Retinoic acid hydroxylation in rainbow trout ( Oncorhynchus mykiss ) and the effect of a coplanar PCB, 3,3′,4,4′-tetrachlorobiphenyl
Identifieur interne : 000840 ( Istex/Corpus ); précédent : 000839; suivant : 000841Retinoic acid hydroxylation in rainbow trout ( Oncorhynchus mykiss ) and the effect of a coplanar PCB, 3,3′,4,4′-tetrachlorobiphenyl
Auteurs : Nicolas L. Gilbert ; Marie-Josée Cloutier ; Philip A. SpearSource :
- Aquatic Toxicology [ 0166-445X ] ; 1995.
Abstract
When liver microsomes of rainbow trout (Oncorhynchus mykiss) were incubated with [14C]-labeled retinoic acid plus NADPH, high performance liquid chromatography revealed the presence of radioactive peaks having elution times identical to those of 4-hydroxy- and 4-oxoretinoic acid. In the absence of NADPH, the radioactive peaks were not detected which is consistent with cytochrome P450-dependent 4-hydroxylation. In trout injected intraperitoneally with 5 μg/g of 3,3′,4,4′-tetrachlorobiphenyl (TCB) and sacrificed 56 days later, the hydroxylation rate was higher (P < 0.0005) compared with control trout. No difference was observed between TCB-treated and control groups 7 days after injection. In contrast, cytochrome P4501-dependent ethoxyresorufin-O-deethylase activity was significantly higher in the TCB-treated group, both at 7 and 56 days. Liver retinoid stores were not affected by TCB treatment. These results clearly demonstrate that fish metabolize retinoic acid through a hydroxylation step which can be accelerated by a cytochrome P4501-inducing coplanar PCB. Given the pronounced biological activity of retinoic acid and closely related retinoids, increased retinoic acid metabolism could explain some of the effects of PCBs in fish.
Url:
DOI: 10.1016/0166-445X(94)00091-4
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Centre-Ville, Montréal, Québec, H3C 3P8, Canada</mods:affiliation></affiliation></author><author><name sortKey="Spear, Philip A" sort="Spear, Philip A" uniqKey="Spear P" first="Philip A." last="Spear">Philip A. Spear</name><affiliation><mods:affiliation>Laboratoire TOXEN and Département des Sciences biologiques, Université du Québec à Montréal, C.P. 8888, Succ. 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Gilbert</name><affiliation><mods:affiliation>Laboratoire TOXEN and Département des Sciences biologiques, Université du Québec à Montréal, C.P. 8888, Succ. Centre-Ville, Montréal, Québec, H3C 3P8, Canada</mods:affiliation></affiliation></author><author><name sortKey="Cloutier, Marie Josee" sort="Cloutier, Marie Josee" uniqKey="Cloutier M" first="Marie-Josée" last="Cloutier">Marie-Josée Cloutier</name><affiliation><mods:affiliation>Laboratoire TOXEN and Département des Sciences biologiques, Université du Québec à Montréal, C.P. 8888, Succ. Centre-Ville, Montréal, Québec, H3C 3P8, Canada</mods:affiliation></affiliation></author><author><name sortKey="Spear, Philip A" sort="Spear, Philip A" uniqKey="Spear P" first="Philip A." last="Spear">Philip A. Spear</name><affiliation><mods:affiliation>Laboratoire TOXEN and Département des Sciences biologiques, Université du Québec à Montréal, C.P. 8888, Succ. Centre-Ville, Montréal, Québec, H3C 3P8, Canada</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="1995">1995</date><biblScope unit="volume">32</biblScope><biblScope unit="issue">2–3</biblScope><biblScope unit="page" from="177">177</biblScope><biblScope unit="page" to="187">187</biblScope></imprint><idno type="ISSN">0166-445X</idno></series><idno type="istex">07B11E4684234DBA1035377C9B0A784538FF1DCA</idno><idno type="DOI">10.1016/0166-445X(94)00091-4</idno><idno type="PII">0166-445X(94)00091-4</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0166-445X</idno></seriesStmt></fileDesc><profileDesc><textClass></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">When liver microsomes of rainbow trout (Oncorhynchus mykiss) were incubated with [14C]-labeled retinoic acid plus NADPH, high performance liquid chromatography revealed the presence of radioactive peaks having elution times identical to those of 4-hydroxy- and 4-oxoretinoic acid. In the absence of NADPH, the radioactive peaks were not detected which is consistent with cytochrome P450-dependent 4-hydroxylation. In trout injected intraperitoneally with 5 μg/g of 3,3′,4,4′-tetrachlorobiphenyl (TCB) and sacrificed 56 days later, the hydroxylation rate was higher (P < 0.0005) compared with control trout. No difference was observed between TCB-treated and control groups 7 days after injection. In contrast, cytochrome P4501-dependent ethoxyresorufin-O-deethylase activity was significantly higher in the TCB-treated group, both at 7 and 56 days. Liver retinoid stores were not affected by TCB treatment. These results clearly demonstrate that fish metabolize retinoic acid through a hydroxylation step which can be accelerated by a cytochrome P4501-inducing coplanar PCB. Given the pronounced biological activity of retinoic acid and closely related retinoids, increased retinoic acid metabolism could explain some of the effects of PCBs in fish.