Subchronic Toxicity of 3,3′,4,4′,5-Pentachlorobiphenyl in the Rat
Identifieur interne : 000D15 ( Istex/Corpus ); précédent : 000D14; suivant : 000D16Subchronic Toxicity of 3,3′,4,4′,5-Pentachlorobiphenyl in the Rat
Auteurs : I. Chu ; D. C. Villeneuve ; A. Yagminas ; P. Lecavalier ; R. Poon ; M. Feeley ; S. W. Kennedy ; R. F. Seegal ; H. H Kansson ; U. G. Ahlborg ; V. E. ValliSource :
- Toxicological Sciences [ 1096-6080 ] ; 1994-04.
Abstract
The systemic, toxicity of 3,3′,4,4′,5-pentachlorobiphenyl (PCB 126) following subchronic dietary exposure was investigated in Sprague-Dawley rats. PCB 126 was administered to rats of both sexes at concentrations of 0.1, 1.0, 10, or 100 ppb in their diet for 13 weeks. Another group of rats received a loading dose of 5 μg PCB/kg body wt at the start of the feeding period followed by exposure to 10 ppb PCB diet for the same period of time as the other groups. Growth suppression and decreased food consumption were observed in the highest dose groups of both sexes. Increased organ/body weight ratios for the liver occurred in the 10 and 100 ppb groups of both sexes. Rats of both sexes exposed to the highest dose of the PCB also exhibited increased relative kidney, spleen, and brain weights. Hematological and most serum biochemical changes were confined to the 100 ppb groups. These included elevated alkaline phosphatase, bilirubin, cholesterol, and aspartate aminotransferase, and decreased serum glucose, hemoglobin, erythrocytes, hematocrit, and platelets. A dose-dependent increase in liver ethoxyre-sorufin-O-deethylase activity was observed in rats of both sexes starting at 0.1 ppb. A dose-dependent increase in liver uroporphyrin levels was observed in both sexes and significant changes occurred in the female rats at 1.0 ppb and higher dose groups. Decreased liver vitamin A was observed in the 10 ppb group and higher in both sexes. Kidney vitamin A was elevated in the 100 ppb group. No statistically significant changes were noted in concentrations of brain biogenic amines. PCB 126 residues were 10-fold higher in liver than in fat. Treatment-related histopathological changes were observed in the thymus, thyroid, bone marrow, and liver of rats exposed to the 10 ppb diet, but increased frequency of mild changes was observed in most of these tissues at the 1.0 ppb level. Based on the above data, the no adverse effect level was judged to be 0.1 ppb in the diet or 0.01 μg/kg body wt/day.
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DOI: 10.1093/toxsci/22.3.457
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Chu</name><affiliation><mods:affiliation>Environmental Health Directorate and Food Directorate, Health Protection Branch Tunney's Pasture, Ottawa, Ontario, Canada KIA 0L2</mods:affiliation></affiliation><affiliation><mods:affiliation>To whom correspondance should be addressed</mods:affiliation></affiliation></author><author><name sortKey="Villeneuve, D C" sort="Villeneuve, D C" uniqKey="Villeneuve D" first="D. C." last="Villeneuve">D. C. Villeneuve</name><affiliation><mods:affiliation>Environmental Health Directorate and Food Directorate, Health Protection Branch Tunney's Pasture, Ottawa, Ontario, Canada KIA 0L2</mods:affiliation></affiliation></author><author><name sortKey="Yagminas, A" sort="Yagminas, A" uniqKey="Yagminas A" first="A." last="Yagminas">A. 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Feeley</name><affiliation><mods:affiliation>Environmental Health Directorate and Food Directorate, Health Protection Branch Tunney's Pasture, Ottawa, Ontario, Canada KIA 0L2</mods:affiliation></affiliation></author><author><name sortKey="Kennedy, S W" sort="Kennedy, S W" uniqKey="Kennedy S" first="S. W." last="Kennedy">S. W. Kennedy</name><affiliation><mods:affiliation>National Wildlife Research Centre Environment Canada, Hull, Quebec, Canada KIA OH3</mods:affiliation></affiliation></author><author><name sortKey="Seegal, R F" sort="Seegal, R F" uniqKey="Seegal R" first="R. F." last="Seegal">R. F. Seegal</name><affiliation><mods:affiliation>New York State Department of Health, Wadworth Center for Laboratory and Research Albany, New York 12201–1509</mods:affiliation></affiliation></author><author><name sortKey="H Kansson, H" sort="H Kansson, H" uniqKey="H Kansson H" first="H." last="H Kansson">H. H Kansson</name><affiliation><mods:affiliation>Unit