Partial contribution of biliary metabolites to nephrotoxicity, renal content and excretion of [14C]hexachloro-1,3-butadiene in rats
Male Sprague Dawley rats with cannulated bile duct (BDC rats) received 100 or 200 mg kg−1 labelled hexachloro‐1,3‐butadiene ([14C]HCBD) by gavage 1 h (BDC1, rats) or 24 h (BDC24 rats) after surgical cannula implantation. Twenty‐four hours after treatment with HCBD, rats were examined histochemically...
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| Veröffentlicht in: | Journal of applied toxicology 1993-01, Vol.13 (1), p.19-24 |
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| creator | Payan, J. P. Beydon, D. Fabry, J. P. Morei, G. Brondeau, M. T. Ban, M. de Ceaurriz, J. |
| description | Male Sprague Dawley rats with cannulated bile duct (BDC rats) received 100 or 200 mg kg−1 labelled hexachloro‐1,3‐butadiene ([14C]HCBD) by gavage 1 h (BDC1, rats) or 24 h (BDC24 rats) after surgical cannula implantation. Twenty‐four hours after treatment with HCBD, rats were examined histochemically and biochemically for kidney damage. Urine, faeces, liver and kidney radioactivities were also measured in 24‐h samples. Results were compared with those obtained from non‐cannulated (NC) rats. Bile‐duct cannulation did not completely protect against HCBD‐induced kidney damage. The 24‐h [14C] urinary excretion and tissue content was 30–50% lower in BDC rats compared to NC rats and correlated well with the toxicity findings.
BDC1 rats appeared to be much more resistant to HCBD treatment than BDC24 rats. Since faecal [14C] radioactivity extractible by diethyl ether at neutral pH in BDC1, rats was twice that measured in BDC24 rats, the greater resistance was attributed to a higher deficiency in the gastrointestinal absorption of unchanged HCBD.
The present results reveal that the biliary metabolites of HCBD are not solely responsible for kidney toxicity as previously assumed. They suggest a sinusoidal efflux of the HCBD conjugates from the liver. |
| doi_str_mv | 10.1002/jat.2550130106 |
| format | Article |
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BDC1 rats appeared to be much more resistant to HCBD treatment than BDC24 rats. Since faecal [14C] radioactivity extractible by diethyl ether at neutral pH in BDC1, rats was twice that measured in BDC24 rats, the greater resistance was attributed to a higher deficiency in the gastrointestinal absorption of unchanged HCBD.
The present results reveal that the biliary metabolites of HCBD are not solely responsible for kidney toxicity as previously assumed. They suggest a sinusoidal efflux of the HCBD conjugates from the liver.</description><identifier>ISSN: 0260-437X</identifier><identifier>EISSN: 1099-1263</identifier><identifier>DOI: 10.1002/jat.2550130106</identifier><identifier>PMID: 8440871</identifier><identifier>CODEN: JJATDK</identifier><language>eng</language><publisher>Chichester: John Wiley & Sons, Ltd</publisher><subject>3-butadiene ; Animals ; Bile - metabolism ; biliary metabolites ; Biological and medical sciences ; Butadienes - toxicity ; Butadienes - urine ; Catheterization, Peripheral ; Chemical and industrial products toxicology. Toxic occupational diseases ; Common Bile Duct ; excretion ; Fungicides, Industrial - toxicity ; Fungicides, Industrial - urine ; Glutathione - metabolism ; hexachloro-1 ; hexachloro‐1,3‐butadiene ; Kidney - metabolism ; Kidney - pathology ; Kidney Diseases - chemically induced ; Kidney Diseases - pathology ; Liver - metabolism ; Male ; Medical sciences ; nephrotoxicity ; Oxidation-Reduction ; Rats ; Rats, Sprague-Dawley ; Toxicology ; Various organic compounds</subject><ispartof>Journal of applied toxicology, 1993-01, Vol.13 (1), p.19-24</ispartof><rights>Copyright © 1993 John Wiley & Sons, Ltd.</rights><rights>1993 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4386-ded863be1fd9ce0c48b7f63de95d1447a5f38cb97568c0f451dfab10a2c823293</citedby><cites>FETCH-LOGICAL-c4386-ded863be1fd9ce0c48b7f63de95d1447a5f38cb97568c0f451dfab10a2c823293</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1002%2Fjat.2550130106$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1002%2Fjat.2550130106$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,776,780,1411,4010,27900,27901,27902,45550,45551</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=4608987$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/8440871$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Payan, J. P.</creatorcontrib><creatorcontrib>Beydon, D.</creatorcontrib><creatorcontrib>Fabry, J. P.</creatorcontrib><creatorcontrib>Morei, G.</creatorcontrib><creatorcontrib>Brondeau, M. T.</creatorcontrib><creatorcontrib>Ban, M.</creatorcontrib><creatorcontrib>de Ceaurriz, J.</creatorcontrib><title>Partial contribution of biliary metabolites to nephrotoxicity, renal content and excretion of [14C]hexachloro-1,3-butadiene in rats</title><title>Journal of applied toxicology</title><addtitle>J. Appl. Toxicol</addtitle><description>Male Sprague Dawley rats with cannulated bile duct (BDC rats) received 100 or 200 mg kg−1 labelled hexachloro‐1,3‐butadiene ([14C]HCBD) by gavage 1 h (BDC1, rats) or 24 h (BDC24 rats) after surgical cannula implantation. Twenty‐four hours after treatment with HCBD, rats were examined histochemically and biochemically for kidney damage. Urine, faeces, liver and kidney radioactivities were also measured in 24‐h samples. Results were compared with those obtained from non‐cannulated (NC) rats. Bile‐duct cannulation did not completely protect against HCBD‐induced kidney damage. The 24‐h [14C] urinary excretion and tissue content was 30–50% lower in BDC rats compared to NC rats and correlated well with the toxicity findings.