</div></front></TEI><istex><corpusName>elsevier</corpusName><author><json:item><name>Nicolas L. Gilbert</name><affiliations><json:string>Laboratoire TOXEN and Département des Sciences biologiques, Université du Québec à Montréal, C.P. 8888, Succ. Centre-Ville, Montréal, Québec, H3C 3P8, Canada</json:string></affiliations></json:item><json:item><name>Marie-Josée Cloutier</name><affiliations><json:string>Laboratoire TOXEN and Département des Sciences biologiques, Université du Québec à Montréal, C.P. 8888, Succ. Centre-Ville, Montréal, Québec, H3C 3P8, Canada</json:string></affiliations></json:item><json:item><name>Philip A. Spear</name><affiliations><json:string>Laboratoire TOXEN and Département des Sciences biologiques, Université du Québec à Montréal, C.P. 8888, Succ. Centre-Ville, Montréal, Québec, H3C 3P8, Canada</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>Oncorhynchus mykiss</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Vitamin A</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>EROD</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>4-hydroxyretinoic acid</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>4-oxoretinoic acid</value></json:item></subject><language><json:string>eng</json:string></language><originalGenre><json:string>Full-length article</json:string></originalGenre><abstract>When liver microsomes of rainbow trout (Oncorhynchus mykiss) were incubated with [14C]-labeled retinoic acid plus NADPH, high performance liquid chromatography revealed the presence of radioactive peaks having elution times identical to those of 4-hydroxy- and 4-oxoretinoic acid. In the absence of NADPH, the radioactive peaks were not detected which is consistent with cytochrome P450-dependent 4-hydroxylation. In trout injected intraperitoneally with 5 μg/g of 3,3′,4,4′-tetrachlorobiphenyl (TCB) and sacrificed 56 days later, the hydroxylation rate was higher (P > 0.0005) compared with control trout. No difference was observed between TCB-treated and control groups 7 days after injection. In contrast, cytochrome P4501-dependent ethoxyresorufin-O-deethylase activity was significantly higher in the TCB-treated group, both at 7 and 56 days. Liver retinoid stores were not affected by TCB treatment. These results clearly demonstrate that fish metabolize retinoic acid through a hydroxylation step which can be accelerated by a cytochrome P4501-inducing coplanar PCB. 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Centre-Ville, Montréal, Québec, H3C 3P8, Canada</affiliation></author><author xml:id="author-2"><persName><forename type="first">Marie-Josée</forename><surname>Cloutier</surname></persName><affiliation>Laboratoire TOXEN and Département des Sciences biologiques, Université du Québec à Montréal, C.P. 8888, Succ. Centre-Ville, Montréal, Québec, H3C 3P8, Canada</affiliation></author><author xml:id="author-3"><persName><forename type="first">Philip A.</forename><surname>Spear</surname></persName><affiliation>Laboratoire TOXEN and Département des Sciences biologiques, Université du Québec à Montréal, C.P. 8888, Succ. Centre-Ville, Montréal, Québec, H3C 3P8, Canada</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)X0010-0</idno><imprint><publisher>ELSEVIER</publisher><date type="published" when="1995"></date><biblScope unit="volume">32</biblScope><biblScope unit="issue">2–3</biblScope><biblScope unit="page" from="177">177</biblScope><biblScope unit="page" to="187">187</biblScope></imprint></monogr><idno type="istex">07B11E4684234DBA1035377C9B0A784538FF1DCA</idno><idno type="DOI">10.1016/0166-445X(94)00091-4</idno><idno type="PII">0166-445X(94)00091-4</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>1995</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>When liver microsomes of rainbow trout (Oncorhynchus mykiss) were incubated with [14C]-labeled retinoic acid plus NADPH, high performance liquid chromatography revealed the presence of radioactive peaks having elution times identical to those of 4-hydroxy- and 4-oxoretinoic acid. In the absence of NADPH, the radioactive peaks were not detected which is consistent with cytochrome P450-dependent 4-hydroxylation. In trout injected intraperitoneally with 5 μg/g of 3,3′,4,4′-tetrachlorobiphenyl (TCB) and sacrificed 56 days later, the hydroxylation rate was higher (P < 0.0005) compared with control trout. No difference was observed between TCB-treated and control groups 7 days after injection. In contrast, cytochrome P4501-dependent ethoxyresorufin-O-deethylase activity was significantly higher in the TCB-treated group, both at 7 and 56 days. Liver retinoid stores were not affected by TCB treatment. These results clearly demonstrate that fish metabolize retinoic acid through a hydroxylation step which can be accelerated by a cytochrome P4501-inducing coplanar PCB. Given the pronounced biological activity of retinoic acid and closely related retinoids, increased retinoic acid metabolism could explain some of the effects of PCBs in fish.</p></abstract><textClass><keywords scheme="keyword"><list><head>Keywords</head><item><term>Oncorhynchus mykiss</term></item><item><term>Vitamin A</term></item><item><term>EROD</term></item><item><term>4-hydroxyretinoic acid</term></item><item><term>4-oxoretinoic acid</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="1995">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><extension>txt</extension><original>false</original><mimetype>text/plain</mimetype><uri>https://api.istex.fr/document/07B11E4684234DBA1035377C9B0A784538FF1DCA/fulltext/txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="Elsevier, elements deleted: 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:docType><istex:document><converted-article version="4.5.2" docsubtype="fla"><item-info><jid>AQTOX</jid><aid>94000914</aid><ce:pii>0166-445X(94)00091-4</ce:pii><ce:doi>10.1016/0166-445X(94)00091-4</ce:doi><ce:copyright type="unknown" year="1995"></ce:copyright></item-info><head><ce:title>Retinoic acid hydroxylation in rainbow trout (<ce:italic>Oncorhynchus mykiss</ce:italic>) and the effect of a coplanar PCB, 3,3′,4,4′-tetrachlorobiphenyl</ce:title><ce:author-group><ce:author><ce:given-name>Nicolas L.</ce:given-name><ce:surname>Gilbert</ce:surname><ce:cross-ref refid="COR1"><ce:sup>∗</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>Marie-Josée</ce:given-name><ce:surname>Cloutier</ce:surname></ce:author><ce:author><ce:given-name>Philip A.</ce:given-name><ce:surname>Spear</ce:surname></ce:author><ce:affiliation><ce:textfn>Laboratoire TOXEN and Département des Sciences biologiques, Université du Québec à Montréal, C.P. 8888, Succ. Centre-Ville, Montréal, Québec, H3C 3P8, Canada</ce:textfn></ce:affiliation><ce:correspondence id="COR1"><ce:label>∗</ce:label><ce:text>Corresponding author.</ce:text></ce:correspondence></ce:author-group><ce:date-received day="13" month="5" year="1994"></ce:date-received><ce:date-accepted day="15" month="11" year="1994"></ce:date-accepted><ce:abstract><ce:section-title>Abstract</ce:section-title><ce:abstract-sec><ce:simple-para>When liver microsomes of rainbow trout (<ce:italic>Oncorhynchus mykiss</ce:italic>) were incubated with [<ce:sup loc="pre">14</ce:sup>C]-labeled retinoic acid plus NADPH, high performance liquid chromatography revealed the presence of radioactive peaks having elution times identical to those of 4-hydroxy- and 4-oxoretinoic acid. In the absence of NADPH, the radioactive peaks were not detected which is consistent with cytochrome P450-dependent 4-hydroxylation. In trout injected intraperitoneally with 5 μg/g of 3,3′,4,4′-tetrachlorobiphenyl (TCB) and sacrificed 56 days later, the hydroxylation rate was higher (<ce:italic>P</ce:italic> < 0.0005) compared with control trout. No difference was observed between TCB-treated and control groups 7 days after injection. In contrast, cytochrome P4501-dependent ethoxyresorufin-<ce:italic>O</ce:italic>-deethylase activity was significantly higher in the TCB-treated group, both at 7 and 56 days. Liver retinoid stores were not affected by TCB treatment. These results clearly demonstrate that fish metabolize retinoic acid through a hydroxylation step which can be accelerated by a cytochrome P4501-inducing coplanar PCB. Given the pronounced biological activity of retinoic acid and closely related retinoids, increased retinoic acid metabolism could explain some of the effects of PCBs in fish.