of Toxicology, The National Institute of Environmental Medicine, Karolinska Institute S-104-0l, Stockholm, Sweden</mods:affiliation></affiliation></author><author><name sortKey="Ahlborg, U G" sort="Ahlborg, U G" uniqKey="Ahlborg U" first="U. G." last="Ahlborg">U. G. Ahlborg</name><affiliation><mods:affiliation>Unit of Toxicology, The National Institute of Environmental Medicine, Karolinska Institute S-104-0l, Stockholm, Sweden</mods:affiliation></affiliation></author><author><name sortKey="Valli, V E" sort="Valli, V E" uniqKey="Valli V" first="V. E." last="Valli">V. E. Valli</name><affiliation><mods:affiliation>College of Veterinary Medicine, University of Illinois Urbana, Illinois 61801</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">Toxicological Sciences</title><idno type="ISSN">1096-6080</idno><idno type="eISSN">1096-0929</idno><imprint><publisher>Oxford University Press</publisher><date type="published" when="1994-04">1994-04</date><biblScope unit="volume">22</biblScope><biblScope unit="issue">3</biblScope><biblScope unit="page" from="457">457</biblScope><biblScope unit="page" to="468">468</biblScope></imprint><idno type="ISSN">1096-6080</idno></series></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">1096-6080</idno></seriesStmt></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract">The systemic, toxicity of 3,3′,4,4′,5-pentachlorobiphenyl (PCB 126) following subchronic dietary exposure was investigated in Sprague-Dawley rats. PCB 126 was administered to rats of both sexes at concentrations of 0.1, 1.0, 10, or 100 ppb in their diet for 13 weeks. Another group of rats received a loading dose of 5 μg PCB/kg body wt at the start of the feeding period followed by exposure to 10 ppb PCB diet for the same period of time as the other groups. Growth suppression and decreased food consumption were observed in the highest dose groups of both sexes. Increased organ/body weight ratios for the liver occurred in the 10 and 100 ppb groups of both sexes. Rats of both sexes exposed to the highest dose of the PCB also exhibited increased relative kidney, spleen, and brain weights. Hematological and most serum biochemical changes were confined to the 100 ppb groups. These included elevated alkaline phosphatase, bilirubin, cholesterol, and aspartate aminotransferase, and decreased serum glucose, hemoglobin, erythrocytes, hematocrit, and platelets. A dose-dependent increase in liver ethoxyre-sorufin-O-deethylase activity was observed in rats of both sexes starting at 0.1 ppb. A dose-dependent increase in liver uroporphyrin levels was observed in both sexes and significant changes occurred in the female rats at 1.0 ppb and higher dose groups. Decreased liver vitamin A was observed in the 10 ppb group and higher in both sexes. Kidney vitamin A was elevated in the 100 ppb group. No statistically significant changes were noted in concentrations of brain biogenic amines. PCB 126 residues were 10-fold higher in liver than in fat. Treatment-related histopathological changes were observed in the thymus, thyroid, bone marrow, and liver of rats exposed to the 10 ppb diet, but increased frequency of mild changes was observed in most of these tissues at the 1.0 ppb level. Based on the above data, the no adverse effect level was judged to be 0.1 ppb in the diet or 0.01 μg/kg body wt/day.</div></front></TEI><istex><corpusName>oup</corpusName><author><json:item><name>I. CHU</name><affiliations><json:string>Environmental Health Directorate and Food Directorate, Health Protection Branch Tunney's Pasture, Ottawa, Ontario, Canada KIA 0L2</json:string><json:string>To whom correspondance should be addressed</json:string></affiliations></json:item><json:item><name>D. C. VILLENEUVE</name><affiliations><json:string>Environmental Health Directorate and Food Directorate, Health Protection Branch Tunney's Pasture, Ottawa, Ontario, Canada KIA 0L2</json:string></affiliations></json:item><json:item><name>A. YAGMINAS</name><affiliations><json:string>Environmental Health Directorate and Food Directorate, Health Protection Branch Tunney's Pasture, Ottawa, Ontario, Canada KIA 0L2</json:string></affiliations></json:item><json:item><name>P. LECAVALIER</name><affiliations><json:string>Environmental Health Directorate and Food Directorate, Health Protection Branch Tunney's Pasture, Ottawa, Ontario, Canada