Distribution of the carcinogenic tryptophan pyrolysis product Trp-P-1 in control, 9-hydroxyellipticine and β-naphthoflavone pretreated mice
Identifieur interne : 001784 ( Istex/Corpus ); précédent : 001783; suivant : 001785Distribution of the carcinogenic tryptophan pyrolysis product Trp-P-1 in control, 9-hydroxyellipticine and β-naphthoflavone pretreated mice
Auteurs : Ingvar Brandt ; Jan- Ke Gustafsson ; Joseph RafterSource :
- Carcinogenesis [ 0143-3334 ] ; 1983.
Abstract
Autoradiograms obtained 1–4 h after i.v. injection of the 14C-labelled carcinogenic tryptophan pyrolysis product Trp-P-1 to albino and pigmented mice showed a pronounced uptake of radioactivity in the lymphatic system (thymus, lymphnodes, bone marrow and spleen), in the endocrine system (hypophysis, thyroid, adrenal medulla) and in the liver, kidney medulla and brain. High radioactivity was present in the excretory pathways, predominantly in the bile/intestinal contents. At longer post-injection times (24 h to 6 days) most of the labelled substance had left the tissues, except for the liver which still retained a high concentration of radioactivity. Trp-P-1 is known to be activated by cytochrome P-448. The uptake of radioactivity in the liver could be reduced by pretreatment with the cylochrome P448 inhibitor 9-hydroxy-ellipticine suggesting that the observed accumulation of radioactivity in the liver was partly due to metabolites of Trp-P-1. After pretreatment with the cytochrome P-448 inducer β-naphthoflavone, the administration of Trp-P-1 resulted in a highly selective accumulation of radioactivity in the lung parenchyma, exceeding all other tissues in the body. β-Naphthoflavone pretreatment also increased the uptake of radioactivity in the kidney cortex and small intestinal mucosa. As indicated by a high labelling of the pigmented tissues of the maternal and fetal eye, the carcinogen and/or its metabolites were accumulated in melanin.
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DOI: 10.1093/carcin/4.10.1291
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ISTEX:28018B9A5C8AE832D902C0000EECBA378C42E09ALe document en format XML
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High radioactivity was present in the excretory pathways, predominantly in the bile/intestinal contents. At longer post-injection times (24 h to 6 days) most of the labelled substance had left the tissues, except for the liver which still retained a high concentration of radioactivity. Trp-P-1 is known to be activated by cytochrome P-448. The uptake of radioactivity in the liver could be reduced by pretreatment with the cylochrome P448 inhibitor 9-hydroxy-ellipticine suggesting that the observed accumulation of radioactivity in the liver was partly due to metabolites of Trp-P-1. After pretreatment with the cytochrome P-448 inducer β-naphthoflavone, the administration of Trp-P-1 resulted in a highly selective accumulation of radioactivity in the lung parenchyma, exceeding all other tissues in the body. β-Naphthoflavone pretreatment also increased the uptake of radioactivity in the kidney cortex and small intestinal mucosa. As indicated by a high labelling of the pigmented tissues of the maternal and fetal eye, the carcinogen and/or its metabolites were accumulated in melanin.</div></front></TEI><istex><corpusName>oup</corpusName><keywords><teeft><json:string>pretreated</json:string><json:string>cytochrome</json:string><json:string>endocrine</json:string><json:string>intestinal</json:string><json:string>labelling</json:string><json:string>pretreatment</json:string><json:string>lymphatic</json:string><json:string>radioactivity</json:string><json:string>lymphatic system</json:string><json:string>control mouse</json:string><json:string>nmri</json:string><json:string>pretreated mouse</json:string><json:string>kidney cortex</json:string><json:string>lymph node</json:string><json:string>female mouse</json:string><json:string>mouse</json:string><json:string>adrenal