatment with PAHs and peaked after 1–3 days, compared to initial induction 4–7 days after treatment with HAHs, and maximum induction not occurring for up to 72 days after exposure. Quantification of halogenated aromatic hydrocarbons (HAH) in the livers of tomcod caught in the Hudson and Miramichi Rivers confirmed exposure and accumulation of known CYP1A1 inducing chemicals including 2,3,7,8-TCDD at concentrations as high as 1.5 μg/kg lipid (554 ng/kg w.w.) and PCB-77 at concentrations as high as 108 μg/kg lipid (15 μg/kg w.w.). These results suggest that hepatic CYP1A1 mRNA concentration can be a useful bioindicator of exposure to some aromatic hydrocarbon compounds in the aquatic environment and that profiles of gene induction and disappearance may help identify environmental inducers provided that gene responsiveness is also evaluated under controlled laboratory conditions.</p></abstract><textClass xml:lang="en"><keywords scheme="keyword"><list><head>Keywords</head><item><term>Atlantic tomcod</term></item><item><term>CYP1A1 mRNA</term></item><item><term>β-NF</term></item><item><term>B[a]P</term></item><item><term>Dose–response</term></item><item><term>PCB-77</term></item><item><term>2,3,7,8-TCDD</term></item><item><term>Time–response</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="1998-12-22">Modified</change><change when="1999">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><extension>txt</extension><original>false</original><mimetype>text/plain</mimetype><uri>https://api.istex.fr/document/06FA3FC513F76E119B4020DF552EB599F1563C37/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>1042</aid><ce:pii>S0166-445X(99)00006-5</ce:pii><ce:doi>10.1016/S0166-445X(99)00006-5</ce:doi><ce:copyright type="full-transfer" year="1999">Elsevier Science B.V.</ce:copyright></item-info><head><ce:title>A comparison of the dose and time response of CYP1A1 mRNA induction in chemically treated Atlantic tomcod from two populations</ce:title><ce:author-group><ce:author><ce:given-name>Simon C</ce:given-name><ce:surname>Courtenay</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>courtenays@mar.dfo-mpo.gc.ca</ce:e-address></ce:author><ce:author><ce:given-name>Cheryl M</ce:given-name><ce:surname>Grunwald</ce:surname><ce:cross-ref refid="AFF2"><ce:sup>b</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>Guat-Lian</ce:given-name><ce:surname>Kreamer</ce:surname><ce:cross-ref refid="AFF2"><ce:sup>b</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>Wayne L</ce:given-name><ce:surname>Fairchild</ce:surname><ce:cross-ref refid="AFF1"><ce:sup>a</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>Jacqueline T</ce:given-name><ce:surname>Arsenault</ce:surname><ce:cross-ref refid="AFF1"><ce:sup>a</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>Michael</ce:given-name><ce:surname>Ikonomou</ce:surname><ce:cross-ref refid="AFF3"><ce:sup>c</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>Isaac I</ce:given-name><ce:surname>Wirgin</ce:surname><ce:cross-ref refid="AFF2"><ce:sup>b</ce:sup></ce:cross-ref></ce:author><ce:affiliation id="AFF1"><ce:label>a</ce:label><ce:textfn>Fisheries and Oceans Canada, Gulf Fisheries Centre, P.O. Box 5030, Moncton, NB E1C 9B6, Canada</ce:textfn></ce:affiliation><ce:affiliation id="AFF2"><ce:label>b</ce:label><ce:textfn>Nelson Institute of Environmental Medicine, New York University Medical Center, Long Meadow Road, Tuxedo, NY 10987, USA</ce:textfn></ce:affiliation><ce:affiliation id="AFF3"><ce:label>c</ce:label><ce:textfn>Fisheries and Oceans Canada, Institute of Ocean Science, P.O. Box 9860, Sidney, BC V8L 4B2, Canada</ce:textfn></ce:affiliation><ce:correspondence id="CORR1"><ce:label>*</ce:label><ce:text>Corresponding author. Tel.: +1-506-851-6709; fax +1-506-851-2079</ce:text></ce:correspondence></ce:author-group><ce:date-received