KIA 0L2</json:string></affiliations></json:item><json:item><name>R. POON</name><affiliations><json:string>Environmental Health Directorate and Food Directorate, Health Protection Branch Tunney's Pasture, Ottawa, Ontario, Canada KIA 0L2</json:string></affiliations></json:item><json:item><name>M. FEELEY</name><affiliations><json:string>Environmental Health Directorate and Food Directorate, Health Protection Branch Tunney's Pasture, Ottawa, Ontario, Canada KIA 0L2</json:string></affiliations></json:item><json:item><name>S. W. KENNEDY</name><affiliations><json:string>National Wildlife Research Centre Environment Canada, Hull, Quebec, Canada KIA OH3</json:string></affiliations></json:item><json:item><name>R. F. SEEGAL</name><affiliations><json:string>New York State Department of Health, Wadworth Center for Laboratory and Research Albany, New York 12201–1509</json:string></affiliations></json:item><json:item><name>H. HÄKANSSON</name><affiliations><json:string>Unit of Toxicology, The National Institute of Environmental Medicine, Karolinska Institute S-104-0l, Stockholm, Sweden</json:string></affiliations></json:item><json:item><name>U. G. AHLBORG</name><affiliations><json:string>Unit of Toxicology, The National Institute of Environmental Medicine, Karolinska Institute S-104-0l, Stockholm, Sweden</json:string></affiliations></json:item><json:item><name>V. E. VALLI</name><affiliations><json:string>College of Veterinary Medicine, University of Illinois Urbana, Illinois 61801</json:string></affiliations></json:item></author><subject><json:item><value>Articles</value></json:item></subject><articleId><json:string>22.3.457</json:string></articleId><language><json:string>unknown</json:string></language><originalGenre><json:string>research-article</json:string></originalGenre><abstract>The systemic, toxicity of 3,3′,4,4′,5-pentachlorobiphenyl (PCB 126) following subchronic dietary exposure was investigated in Sprague-Dawley rats. PCB 126 was administered to rats of both sexes at concentrations of 0.1, 1.0, 10, or 100 ppb in their diet for 13 weeks. Another group of rats received a loading dose of 5 μg PCB/kg body wt at the start of the feeding period followed by exposure to 10 ppb PCB diet for the same period of time as the other groups. Growth suppression and decreased food consumption were observed in the highest dose groups of both sexes. Increased organ/body weight ratios for the liver occurred in the 10 and 100 ppb groups of both sexes. Rats of both sexes exposed to the highest dose of the PCB also exhibited increased relative kidney, spleen, and brain weights. Hematological and most serum biochemical changes were confined to the 100 ppb groups. These included elevated alkaline phosphatase, bilirubin, cholesterol, and aspartate aminotransferase, and decreased serum glucose, hemoglobin, erythrocytes, hematocrit, and platelets. A dose-dependent increase in liver ethoxyre-sorufin-O-deethylase activity was observed in rats of both sexes starting at 0.1 ppb. A dose-dependent increase in liver uroporphyrin levels was observed in both sexes and significant changes occurred in the female rats at 1.0 ppb and higher dose groups. Decreased liver vitamin A was observed in the 10 ppb group and higher in both sexes. Kidney vitamin A was elevated in the 100 ppb group. No statistically significant changes were noted in concentrations of brain biogenic amines. PCB 126 residues were 10-fold higher in liver than in fat. Treatment-related histopathological changes were observed in the thymus, thyroid, bone marrow, and liver of rats exposed to the 10 ppb diet, but increased frequency of mild changes was observed in most of these tissues at the 1.0 ppb level. Based on the above data, the no adverse effect level was judged to be 0.1 ppb in the diet or 0.01 μg/kg body wt/day.