PCBs and PBBs: Biologic and toxic effects on C57BL/6J and DBA/2J inbred mice
Identifieur interne : 004F89 ( Main/Exploration ); précédent : 004F88; suivant : 004F90PCBs and PBBs: Biologic and toxic effects on C57BL/6J and DBA/2J inbred mice
Auteurs : Larry W. Robertson [États-Unis, Allemagne] ; Andrew Parkinson [Canada, États-Unis] ; Stelvio Bandiera [États-Unis] ; Iain Lambert [États-Unis] ; Jill Merrill [États-Unis] ; Stephen H. Safe [Canada]Source :
- Toxicology [ 0300-483X ] ; 1984.
Abstract
Treatment of genetically inbred “responsive” C57BL/6J and ”non-responsive” DBA/2J mice with Aroclor 1254 or fireMaster BP-6 resulted in the induction of hepatic microsomal benzo[a]pyrene hydroxylase only in the former mouse strain and aminopyrine N-demethylase in both strains of mice. In contrast, 3,3′,4,4′,5-pentachlorobiphenyl and 3,3′,4,4′-tetrabromobiphenyl, induced benzo[a]pyrene hydroxylase in both C57BL/6J and DBA/2J but did not enhance aminopyrine N-demethylase in either strain of mouse. Boo these coplanar halogenated biphenyls also caused thymic atrophy in the responsive and non-responsive mice and their effects resembled those of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). Treatment of the inbred mice with several mono-ortho substituted analogs of the coplanar halogenated biphenyls, including 2,3,3′,4,4′-pentachloro-, 2,3′,4,4′,5-pentabromo, 2,3,3′,4,4′,5-hexachloro- and 3′,4′-dibromo-2,3,4,5-tetrachlorobiphenyl, gave hepatic enzyme-induction results similar to those observed for the commercial halogenated biphenyls. At dose levels of 1500 μmol/kg, most of these compounds caused thymic atrophy in C57BL/6J mice but not in DBA/2J mice. The structure-activity correlations in the mice complement similar studies with the halogenated biphenyls in rats and support the proposed receptor-mediated mechanism for the toxic halogenated aromatics.
Url:
DOI: 10.1016/0300-483X(84)90101-X
Affiliations:
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Robertson</name><affiliation wicri:level="1"><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Veterinary Physiology and Pharmacology, Texas A&M University, College Station</wicri:regionArea><wicri:noRegion>College Station</wicri:noRegion></affiliation><affiliation wicri:level="3"><country xml:lang="fr" wicri:curation="lc">Allemagne</country><wicri:regionArea>∗ Present address: Pharmakologisches Institute, Obere Zahlbacher Strasse 67, D-6500 Mainz</wicri:regionArea><placeName><region type="land" nuts="2">Rhénanie-Palatinat</region><settlement type="city">Mayence</settlement></placeName></affiliation></author><author><name sortKey="Parkinson, Andrew" sort="Parkinson, Andrew" uniqKey="Parkinson A" first="Andrew" last="Parkinson">Andrew Parkinson</name><affiliation wicri:level="1"><country xml:lang="fr">Canada</country><wicri:regionArea>Department of Chemistry and Biochemistry, University of Guelph, Guelph</wicri:regionArea><wicri:noRegion>Guelph</wicri:noRegion></affiliation><affiliation wicri:level="2"><country xml:lang="fr">États-Unis</country><wicri:regionArea>∗∗ Present address: Department of Pharmacology, Toxicology and Therapeutics, Kansas University Medical Center, 39th St. at Rainbow Blvd., Kansas City, KS 66103</wicri:regionArea><placeName><region type="state">Kansas</region></placeName></affiliation></author><author><name sortKey="Bandiera, Stelvio" sort="Bandiera, Stelvio" uniqKey="Bandiera S" first="Stelvio" last="Bandiera">Stelvio Bandiera</name><affiliation wicri:level="1"><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Veterinary Physiology and Pharmacology, Texas A&M University, College Station</wicri:regionArea><wicri:noRegion>College Station</wicri:noRegion></affiliation></author><author><name sortKey="Lambert, Iain" sort="Lambert, Iain" uniqKey="Lambert I" first="Iain" last="Lambert">Iain Lambert</name><affiliation