medulla</json:string><json:string>small intestinal mucosa</json:string><json:string>high concentration</json:string><json:string>factor present</json:string><json:string>bone marrow</json:string><json:string>cigarette smoke</json:string><json:string>citrate buffer</json:string><json:string>lung parenchyma</json:string><json:string>proximal segment</json:string><json:string>high level</json:string><json:string>other tissue</json:string><json:string>endocrine system</json:string><json:string>small intestine</json:string><json:string>wide range</json:string><json:string>amino acid</json:string><json:string>experimental protocol</json:string><json:string>body weight</json:string><json:string>polypeptide hormone</json:string><json:string>selective accumulation</json:string><json:string>intestinal mucosa</json:string><json:string>human cancer</json:string><json:string>nmri male</json:string><json:string>corpus lutea</json:string><json:string>male mouse</json:string><json:string>germinal center</json:string><json:string>high radioactivity</json:string><json:string>pyrolysis product</json:string><json:string>high accumulation</json:string><json:string>distribution pattern</json:string><json:string>fetal eye</json:string><json:string>mouse pretreated</json:string><json:string>central vein</json:string><json:string>quantitative measurement</json:string><json:string>excretory pathway</json:string><json:string>carcinogenic action</json:string><json:string>intestinal content</json:string><json:string>liver microsome</json:string><json:string>carcinogenic tryptophan pyrolysis product</json:string><json:string>cell system</json:string><json:string>uptake</json:string><json:string>injection</json:string></teeft></keywords><author><json:item><name>Ingvar Brandt</name><affiliations><json:string>Department of Pharmacology, SLU, Uppsala Biomedical Centre, Box 573, S-75 1 23 Uppsala Sweeden, F-69, S-141 86 Huddinge, Sweden</json:string></affiliations></json:item><json:item><name>Jan-Åke Gustafsson</name><affiliations><json:string>Department of Medical Nutrition, Karolinska Institute, Huddinge University Hospital F-69, S-141 86 Huddinge, Sweden</json:string></affiliations></json:item><json:item><name>Joseph Rafter</name><affiliations><json:string>Department of Medical Nutrition, Karolinska Institute, Huddinge University Hospital F-69, S-141 86 Huddinge, Sweden</json:string></affiliations></json:item></author><articleId><json:string>4.10.1291</json:string></articleId><arkIstex>ark:/67375/HXZ-GZ37N969-F</arkIstex><language><json:string>unknown</json:string></language><originalGenre><json:string>research-article</json:string></originalGenre><abstract>Autoradiograms obtained 1–4 h after i.v. injection of the 14C-labelled carcinogenic tryptophan pyrolysis product Trp-P-1 to albino and pigmented mice showed a pronounced uptake of radioactivity in the lymphatic system (thymus, lymphnodes, bone marrow and spleen), in the endocrine system (hypophysis, thyroid, adrenal medulla) and in the liver, kidney medulla and brain. 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<front>
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<journal-id journal-id-type="hwp">carcin</journal-id>
<journal-id journal-id-type="publisher-id">carcin</journal-id>
<journal-id journal-id-type="pmc">carcin</journal-id>
<journal-title>Carcinogenesis</journal-title>
<issn pub-type="epub">1460-2180</issn>
<issn pub-type="ppub">0143-3334</issn>
<publisher>
<publisher-name>Oxford University Press</publisher-name>
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<title-group>
<article-title>Distribution of the carcinogenic tryptophan pyrolysis product Trp-P-1 in control, 9-hydroxyellipticine and <italic>β</italic>-naphthoflavone pretreated mice</article-title>
</title-group>
<contrib-group>
<contrib contrib-type="author">
<name><surname>Brandt</surname><given-names>Ingvar</given-names></name>
</contrib>
<contrib contrib-type="author">