</abstract><qualityIndicators><score>10</score><pdfWordCount>6198</pdfWordCount><pdfCharCount>38387</pdfCharCount><pdfVersion>1.2</pdfVersion><pdfPageCount>12</pdfPageCount><pdfPageSize>615 x 804 pts</pdfPageSize><refBibsNative>false</refBibsNative><abstractWordCount>323</abstractWordCount><abstractCharCount>2010</abstractCharCount><keywordCount>1</keywordCount></qualityIndicators><title>Subchronic Toxicity of 3,3′,4,4′,5-Pentachlorobiphenyl in the Rat</title><genre><json:string>research-article</json:string></genre><host><title>Toxicological Sciences</title><language><json:string>unknown</json:string></language><issn><json:string>1096-6080</json:string></issn><eissn><json:string>1096-0929</json:string></eissn><publisherId><json:string>toxsci</json:string></publisherId><volume>22</volume><issue>3</issue><pages><first>457</first><last>468</last></pages><genre><json:string>journal</json:string></genre></host><categories><wos><json:string>science</json:string><json:string>toxicology</json:string></wos><scienceMetrix><json:string>health sciences</json:string><json:string>biomedical research</json:string><json:string>toxicology</json:string></scienceMetrix></categories><publicationDate>1994</publicationDate><copyrightDate>1994</copyrightDate><doi><json:string>10.1093/toxsci/22.3.457</json:string></doi><id>44BC2BB0125471F3F103B643D0F5686F9DBB1573</id><fulltext><json:item><extension>pdf</extension><original>true</original><mimetype>application/pdf</mimetype><uri>https://api-v5.istex.fr/document/44BC2BB0125471F3F103B643D0F5686F9DBB1573/fulltext/pdf</uri></json:item><json:item><extension>zip</extension><original>false</original><mimetype>application/zip</mimetype><uri>https://api-v5.istex.fr/document/44BC2BB0125471F3F103B643D0F5686F9DBB1573/fulltext/zip</uri></json:item><istex:fulltextTEI uri="https://api-v5.istex.fr/document/44BC2BB0125471F3F103B643D0F5686F9DBB1573/fulltext/tei"><teiHeader><fileDesc><titleStmt><title level="a">Subchronic Toxicity of 3,3′,4,4′,5-Pentachlorobiphenyl in the Rat</title><title level="a" type="sub">I. Clinical, Biochemical, Hematological, and Histopathological Changes</title></titleStmt><publicationStmt><authority>ISTEX</authority><publisher>Oxford University Press</publisher><availability><p>© 1994 by the Society of Toxicology</p></availability><date>1994</date></publicationStmt><notesStmt><note>1 To whom correspondance should be addressed</note></notesStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a">Subchronic Toxicity of 3,3′,4,4′,5-Pentachlorobiphenyl in the Rat</title><title level="a" type="sub">I. Clinical, Biochemical, Hematological, and Histopathological Changes</title><author xml:id="author-0000"><persName><forename type="first">I.</forename><surname>CHU</surname></persName><affiliation>Environmental Health Directorate and Food Directorate, Health Protection Branch Tunney's Pasture, Ottawa, Ontario, Canada KIA 0L2</affiliation><affiliation>To whom correspondance should be addressed</affiliation></author><author xml:id="author-0001"><persName><forename type="first">D. C.</forename><surname>VILLENEUVE</surname></persName><affiliation>Environmental Health Directorate and Food Directorate, Health Protection Branch Tunney's Pasture, Ottawa, Ontario, Canada KIA 0L2</affiliation></author><author xml:id="author-0002"><persName><forename type="first">A.</forename><surname>YAGMINAS</surname></persName><affiliation>Environmental Health Directorate and Food Directorate, Health Protection Branch Tunney's Pasture, Ottawa, Ontario, Canada KIA 0L2</affiliation></author><author xml:id="author-0003"><persName><forename type="first">P.</forename><surname>LECAVALIER</surname></persName><affiliation>Environmental Health Directorate and Food Directorate, Health Protection Branch Tunney's Pasture, Ottawa, Ontario, Canada KIA 0L2</affiliation></author><author xml:id="author-0004"><persName><forename type="first">R.</forename><surname>POON</surname></persName><affiliation>Environmental Health Directorate and Food Directorate, Health Protection Branch Tunney's Pasture, Ottawa, Ontario, Canada KIA 0L2</affiliation></author><author xml:id="author-0005"><persName><forename type="first">M.</forename><surname>FEELEY</surname></persName><affiliation>Environmental Health Directorate and Food Directorate, Health Protection Branch Tunney's Pasture, Ottawa, Ontario, Canada KIA 0L2</affiliation></author><author xml:id="author-0006"><persName><forename type="first">S. W.</forename><surname>KENNEDY</surname></persName><affiliation>National Wildlife Research Centre Environment Canada, Hull, Quebec, Canada KIA OH3</affiliation></author><author xml:id="author-0007"><persName><forename type="first">R. F.</forename><surname>SEEGAL</surname></persName><affiliation>New York State Department of Health, Wadworth Center for Laboratory and Research Albany, New York 12201–1509</affiliation></author><author xml:id="author-0008"><persName><forename type="first">H.