day="20" month="3" year="1997"></ce:date-received><ce:date-revised day="22" month="12" year="1998"></ce:date-revised><ce:date-accepted day="17" month="1" year="1999"></ce:date-accepted><ce:abstract><ce:section-title>Abstract</ce:section-title><ce:abstract-sec><ce:simple-para>Quantification of cytochrome P4501A1 (CYP1A1) mRNA levels in environmentally exposed Atlantic tomcod (<ce:italic>Microgadus tomcod</ce:italic>) has revealed significantly induced gene expression in fish from contaminated locales including the Hudson River, New York, and the Miramichi River, New Brunswick. In order to calibrate this response, determine its sensitivity and dose-responsiveness, levels of hepatic CYP1A1 mRNA were quantified in depurated Atlantic tomcod intraperitoneally (i.p.) injected with various concentrations of: β-naphthoflavone (β-NF), the PAH benzo[<ce:italic>a</ce:italic>]pyrene (B[<ce:italic>a</ce:italic>]P), the non-<ce:italic>ortho</ce:italic> coplanar PCB congener-3,3′,4,4′- tetrachlorobiphenyl (IUPAC: PCB-77), and the dioxin 2,3,7,8-tetrachlorodibenzo<ce:italic>-p-</ce:italic>dioxin (2,3,7,8-TCDD). Additionally, the rates of CYP1A1 mRNA induction and disappearance were quantified in depurated Atlantic tomcod i.p. injected with single doses of these chemicals and sacrificed at times ranging up to 72 days. Levels of CYP1A1 mRNA were dose-responsive for all four chemicals with maximum induction ranging from 50- to 460-fold and first significant induction being observed in the low mg per kg fish (wet weight) range for β-NF and B[<ce:italic>a</ce:italic>]P, μg/kg range for PCB-77 and ng/kg range for 2,3,7,8-TCDD. However, while tomcod from the Miramichi River responded to both PAHs and halogenated aromatic hydrocarbons (HAHs), Hudson River tomcod responded only to PAHs indicating population level differences in CYP1A1 mRNA inducibility in tomcod. Furthermore, differences in the responsiveness to PAHs and HAHs suggest that more than one molecular mechanism mediates CYP1A1 transcription in Atlantic tomcod. Kinetic profiles of CYP1A1 mRNA induction differed greatly between tomcod treated with HAHs and PAHs. Initial induction occurred within hours of treatment with PAHs and peaked after 1–3 days, compared to initial induction 4–7 days after treatment with HAHs, and maximum induction not occurring for up to 72 days after exposure. Quantification of halogenated aromatic hydrocarbons (HAH) in the livers of tomcod caught in the Hudson and Miramichi Rivers confirmed exposure and accumulation of known CYP1A1 inducing chemicals including 2,3,7,8-TCDD at concentrations as high as 1.5 μg/kg lipid (554 ng/kg w.w.) and PCB-77 at concentrations as high as 108 μg/kg lipid (15 μg/kg w.w.). These results suggest that hepatic CYP1A1 mRNA concentration can be a useful bioindicator of exposure to some aromatic hydrocarbon compounds in the aquatic environment and that profiles of gene induction and disappearance may help identify environmental inducers provided that gene responsiveness is also evaluated under controlled laboratory conditions.</ce:simple-para></ce:abstract-sec></ce:abstract><ce:keywords class="keyword"><ce:section-title>Keywords</ce:section-title><ce:keyword><ce:text>Atlantic tomcod</ce:text></ce:keyword><ce:keyword><ce:text>CYP1A1 mRNA</ce:text></ce:keyword><ce:keyword><ce:text>β-NF</ce:text></ce:keyword><ce:keyword><ce:text>B[<ce:italic>a</ce:italic>]P</ce:text></ce:keyword><ce:keyword><ce:text>Dose–response</ce:text></ce:keyword><ce:keyword><ce:text>PCB-77</ce:text></ce:keyword><ce:keyword><ce:text>2,3,7,8-TCDD</ce:text></ce:keyword><ce:keyword><ce:text>Time–response</ce:text></ce:keyword></ce:keywords></head></converted-article></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>A comparison of the dose and time response