<name><surname>Gustafsson</surname><given-names>Jan-Åke</given-names></name><xref ref-type="aff" rid="au1"><sup>1</sup></xref>
</contrib>
<contrib contrib-type="author">
<name><surname>Rafter</surname><given-names>Joseph</given-names></name><xref ref-type="aff" rid="au1"><sup>1</sup></xref>
</contrib>
<aff><institution>Department of Pharmacology, SLU, Uppsala Biomedical Centre</institution> <addr-line>Box 573, S-75 1 23 Uppsala Sweeden</addr-line></aff>
<aff id="au1"><sup>1</sup><institution>Department of Medical Nutrition, Karolinska Institute, Huddinge University Hospital</institution> <addr-line>F-69, S-141 86 Huddinge, Sweden</addr-line></aff>
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<pub-date pub-type="ppub">
<month>10</month>
<year>1983</year>
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<volume>4</volume>
<issue>10</issue>
<fpage>1291</fpage>
<lpage>1296</lpage>
<history>
<date date-type="received">
<day>09</day>
<month>5</month>
<year>1983</year>
</date>
<date date-type="accepted">
<day>03</day>
<month>8</month>
<year>1983</year>
</date>
</history>
<copyright-statement>© IRL Press Ltd.</copyright-statement>
<copyright-year>1983</copyright-year>
<abstract>
<p>Autoradiograms obtained 1–4 h after i.v. injection of the <sup>14</sup>C-labelled carcinogenic tryptophan pyrolysis product Trp-P-1 to albino and pigmented mice showed a pronounced uptake of radioactivity in the lymphatic system (thymus, lymphnodes, bone marrow and spleen), in the endocrine system (hypophysis, thyroid, adrenal medulla) and in the liver, kidney medulla and brain. High radioactivity was present in the excretory pathways, predominantly in the bile/intestinal contents. At longer post-injection times (24 h to 6 days) most of the labelled substance had left the tissues, except for the liver which still retained a high concentration of radioactivity. Trp-P-1 is known to be activated by cytochrome P-448. The uptake of radioactivity in the liver could be reduced by pretreatment with the cylochrome P448 inhibitor 9-hydroxy-ellipticine suggesting that the observed accumulation of radioactivity in the liver was partly due to metabolites of Trp-P-1. After pretreatment with the cytochrome P-448 inducer <italic>β</italic>-naphthoflavone, the administration of Trp-P-1 resulted in a highly selective accumulation of radioactivity in the lung parenchyma, exceeding all other tissues in the body. <italic>β</italic>-Naphthoflavone pretreatment also increased the uptake of radioactivity in the kidney cortex and small intestinal mucosa. As indicated by a high labelling of the pigmented tissues of the maternal and fetal eye, the carcinogen and/or its metabolites were accumulated in melanin.</p>
</abstract>
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</article></istex:document></istex:metadataXml><mods version="3.6"><titleInfo><title>Distribution of the carcinogenic tryptophan pyrolysis product Trp-P-1 in control, 9-hydroxyellipticine and β-naphthoflavone pretreated mice</title></titleInfo><titleInfo type="alternative" contentType="CDATA"><title>Distribution of the carcinogenic tryptophan pyrolysis product Trp-P-1 in control, 9-hydroxyellipticine and β-naphthoflavone pretreated mice</title></titleInfo><name type="personal"><namePart type="given">Ingvar</namePart><namePart type="family">Brandt</namePart><affiliation>Department of Pharmacology, SLU, Uppsala Biomedical Centre, Box 573, S-75 1 23 Uppsala Sweeden, F-69, S-141 86 Huddinge, Sweden</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Jan-Åke</namePart><namePart type="family">Gustafsson</namePart><affiliation>Department of Medical Nutrition, Karolinska Institute, Huddinge University Hospital F-69, S-141 86 Huddinge, Sweden</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Joseph</namePart><namePart type="family">Rafter</namePart><affiliation>Department of Medical Nutrition, Karolinska Institute, Huddinge University Hospital F-69, S-141 86 