</forename><surname>HÄKANSSON</surname></persName><affiliation>Unit of Toxicology, The National Institute of Environmental Medicine, Karolinska Institute S-104-0l, Stockholm, Sweden</affiliation></author><author xml:id="author-0009"><persName><forename type="first">U. G.</forename><surname>AHLBORG</surname></persName><affiliation>Unit of Toxicology, The National Institute of Environmental Medicine, Karolinska Institute S-104-0l, Stockholm, Sweden</affiliation></author><author xml:id="author-0010"><persName><forename type="first">V. E.</forename><surname>VALLI</surname></persName><affiliation>College of Veterinary Medicine, University of Illinois Urbana, Illinois 61801</affiliation></author><idno type="istex">44BC2BB0125471F3F103B643D0F5686F9DBB1573</idno><idno type="DOI">10.1093/toxsci/22.3.457</idno><idno type="ArticleID">22.3.457</idno></analytic><monogr><title level="j">Toxicological Sciences</title><idno type="pISSN">1096-6080</idno><idno type="eISSN">1096-0929</idno><idno type="PublisherID">toxsci</idno><idno type="PublisherID-hwp">toxsci</idno><imprint><publisher>Oxford University Press</publisher><date type="published" when="1994-04"></date><biblScope unit="volume">22</biblScope><biblScope unit="issue">3</biblScope><biblScope unit="page" from="457">457</biblScope><biblScope unit="page" to="468">468</biblScope></imprint></monogr></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>1994</date></creation><abstract><p>The systemic, toxicity of 3,3′,4,4′,5-pentachlorobiphenyl (PCB 126) following subchronic dietary exposure was investigated in Sprague-Dawley rats. PCB 126 was administered to rats of both sexes at concentrations of 0.1, 1.0, 10, or 100 ppb in their diet for 13 weeks. Another group of rats received a loading dose of 5 μg PCB/kg body wt at the start of the feeding period followed by exposure to 10 ppb PCB diet for the same period of time as the other groups. Growth suppression and decreased food consumption were observed in the highest dose groups of both sexes. Increased organ/body weight ratios for the liver occurred in the 10 and 100 ppb groups of both sexes. Rats of both sexes exposed to the highest dose of the PCB also exhibited increased relative kidney, spleen, and brain weights. Hematological and most serum biochemical changes were confined to the 100 ppb groups. These included elevated alkaline phosphatase, bilirubin, cholesterol, and aspartate aminotransferase, and decreased serum glucose, hemoglobin, erythrocytes, hematocrit, and platelets. A dose-dependent increase in liver ethoxyre-sorufin-O-deethylase activity was observed in rats of both sexes starting at 0.1 ppb. A dose-dependent increase in liver uroporphyrin levels was observed in both sexes and significant changes occurred in the female rats at 1.0 ppb and higher dose groups. Decreased liver vitamin A was observed in the 10 ppb group and higher in both sexes. Kidney vitamin A was elevated in the 100 ppb group. No statistically significant changes were noted in concentrations of brain biogenic amines. PCB 126 residues were 10-fold higher in liver than in fat. Treatment-related histopathological changes were observed in the thymus, thyroid, bone marrow, and liver of rats exposed to the 10 ppb diet, but increased frequency of mild changes was observed in most of these tissues at the 1.0 ppb level. Based on the above data, the no adverse effect level was judged to be 0.1 ppb in the diet or 0.01 μg/kg body wt/day.</p></abstract><textClass><keywords scheme="keyword"><list><item><term>Articles</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="1994-04">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><extension>txt</extension><original>false</original><mimetype>text/plain</mimetype><uri>https://api-v5.istex.fr/document/44BC2BB0125471F3F103B643D0F5686F9DBB1573/fulltext/txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="corpus oup" wicri:toSee="no header"><istex:docType PUBLIC="-//NLM//DTD Journal Publishing DTD v2.3 20070202//EN" URI="journalpublishing.dtd" name="istex:docType"></istex:docType><istex:document><article article-type="research-article"><front><journal-meta><journal-id journal-id-type="hwp">toxsci</journal-id><journal-id journal-id-type="publisher-id">toxsci</journal-id><journal-id journal-id-type="pmc">toxsci</journal-id><journal-title>Toxicological