BDC1 rats appeared to be much more resistant to HCBD treatment than BDC24 rats. Since faecal [14C] radioactivity extractible by diethyl ether at neutral pH in BDC1, rats was twice that measured in BDC24 rats, the greater resistance was attributed to a higher deficiency in the gastrointestinal absorption of unchanged HCBD.
The present results reveal that the biliary metabolites of HCBD are not solely responsible for kidney toxicity as previously assumed. They suggest a sinusoidal efflux of the HCBD conjugates from the liver.</description><subject>3-butadiene</subject><subject>Animals</subject><subject>Bile - metabolism</subject><subject>biliary metabolites</subject><subject>Biological and medical sciences</subject><subject>Butadienes - toxicity</subject><subject>Butadienes - urine</subject><subject>Catheterization, Peripheral</subject><subject>Chemical and industrial products toxicology. Toxic occupational diseases</subject><subject>Common Bile Duct</subject><subject>excretion</subject><subject>Fungicides, Industrial - toxicity</subject><subject>Fungicides, Industrial - urine</subject><subject>Glutathione - metabolism</subject><subject>hexachloro-1</subject><subject>hexachloro‐1,3‐butadiene</subject><subject>Kidney - metabolism</subject><subject>Kidney - pathology</subject><subject>Kidney Diseases - chemically induced</subject><subject>Kidney Diseases - pathology</subject><subject>Liver - metabolism</subject><subject>Male</subject><subject>Medical sciences</subject><subject>nephrotoxicity</subject><subject>Oxidation-Reduction</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Toxicology</subject><subject>Various organic compounds</subject><issn>0260-437X</issn><issn>1099-1263</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1993</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkM9v0zAYhi0EGmXjyg3JB8RpKZ9jJ3GOU8TKULWhafyQELIc54vqkdrFdkV73j9OUEMRJ04-vM_7ftZDyAsGcwaQv7nXaZ4XBTAODMpHZMagrjOWl_wxmUFeQiZ49eUpeRbjPcCY5fKEnEghQFZsRh4-6JCsHqjxLgXbbpP1jvqetnawOuzpGpNu_WATRpo8dbhZBZ_8zhqb9uc0oJvK6BLVrqO4MwH_rHxlovm2wp02q8EHn7Fzno03dGfRIbWOBp3iGXnS6yHi8-k9JR8v394177LlzeKquVhmRnBZZh12suQtsr6rDYIRsq36kndYFx0TotJFz6Vp66oopYFeFKzrdctA50bmPK_5KXl92N0E_2OLMam1jQaHQTv026iY4FAwKEZwfgBN8DEG7NUm2PVoQzFQv62r0br6a30svJyWt-0auyM-aR7zV1Ouo9FDH7QzNh4xUYKsZTVi9QH7aQfc_-eoen9x988XskPXxoS7Y1eH76qseFWoz9cL9UksmsvmVqgl_wWfB6xA</recordid><startdate>199301</startdate><enddate>199301</enddate><creator>Payan, J. P.</creator><creator>Beydon, D.</creator><creator>Fabry, J. P.</creator><creator>Morei, G.</creator><creator>Brondeau, M. T.</creator><creator>Ban, M.</creator><creator>de Ceaurriz, J.</creator><general>John Wiley & Sons, Ltd</general><general>Wiley</general><scope>BSCLL</scope><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7ST</scope><scope>C1K</scope><scope>SOI</scope></search><sort><creationdate>199301</creationdate><title>Partial contribution of biliary metabolites to nephrotoxicity, renal content and excretion of [14C]hexachloro-1,3-butadiene in rats</title><author>Payan, J. P. ; Beydon, D. ; Fabry, J. P. ; Morei, G. ; Brondeau, M. T. ; Ban, M. ; de Ceaurriz, J.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4386-ded863be1fd9ce0c48b7f63de95d1447a5f38cb97568c0f451dfab10a2c823293</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1993</creationdate><topic>3-butadiene</topic><topic>Animals</topic><topic>Bile - metabolism</topic><topic>biliary metabolites</topic><topic>Biological and medical sciences</topic><topic>Butadienes - toxicity</topic><topic>Butadienes - urine</topic><topic>Catheterization, Peripheral</topic><topic>Chemical and industrial products toxicology. Toxic occupational diseases</topic><topic>Common Bile Duct</topic><topic>excretion</topic><topic>Fungicides, Industrial - toxicity</topic><topic>Fungicides, Industrial - urine</topic><topic>Glutathione - metabolism</topic><topic>hexachloro-1</topic><topic>hexachloro‐1,3‐butadiene</topic><topic>Kidney - metabolism</topic><topic>Kidney - pathology</topic><topic>Kidney Diseases - chemically induced</topic><topic>Kidney Diseases - pathology</topic><topic>Liver - metabolism</topic><topic>Male</topic><topic>Medical sciences</topic><topic>nephrotoxicity</topic><topic>Oxidation-Reduction</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Toxicology</topic><topic>Various organic compounds</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Payan, J. P.