of CYP1A1 mRNA induction in chemically treated Atlantic tomcod from two populations</title></titleInfo><titleInfo type="alternative" lang="en" contentType="CDATA"><title>A comparison of the dose and time response of CYP1A1 mRNA induction in chemically treated Atlantic tomcod from two populations</title></titleInfo><name type="personal"><namePart type="given">Simon C</namePart><namePart type="family">Courtenay</namePart><affiliation>E-mail: courtenays@mar.dfo-mpo.gc.ca</affiliation><affiliation>Fisheries and Oceans Canada, Gulf Fisheries Centre, P.O. Box 5030, Moncton, NB E1C 9B6, Canada</affiliation><description>Corresponding author. Tel.: +1-506-851-6709; fax +1-506-851-2079</description><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Cheryl M</namePart><namePart type="family">Grunwald</namePart><affiliation>Nelson Institute of Environmental Medicine, New York University Medical Center, Long Meadow Road, Tuxedo, NY 10987, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Guat-Lian</namePart><namePart type="family">Kreamer</namePart><affiliation>Nelson Institute of Environmental Medicine, New York University Medical Center, Long Meadow Road, Tuxedo, NY 10987, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Wayne L</namePart><namePart type="family">Fairchild</namePart><affiliation>Fisheries and Oceans Canada, Gulf Fisheries Centre, P.O. Box 5030, Moncton, NB E1C 9B6, Canada</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Jacqueline T</namePart><namePart type="family">Arsenault</namePart><affiliation>Fisheries and Oceans Canada, Gulf Fisheries Centre, P.O. Box 5030, Moncton, NB E1C 9B6, Canada</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Michael</namePart><namePart type="family">Ikonomou</namePart><affiliation>Fisheries and Oceans Canada, Institute of Ocean Science, P.O. Box 9860, Sidney, BC V8L 4B2, Canada</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Isaac I</namePart><namePart type="family">Wirgin</namePart><affiliation>Nelson Institute of Environmental Medicine, New York University Medical Center, Long Meadow Road, Tuxedo, NY 10987, USA</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">1999</dateIssued><dateModified encoding="w3cdtf">1998-12-22</dateModified><copyrightDate encoding="w3cdtf">1999</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">Quantification of cytochrome P4501A1 (CYP1A1) mRNA levels in environmentally exposed Atlantic tomcod (Microgadus tomcod) has revealed significantly induced gene expression in fish from contaminated locales including the Hudson River, New York, and the Miramichi River, New Brunswick. In order to calibrate this response, determine its sensitivity and dose-responsiveness, levels of hepatic CYP1A1 mRNA were quantified in depurated Atlantic tomcod intraperitoneally (i.p.) injected with various concentrations of: β-naphthoflavone (β-NF), the PAH benzo[a]pyrene (B[a]P), the non-ortho coplanar PCB congener-3,3′,4,4′- tetrachlorobiphenyl (IUPAC: PCB-77), and the dioxin 2,3,7,8-tetrachlorodibenzo-p-dioxin (2,3,7,8-TCDD). Additionally, the rates of CYP1A1 mRNA induction and disappearance were quantified in depurated Atlantic tomcod i.p. injected with single doses of these chemicals and sacrificed at times ranging up to 72 days. Levels of CYP1A1 mRNA were dose-responsive for all four chemicals with maximum induction ranging from 50- to 460-fold and first significant induction being observed in the low mg per kg fish (wet weight) range for β-NF and B[a]P, μg/kg range for PCB-77 and ng/kg range for 2,3,7,8-TCDD. However, while tomcod from the Miramichi River responded to both PAHs and halogenated aromatic hydrocarbons (HAHs), Hudson River tomcod responded only to PAHs indicating population level differences in CYP1A1 mRNA inducibility in tomcod. Furthermore, differences