Sciences</journal-title><issn pub-type="epub">1096-0929</issn><issn pub-type="ppub">1096-6080</issn><publisher><publisher-name>Oxford University Press</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="publisher-id">22.3.457</article-id><article-id pub-id-type="doi">10.1093/toxsci/22.3.457</article-id><article-categories><subj-group><subject>Articles</subject></subj-group></article-categories><title-group><article-title>Subchronic Toxicity of 3,3′,4,4′,5-Pentachlorobiphenyl in the Rat</article-title><subtitle>I. Clinical, Biochemical, Hematological, and Histopathological Changes</subtitle></title-group><contrib-group><contrib contrib-type="author"><name><surname>CHU</surname><given-names>I.</given-names></name><xref ref-type="aff" rid="au1"><sup>*</sup></xref><xref ref-type="corresp" rid="cor1"><sup>1</sup></xref></contrib><contrib contrib-type="author"><name><surname>VILLENEUVE</surname><given-names>D. C.</given-names></name><xref ref-type="aff" rid="au1"><sup>*</sup></xref></contrib><contrib contrib-type="author"><name><surname>YAGMINAS</surname><given-names>A.</given-names></name><xref ref-type="aff" rid="au1"><sup>*</sup></xref></contrib><contrib contrib-type="author"><name><surname>LECAVALIER</surname><given-names>P.</given-names></name><xref ref-type="aff" rid="au1"><sup>*</sup></xref></contrib><contrib contrib-type="author"><name><surname>POON</surname><given-names>R.</given-names></name><xref ref-type="aff" rid="au1"><sup>*</sup></xref></contrib><contrib contrib-type="author"><name><surname>FEELEY</surname><given-names>M.</given-names></name><xref ref-type="aff" rid="au1"><sup>*</sup></xref></contrib><contrib contrib-type="author"><name><surname>KENNEDY</surname><given-names>S. W.</given-names></name><xref ref-type="aff" rid="au2"><sup>†</sup></xref></contrib><contrib contrib-type="author"><name><surname>SEEGAL</surname><given-names>R. F.</given-names></name><xref ref-type="aff" rid="au3"><sup>‡</sup></xref></contrib><contrib contrib-type="author"><name><surname>HÄKANSSON</surname><given-names>H.</given-names></name><xref ref-type="aff" rid="au4"><sup>§</sup></xref></contrib><contrib contrib-type="author"><name><surname>AHLBORG</surname><given-names>U. G.</given-names></name><xref ref-type="aff" rid="au4"><sup>§</sup></xref></contrib><contrib contrib-type="author"><name><surname>VALLI</surname><given-names>V. E.</given-names></name><xref ref-type="aff" rid="au5"><sup>¶</sup></xref></contrib><aff id="au1"><sup>*</sup><institution>Environmental Health Directorate and Food Directorate, Health Protection Branch</institution> <addr-line>Tunney's Pasture, Ottawa, Ontario, Canada KIA 0L2</addr-line></aff><aff id="au2"><sup>†</sup><institution>National Wildlife Research Centre</institution> <addr-line>Environment Canada, Hull, Quebec, Canada KIA OH3</addr-line></aff><aff id="au3"><sup>‡</sup><institution>New York State Department of Health, Wadworth Center for Laboratory and Research</institution> <addr-line>Albany, New York 12201–1509</addr-line></aff><aff id="au4"><sup>§</sup><institution>Unit of Toxicology, The National Institute of Environmental Medicine, Karolinska Institute</institution> <addr-line>S-104-0l, Stockholm, Sweden</addr-line></aff><aff id="au5"><sup>¶</sup><institution>College of Veterinary Medicine, University of Illinois</institution> <addr-line>Urbana, Illinois 61801</addr-line></aff></contrib-group><author-notes><corresp id="cor1"><sup>1</sup> To whom correspondance should be addressed</corresp></author-notes><pub-date pub-type="ppub"><month>4</month><year>1994</year></pub-date><volume>22</volume><issue>3</issue><fpage>457</fpage><lpage>468</lpage><history><date date-type="received"><day>13</day><month>11</month><year>1992</year></date><date date-type="accepted"><day>28</day><month>9</month><year>1993</year></date></history><copyright-statement>© 1994 by the Society of Toxicology</copyright-statement><copyright-year>1994</copyright-year><abstract><p>The systemic, toxicity of 3,3′,4,4′,5-pentachlorobiphenyl (PCB 126) following subchronic dietary exposure was investigated in Sprague-Dawley rats. PCB 126 was administered to rats of both sexes at concentrations of 0.1, 1.0, 10, or 100 ppb in their diet for 13 weeks. Another group of rats received a loading dose of 5 μg PCB/kg body wt at the start of the feeding period followed by exposure