wicri:level="1"><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Veterinary Physiology and Pharmacology, Texas A&M University, College Station</wicri:regionArea><wicri:noRegion>College Station</wicri:noRegion></affiliation></author><author><name sortKey="Merrill, Jill" sort="Merrill, Jill" uniqKey="Merrill J" first="Jill" last="Merrill">Jill Merrill</name><affiliation wicri:level="1"><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Veterinary Physiology and Pharmacology, Texas A&M University, College Station</wicri:regionArea><wicri:noRegion>College Station</wicri:noRegion></affiliation></author><author><name sortKey="Safe, Stephen H" sort="Safe, Stephen H" uniqKey="Safe S" first="Stephen H." last="Safe">Stephen H. Safe</name><affiliation></affiliation><affiliation wicri:level="1"><country xml:lang="fr">Canada</country><wicri:regionArea>Department of Chemistry and Biochemistry, University of Guelph, Guelph</wicri:regionArea><wicri:noRegion>Guelph</wicri:noRegion></affiliation></author></analytic><monogr></monogr><series><title level="j">Toxicology</title><title level="j" type="abbrev">TOX</title><idno type="ISSN">0300-483X</idno><imprint><publisher>ELSEVIER</publisher><date type="published" when="1984">1984</date><biblScope unit="volume">31</biblScope><biblScope unit="issue">3–4</biblScope><biblScope unit="page" from="191">191</biblScope><biblScope unit="page" to="206">206</biblScope></imprint><idno type="ISSN">0300-483X</idno></series></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0300-483X</idno></seriesStmt></fileDesc><profileDesc><textClass></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Treatment of genetically inbred “responsive” C57BL/6J and ”non-responsive” DBA/2J mice with Aroclor 1254 or fireMaster BP-6 resulted in the induction of hepatic microsomal benzo[a]pyrene hydroxylase only in the former mouse strain and aminopyrine N-demethylase in both strains of mice. In contrast, 3,3′,4,4′,5-pentachlorobiphenyl and 3,3′,4,4′-tetrabromobiphenyl, induced benzo[a]pyrene hydroxylase in both C57BL/6J and DBA/2J but did not enhance aminopyrine N-demethylase in either strain of mouse. Boo these coplanar halogenated biphenyls also caused thymic atrophy in the responsive and non-responsive mice and their effects resembled those of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). Treatment of the inbred mice with several mono-ortho substituted analogs of the coplanar halogenated biphenyls, including 2,3,3′,4,4′-pentachloro-, 2,3′,4,4′,5-pentabromo, 2,3,3′,4,4′,5-hexachloro- and 3′,4′-dibromo-2,3,4,5-tetrachlorobiphenyl, gave hepatic enzyme-induction results similar to those observed for the commercial halogenated biphenyls. At dose levels of 1500 μmol/kg, most of these compounds caused thymic atrophy in C57BL/6J mice but not in DBA/2J mice. The structure-activity correlations in the mice complement similar studies with the halogenated biphenyls in rats and support the proposed receptor-mediated mechanism for the toxic halogenated aromatics.</div></front></TEI><affiliations><list><country><li>Allemagne</li><li>Canada</li><li>États-Unis</li></country><region><li>Kansas</li><li>Rhénanie-Palatinat</li></region><settlement><li>Mayence</li></settlement></list><tree><country name="États-Unis"><noRegion><name sortKey="Robertson, Larry W" sort="Robertson, Larry W" uniqKey="Robertson L" first="Larry W." last="Robertson">Larry W. 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Robertson</name></region></country><country name="Canada"><noRegion><name sortKey="Parkinson, Andrew" sort="Parkinson, Andrew" uniqKey="Parkinson A" first="Andrew" last="Parkinson">Andrew Parkinson</name></noRegion><name sortKey="Safe, Stephen H" sort="Safe, Stephen H" uniqKey="Safe S" first="Stephen H." last="Safe">Stephen H. Safe</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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