Huddinge, Sweden</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="research-article" displayLabel="research-article" authority="ISTEX" authorityURI="https://content-type.data.istex.fr" valueURI="https://content-type.data.istex.fr/ark:/67375/XTP-1JC4F85T-7">research-article</genre><originInfo><publisher>Oxford University Press</publisher><dateIssued encoding="w3cdtf">1983-10</dateIssued><dateCreated encoding="w3cdtf">1983-08-03</dateCreated><copyrightDate encoding="w3cdtf">1983</copyrightDate></originInfo><abstract>Autoradiograms obtained 1–4 h after i.v. injection of the 14C-labelled carcinogenic tryptophan pyrolysis product Trp-P-1 to albino and pigmented mice showed a pronounced uptake of radioactivity in the lymphatic system (thymus, lymphnodes, bone marrow and spleen), in the endocrine system (hypophysis, thyroid, adrenal medulla) and in the liver, kidney medulla and brain. High radioactivity was present in the excretory pathways, predominantly in the bile/intestinal contents. At longer post-injection times (24 h to 6 days) most of the labelled substance had left the tissues, except for the liver which still retained a high concentration of radioactivity. Trp-P-1 is known to be activated by cytochrome P-448. The uptake of radioactivity in the liver could be reduced by pretreatment with the cylochrome P448 inhibitor 9-hydroxy-ellipticine suggesting that the observed accumulation of radioactivity in the liver was partly due to metabolites of Trp-P-1. After pretreatment with the cytochrome P-448 inducer β-naphthoflavone, the administration of Trp-P-1 resulted in a highly selective accumulation of radioactivity in the lung parenchyma, exceeding all other tissues in the body. β-Naphthoflavone pretreatment also increased the uptake of radioactivity in the kidney cortex and small intestinal mucosa. As indicated by a high labelling of the pigmented tissues of the maternal and fetal eye, the carcinogen and/or its metabolites were accumulated in melanin.</abstract><relatedItem type="host"><titleInfo><title>Carcinogenesis</title></titleInfo><genre type="journal" authority="ISTEX" authorityURI="https://publication-type.data.istex.fr" valueURI="https://publication-type.data.istex.fr/ark:/67375/JMC-0GLKJH51-B">journal</genre><subject><topic>Original Articles</topic></subject><identifier type="ISSN">0143-3334</identifier><identifier type="eISSN">1460-2180</identifier><identifier type="PublisherID">carcin</identifier><identifier type="PublisherID-hwp">carcin</identifier><part><date>1983</date><detail type="volume"><caption>vol.</caption><number>4</number></detail><detail type="issue"><caption>no.</caption><number>10</number></detail><extent unit="pages"><start>1291</start><end>1296</end></extent></part></relatedItem><identifier type="istex">28018B9A5C8AE832D902C0000EECBA378C42E09A</identifier><identifier type="ark">ark:/67375/HXZ-GZ37N969-F</identifier><identifier type="DOI">10.1093/carcin/4.10.1291</identifier><identifier type="ArticleID">4.10.1291</identifier><accessCondition type="use and reproduction" contentType="copyright">© IRL Press Ltd.</accessCondition><recordInfo><recordContentSource authority="ISTEX" authorityURI="https://loaded-corpus.data.istex.fr" valueURI="https://loaded-corpus.data.istex.fr/ark:/67375/XBH-GTWS0RDP-M">oup</recordContentSource><recordOrigin>Converted from (version 1.2.0) to MODS version 3.6.</recordOrigin><recordCreationDate encoding="w3cdtf">2019-12-09</recordCreationDate></recordInfo></mods><json:item><extension>json</extension><original>false</original><mimetype>application/json</mimetype><uri>https://api.istex.fr/ark:/67375/HXZ-GZ37N969-F/record.json</uri></json:item></metadata><annexes><json:item><extension>pdf</extension><original>true</original><mimetype>application/pdf</mimetype><uri>https://api.istex.fr/ark:/67375/HXZ-GZ37N969-F/annexes.pdf</uri></json:item></annexes><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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