to 10 ppb PCB diet for the same period of time as the other groups. Growth suppression and decreased food consumption were observed in the highest dose groups of both sexes. Increased organ/body weight ratios for the liver occurred in the 10 and 100 ppb groups of both sexes. Rats of both sexes exposed to the highest dose of the PCB also exhibited increased relative kidney, spleen, and brain weights. Hematological and most serum biochemical changes were confined to the 100 ppb groups. These included elevated alkaline phosphatase, bilirubin, cholesterol, and aspartate aminotransferase, and decreased serum glucose, hemoglobin, erythrocytes, hematocrit, and platelets. A dose-dependent increase in liver ethoxyre-sorufin-<italic>O</italic>-deethylase activity was observed in rats of both sexes starting at 0.1 ppb. A dose-dependent increase in liver uroporphyrin levels was observed in both sexes and significant changes occurred in the female rats at 1.0 ppb and higher dose groups. Decreased liver vitamin A was observed in the 10 ppb group and higher in both sexes. Kidney vitamin A was elevated in the 100 ppb group. No statistically significant changes were noted in concentrations of brain biogenic amines. PCB 126 residues were 10-fold higher in liver than in fat. Treatment-related histopathological changes were observed in the thymus, thyroid, bone marrow, and liver of rats exposed to the 10 ppb diet, but increased frequency of mild changes was observed in most of these tissues at the 1.0 ppb level. Based on the above data, the no adverse effect level was judged to be 0.1 ppb in the diet or 0.01 μg/kg body wt/day.</p></abstract></article-meta></front></article></istex:document></istex:metadataXml><mods version="3.6"><titleInfo><title>Subchronic Toxicity of 3,3′,4,4′,5-Pentachlorobiphenyl in the Rat</title><subTitle>I. Clinical, Biochemical, Hematological, and Histopathological Changes</subTitle></titleInfo><titleInfo type="alternative" contentType="CDATA"><title>Subchronic Toxicity of 3,3′,4,4′,5-Pentachlorobiphenyl in the Rat</title><subTitle>I. Clinical, Biochemical, Hematological, and Histopathological Changes</subTitle></titleInfo><name type="personal"><namePart type="given">I.</namePart><namePart type="family">CHU</namePart><affiliation>Environmental Health Directorate and Food Directorate, Health Protection Branch Tunney's Pasture, Ottawa, Ontario, Canada KIA 0L2</affiliation><affiliation>To whom correspondance should be addressed</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">D. C.</namePart><namePart type="family">VILLENEUVE</namePart><affiliation>Environmental Health Directorate and Food Directorate, Health Protection Branch Tunney's Pasture, Ottawa, Ontario, Canada KIA 0L2</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">A.</namePart><namePart type="family">YAGMINAS</namePart><affiliation>Environmental Health Directorate and Food Directorate, Health Protection Branch Tunney's Pasture, Ottawa, Ontario, Canada KIA 0L2</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">P.</namePart><namePart type="family">LECAVALIER</namePart><affiliation>Environmental Health Directorate and Food Directorate, Health Protection Branch Tunney's Pasture, Ottawa, Ontario, Canada KIA 0L2</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">R.</namePart><namePart type="family">POON</namePart><affiliation>Environmental Health Directorate and Food Directorate, Health Protection Branch Tunney's Pasture, Ottawa, Ontario, Canada KIA 0L2</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">M.</namePart><namePart type="family">FEELEY</namePart><affiliation>Environmental Health Directorate and Food Directorate, Health Protection Branch Tunney's Pasture, Ottawa, Ontario, Canada KIA 0L2</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">S. W.</namePart><namePart type="family">KENNEDY</namePart><affiliation>National Wildlife Research Centre Environment Canada, Hull, Quebec, Canada KIA OH3</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">R. F.</namePart><namePart type="family">SEEGAL</namePart><affiliation>New York State Department of Health, Wadworth Center for Laboratory and Research Albany, New York 12201–1509</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">H.