</creatorcontrib><creatorcontrib>Beydon, D.</creatorcontrib><creatorcontrib>Fabry, J. P.</creatorcontrib><creatorcontrib>Morei, G.</creatorcontrib><creatorcontrib>Brondeau, M. T.</creatorcontrib><creatorcontrib>Ban, M.</creatorcontrib><creatorcontrib>de Ceaurriz, J.</creatorcontrib><collection>Istex</collection><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Environment Abstracts</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Environment Abstracts</collection><jtitle>Journal of applied toxicology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Payan, J. P.</au><au>Beydon, D.</au><au>Fabry, J. P.</au><au>Morei, G.</au><au>Brondeau, M. T.</au><au>Ban, M.</au><au>de Ceaurriz, J.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Partial contribution of biliary metabolites to nephrotoxicity, renal content and excretion of [14C]hexachloro-1,3-butadiene in rats</atitle><jtitle>Journal of applied toxicology</jtitle><addtitle>J. Appl. Toxicol</addtitle><date>1993-01</date><risdate>1993</risdate><volume>13</volume><issue>1</issue><spage>19</spage><epage>24</epage><pages>19-24</pages><issn>0260-437X</issn><eissn>1099-1263</eissn><coden>JJATDK</coden><abstract>Male Sprague Dawley rats with cannulated bile duct (BDC rats) received 100 or 200 mg kg−1 labelled hexachloro‐1,3‐butadiene ([14C]HCBD) by gavage 1 h (BDC1, rats) or 24 h (BDC24 rats) after surgical cannula implantation. Twenty‐four hours after treatment with HCBD, rats were examined histochemically and biochemically for kidney damage. Urine, faeces, liver and kidney radioactivities were also measured in 24‐h samples. Results were compared with those obtained from non‐cannulated (NC) rats. Bile‐duct cannulation did not completely protect against HCBD‐induced kidney damage. The 24‐h [14C] urinary excretion and tissue content was 30–50% lower in BDC rats compared to NC rats and correlated well with the toxicity findings.
BDC1 rats appeared to be much more resistant to HCBD treatment than BDC24 rats. Since faecal [14C] radioactivity extractible by diethyl ether at neutral pH in BDC1, rats was twice that measured in BDC24 rats, the greater resistance was attributed to a higher deficiency in the gastrointestinal absorption of unchanged HCBD.
The present results reveal that the biliary metabolites of HCBD are not solely responsible for kidney toxicity as previously assumed. They suggest a sinusoidal efflux of the HCBD conjugates from the liver.</abstract><cop>Chichester</cop><pub>John Wiley & Sons, Ltd</pub><pmid>8440871</pmid><doi>10.1002/jat.2550130106</doi><tpages>6</tpages></addata></record> |
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| source | MEDLINE; Wiley Online Library Journals Frontfile Complete |
| subjects | 3-butadiene Animals Bile - metabolism biliary metabolites Biological and medical sciences Butadienes - toxicity Butadienes - urine Catheterization, Peripheral Chemical and industrial products toxicology. Toxic occupational diseases Common Bile Duct excretion Fungicides, Industrial - toxicity Fungicides, Industrial - urine Glutathione - metabolism hexachloro-1 hexachloro‐1,3‐butadiene Kidney - metabolism Kidney - pathology Kidney Diseases - chemically induced Kidney Diseases - pathology Liver - metabolism Male Medical sciences nephrotoxicity Oxidation-Reduction Rats Rats, Sprague-Dawley Toxicology Various organic compounds |
| title | Partial contribution of biliary metabolites to nephrotoxicity, renal content and excretion of [14C]hexachloro-1,3-butadiene in rats |
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