in the responsiveness to PAHs and HAHs suggest that more than one molecular mechanism mediates CYP1A1 transcription in Atlantic tomcod. Kinetic profiles of CYP1A1 mRNA induction differed greatly between tomcod treated with HAHs and PAHs. Initial induction occurred within hours of treatment with PAHs and peaked after 1–3 days, compared to initial induction 4–7 days after treatment with HAHs, and maximum induction not occurring for up to 72 days after exposure. Quantification of halogenated aromatic hydrocarbons (HAH) in the livers of tomcod caught in the Hudson and Miramichi Rivers confirmed exposure and accumulation of known CYP1A1 inducing chemicals including 2,3,7,8-TCDD at concentrations as high as 1.5 μg/kg lipid (554 ng/kg w.w.) and PCB-77 at concentrations as high as 108 μg/kg lipid (15 μg/kg w.w.). These results suggest that hepatic CYP1A1 mRNA concentration can be a useful bioindicator of exposure to some aromatic hydrocarbon compounds in the aquatic environment and that profiles of gene induction and disappearance may help identify environmental inducers provided that gene responsiveness is also evaluated under controlled laboratory conditions.</abstract><note type="content">Fig. 1: A northern gel and hybridizations with total RNAs from Atlantic tomcod from the Miramichi River that were depurated for 75 days in clean laboratory water and treated with graded doses of 2,3,7,8-TCDD (1–500 ng/kg) as described in the text or corn oil vehicle. Gel contains five tiers of samples with up to 25 samples per tier. In Panel 1, the gel was stained with ethidium bromide and 28S and 18S rRNAs are visible. In Panel 2, RNAs were transferred to a nylon hybridization membrane and hybridized to a 32P-radiolabeled Atlantic tomcod CYP1A1 cDNA probe. In Panel 3, membrane was stripped of the CYP1A1 probe and rehybridized to a 32P-radiolabeled rat 18S rRNA probe which served as a housekeeping gene.</note><note type="content">Fig. 2: Relative mean (±1 SEM) levels of hepatic CYP1A1 mRNA (integrated optical density units) in Hudson River tomcod i.p. injected with different doses of β-naphthoflavone (β-NF) dissolved in corn oil and sacrificed 70 h later. Doses are represented on a log scale. Controls (0 mg/kg fish) were injected with corn oil and sacrificed 7 days later. *Significantly different than control at P<0.05. Numbers above bars represent sample size.</note><note type="content">Fig. 3: Relative mean (±1 SEM) levels of hepatic CYP1A1 mRNA (integrated optical density units) in Hudson River tomcod i.p. injected with different doses of benzo[a]pyrene (B[a]P) dissolved in 1:1 emulphor:acetone and sacrificed 24 h later. Doses are represented on a log scale. Controls (0 mg/kg fish) injected with 1:1 emulphor:acetone and sacrificed 24 or 48 h later (four per group) did not differ significantly and were pooled for comparison with B[a]P exposed fish. *Significantly different than control at P<0.05. Numbers above bars represent sample size.</note><note type="content">Fig. 4: Relative mean (±1 SEM) levels of hepatic CYP1A1 mRNA (integrated optical density units) in Miramichi River tomcod i.p. injected with different doses of 3,3′,4,4′- tetrachlorobiphenyl (PCB-77) dissolved in corn oil and sacrificed 7 days later. Doses are represented on a log scale. Controls (0 mg/kg fish) were injected with corn oil and sacrificed 7 days later. *Significantly different than control at P<0.05. Numbers above bars represent sample size.</note><note type="content">Fig. 5: Relative mean (±1 SEM) levels of hepatic CYP1A1 mRNA (integrated optical density units) in Miramichi River tomcod i.p. injected with different doses of 2,3,7,8-tetrachlorodibenzo-p-dioxin (2,3,7,8-TCDD) dissolved in corn oil and sacrificed 10 days later. Doses are represented on a log scale. Controls (0 mg/kg fish) were injected with corn oil and sacrificed 10 days later. *Significantly different than control at P<0.05. Numbers above bars represent sample size.