</namePart><namePart type="family">HÄKANSSON</namePart><affiliation>Unit of Toxicology, The National Institute of Environmental Medicine, Karolinska Institute S-104-0l, Stockholm, Sweden</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">U. G.</namePart><namePart type="family">AHLBORG</namePart><affiliation>Unit of Toxicology, The National Institute of Environmental Medicine, Karolinska Institute S-104-0l, Stockholm, Sweden</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">V. E.</namePart><namePart type="family">VALLI</namePart><affiliation>College of Veterinary Medicine, University of Illinois Urbana, Illinois 61801</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="research-article" displayLabel="research-article"></genre><subject><topic>Articles</topic></subject><originInfo><publisher>Oxford University Press</publisher><dateIssued encoding="w3cdtf">1994-04</dateIssued><copyrightDate encoding="w3cdtf">1994</copyrightDate></originInfo><physicalDescription><internetMediaType>text/html</internetMediaType></physicalDescription><abstract>The systemic, toxicity of 3,3′,4,4′,5-pentachlorobiphenyl (PCB 126) following subchronic dietary exposure was investigated in Sprague-Dawley rats. PCB 126 was administered to rats of both sexes at concentrations of 0.1, 1.0, 10, or 100 ppb in their diet for 13 weeks. Another group of rats received a loading dose of 5 μg PCB/kg body wt at the start of the feeding period followed by exposure to 10 ppb PCB diet for the same period of time as the other groups. Growth suppression and decreased food consumption were observed in the highest dose groups of both sexes. Increased organ/body weight ratios for the liver occurred in the 10 and 100 ppb groups of both sexes. Rats of both sexes exposed to the highest dose of the PCB also exhibited increased relative kidney, spleen, and brain weights. Hematological and most serum biochemical changes were confined to the 100 ppb groups. These included elevated alkaline phosphatase, bilirubin, cholesterol, and aspartate aminotransferase, and decreased serum glucose, hemoglobin, erythrocytes, hematocrit, and platelets. A dose-dependent increase in liver ethoxyre-sorufin-O-deethylase activity was observed in rats of both sexes starting at 0.1 ppb. A dose-dependent increase in liver uroporphyrin levels was observed in both sexes and significant changes occurred in the female rats at 1.0 ppb and higher dose groups. Decreased liver vitamin A was observed in the 10 ppb group and higher in both sexes. Kidney vitamin A was elevated in the 100 ppb group. No statistically significant changes were noted in concentrations of brain biogenic amines. PCB 126 residues were 10-fold higher in liver than in fat. Treatment-related histopathological changes were observed in the thymus, thyroid, bone marrow, and liver of rats exposed to the 10 ppb diet, but increased frequency of mild changes was observed in most of these tissues at the 1.0 ppb level. Based on the above data, the no adverse effect level was judged to be 0.1 ppb in the diet or 0.01 μg/kg body wt/day.</abstract><note type="author-notes">1 To whom correspondance should be addressed</note><relatedItem type="host"><titleInfo><title>Toxicological Sciences</title></titleInfo><genre type="journal">journal</genre><identifier type="ISSN">1096-6080</identifier><identifier type="eISSN">1096-0929</identifier><identifier type="PublisherID">toxsci</identifier><identifier type="PublisherID-hwp">toxsci</identifier><part><date>1994</date><detail type="volume"><caption>vol.</caption><number>22</number></detail><detail type="issue"><caption>no.</caption><number>3</number></detail><extent unit="pages"><start>457</start><end>468</end></extent></part></relatedItem><identifier type="istex">44BC2BB0125471F3F103B643D0F5686F9DBB1573</identifier><identifier type="DOI">10.1093/toxsci/22.3.457</identifier><identifier type="ArticleID">22.3.457</identifier><accessCondition type="use and reproduction" contentType="copyright">© 1994 by the Society of Toxicology</accessCondition><recordInfo><recordContentSource>OUP</recordContentSource></recordInfo></mods></metadata><annexes><json:item><extension>pdf</extension><original>true</original><mimetype>application/pdf</mimetype><uri>https://api-v5.istex.fr/document/44BC2BB0125471F3F103B643D0F5686F9DBB1573/annexes/pdf</uri></json:item></annexes><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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