</ce:simple-para></ce:abstract-sec></ce:abstract><ce:keywords><ce:section-title>Keywords</ce:section-title><ce:keyword><ce:text><ce:italic>Oncorhynchus mykiss</ce:italic></ce:text></ce:keyword><ce:keyword><ce:text>Vitamin A</ce:text></ce:keyword><ce:keyword><ce:text>EROD</ce:text></ce:keyword><ce:keyword><ce:text>4-hydroxyretinoic acid</ce:text></ce:keyword><ce:keyword><ce:text>4-oxoretinoic acid</ce:text></ce:keyword></ce:keywords></head></converted-article></istex:document></istex:metadataXml><mods version="3.6"><titleInfo><title>Retinoic acid hydroxylation in rainbow trout ( Oncorhynchus mykiss ) and the effect of a coplanar PCB, 3,3′,4,4′-tetrachlorobiphenyl</title></titleInfo><titleInfo type="alternative" contentType="CDATA"><title>Retinoic acid hydroxylation in rainbow trout (</title></titleInfo><name type="personal"><namePart type="given">Nicolas L.</namePart><namePart type="family">Gilbert</namePart><affiliation>Laboratoire TOXEN and Département des Sciences biologiques, Université du Québec à Montréal, C.P. 8888, Succ. Centre-Ville, Montréal, Québec, H3C 3P8, Canada</affiliation><description>Corresponding author.</description><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Marie-Josée</namePart><namePart type="family">Cloutier</namePart><affiliation>Laboratoire TOXEN and Département des Sciences biologiques, Université du Québec à Montréal, C.P. 8888, Succ. Centre-Ville, Montréal, Québec, H3C 3P8, Canada</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Philip A.</namePart><namePart type="family">Spear</namePart><affiliation>Laboratoire TOXEN and Département des Sciences biologiques, Université du Québec à Montréal, C.P. 8888, Succ. Centre-Ville, Montréal, Québec, H3C 3P8, Canada</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">1995</dateIssued><copyrightDate encoding="w3cdtf">1995</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">When liver microsomes of rainbow trout (Oncorhynchus mykiss) were incubated with [14C]-labeled retinoic acid plus NADPH, high performance liquid chromatography revealed the presence of radioactive peaks having elution times identical to those of 4-hydroxy- and 4-oxoretinoic acid. In the absence of NADPH, the radioactive peaks were not detected which is consistent with cytochrome P450-dependent 4-hydroxylation. In trout injected intraperitoneally with 5 μg/g of 3,3′,4,4′-tetrachlorobiphenyl (TCB) and sacrificed 56 days later, the hydroxylation rate was higher (P < 0.0005) compared with control trout. No difference was observed between TCB-treated and control groups 7 days after injection. In contrast, cytochrome P4501-dependent ethoxyresorufin-O-deethylase activity was significantly higher in the TCB-treated group, both at 7 and 56 days. Liver retinoid stores were not affected by TCB treatment. These results clearly demonstrate that fish metabolize retinoic acid through a hydroxylation step which can be accelerated by a cytochrome P4501-inducing coplanar PCB. Given the pronounced biological activity of retinoic acid and closely related retinoids, increased retinoic acid metabolism could explain some of the effects of PCBs in fish.</abstract><subject><genre>Keywords</genre><topic>Oncorhynchus mykiss</topic><topic>Vitamin A</topic><topic>EROD</topic><topic>4-hydroxyretinoic acid</topic><topic>4-oxoretinoic acid</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">199506</dateIssued></originInfo><identifier type="ISSN">0166-445X</identifier><identifier type="PII">S0166-445X(00)X0010-0</identifier><part><date>199506</date><detail type="volume"><number>32</number><caption>vol.</caption></detail><detail type="issue"><number>2–3</number><caption>no.</caption></detail><extent unit="issue pages"><start>93</start><end>269</end></extent><extent unit="pages"><start>177</start><end>187</end></extent></part></relatedItem><identifier type="istex">07B11E4684234DBA1035377C9B0A784538FF1DCA</identifier><identifier type="DOI">10.1016/0166-445X(94)00091-4</identifier><identifier type="PII">0166-445X(94)00091-4</identifier><recordInfo><recordContentSource>ELSEVIER</recordContentSource></recordInfo></mods></metadata></istex></record>Pour manipuler ce document sous Unix (Dilib)
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