</note><note type="content">Table 1: Relative mean (±1 SEM) levels of hepatic CYP1A1 mRNA in Hudson River tomcod treated with a single i.p. injection of β-naphthoflavone (β-NF) (100 mg/kg fish) dissolved in corn oil and sacrificed 4, 8, 26, 72, 120 or 168 h after treatmenta</note><note type="content">Table 2: Relative mean (±1 SEM) levels of hepatic CYP1A1 mRNA in Miramichi River tomcod treated with a single i.p. injection of β-naphthoflavone (β-NF) (100 mg/kg fish) dissolved in corn oil and sacrificed 72 h after treatmenta</note><note type="content">Table 3: Relative mean (±1 SEM) levels of hepatic CYP1A1 mRNA in Hudson River tomcod i.p. injected with benzo[a]pyrene (B[a]P) (10 mg/kg fish) dissolved in 1:1 emulphor:acetone and sacrificed 8, 24, 48, 80, 120 or 168 h after treatmenta</note><note type="content">Table 4: Relative mean (±1 SEM) levels of hepatic CYP1A1 mRNA in Hudson River tomcod i.p. injected with 3,3′,4,4′-tetrachlorobiphenyl (PCB-77) dissolved in corn oil and sacrificed 4 or 7 days latera</note><note type="content">Table 5: Relative mean (±1 SEM) levels of hepatic CYP1A1 mRNA in Miramichi River tomcod i.p. injected with 3,3′,4,4′-tetrachlorobiphenyl (PCB-77) (1 mg/kg fish) dissolved in corn oila</note><note type="content">Table 6: Relative mean (±1 SEM) levels of hepatic CYP1A1 mRNA in Hudson River tomcod i.p. injected with 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) (0.5 μg/kg fish) dissolved in corn oila</note><note type="content">Table 7: Relative mean (±1 SEM) levels of hepatic CYP1A1 mRNA in Miramichi River tomcod treated with a single i.p. injection of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) (0.5 μg/kg fish) dissolved in corn oila</note><note type="content">Table 8: Concentrations of chlorinated hydrocarbons that have been shown to induce CYP1A in fish (Stegeman and Hahn 1994) found in livers of Atlantic tomcod from the relatively undeveloped Margaree River (Nova Scotia, Canada; 13 October 1993), the moderately industrialized Miramichi River (New Brunswick, Canada; 8 September 1993) and from two sites in the heavily industrialized Hudson River estuary (New York, USA): Garrison, NY, on the main Hudson River at River Mile 50 (22 December 1997), and the Hackensack River approximately 2–5 km upstream from Newark Bay (17 December 1996)a</note><subject lang="en"><genre>Keywords</genre><topic>Atlantic tomcod</topic><topic>CYP1A1 mRNA</topic><topic>β-NF</topic><topic>B[a]P</topic><topic>Dose–response</topic><topic>PCB-77</topic><topic>2,3,7,8-TCDD</topic><topic>Time–response</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">199910</dateIssued></originInfo><identifier type="ISSN">0166-445X</identifier><identifier type="PII">S0166-445X(00)X0050-1</identifier><part><date>199910</date><detail type="volume"><number>47</number><caption>vol.</caption></detail><detail type="issue"><number>1</number><caption>no.</caption></detail><extent unit="issue pages"><start>1</start><end>76</end></extent><extent unit="pages"><start>43</start><end>69</end></extent></part></relatedItem><identifier type="istex">06FA3FC513F76E119B4020DF552EB599F1563C37</identifier><identifier type="DOI">10.1016/S0166-445X(99)00006-5</identifier><identifier type="PII">S0166-445X(99)00006-5</identifier><accessCondition type="use and reproduction" contentType="copyright">©1999 Elsevier Science B.V.</accessCondition><recordInfo><recordContentSource>ELSEVIER</recordContentSource><recordOrigin>Elsevier Science B.V., ©1999</recordOrigin></recordInfo></mods></metadata></istex></record>Pour manipuler ce document sous Unix (Dilib)
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