Nephrotoxicity of bromobenzene in mice
I.p. administration of bromobenzene to male mice at doses ranging from 0 to 9.4 mmol kg resulted in a dose-dependent increase in blood urea nitrogen (BUN) and serum glutamic-pyruvic transaminase (SGPT) activity and a decrease in renal cortical accumulation of para-aminohippurate (PAH) and tetraethyl...
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| Veröffentlicht in: | Toxicology letters 1984, Vol.20 (1), p.23-32 |
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| creator | Rush, Glenn F. Kuo, Chao-Hen Hook, Jerry B. |
| description | I.p. administration of bromobenzene to male mice at doses ranging from 0 to 9.4
mmol
kg
resulted in a dose-dependent increase in blood urea nitrogen (BUN) and serum glutamic-pyruvic transaminase (SGPT) activity and a decrease in renal cortical accumulation of
para-aminohippurate (PAH) and tetraethylammonium (TEA). Induction of renal and hepatic mixed-function oxidases by β-naphthoflavone (BNF) did not result in any alterations in the hepatotoxic or nephrotoxic response to bromobenzene. Renal and hepatic non-protein sulfhydryl (NPSH) concentrations were decreased significantly 1 h after administration of bromobenzene (7.5
mmol
kg
) and were maximally depleted in both organs to 18% of control after 7 h. Depletion of renal NPSH by bromobenzene was dose-dependent up to 9.4
mmol
kg
. Treatment of mice with diethyl maleate (DEM) (0.6
ml
kg
) 60 min prior to bromobenzene administration resulted in greater hepatotoxicity, evidenced by increased SGPT, while renal toxicity was unchanged. These data demonstrate that large doses of bromobenzene produce functional alterations in the kidney. |
| doi_str_mv | 10.1016/0378-4274(84)90178-4 |
| format | Article |
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mmol
kg
resulted in a dose-dependent increase in blood urea nitrogen (BUN) and serum glutamic-pyruvic transaminase (SGPT) activity and a decrease in renal cortical accumulation of
para-aminohippurate (PAH) and tetraethylammonium (TEA). Induction of renal and hepatic mixed-function oxidases by β-naphthoflavone (BNF) did not result in any alterations in the hepatotoxic or nephrotoxic response to bromobenzene. Renal and hepatic non-protein sulfhydryl (NPSH) concentrations were decreased significantly 1 h after administration of bromobenzene (7.5
mmol
kg
) and were maximally depleted in both organs to 18% of control after 7 h. Depletion of renal NPSH by bromobenzene was dose-dependent up to 9.4
mmol
kg
. Treatment of mice with diethyl maleate (DEM) (0.6
ml
kg
) 60 min prior to bromobenzene administration resulted in greater hepatotoxicity, evidenced by increased SGPT, while renal toxicity was unchanged. These data demonstrate that large doses of bromobenzene produce functional alterations in the kidney.</description><identifier>ISSN: 0378-4274</identifier><identifier>EISSN: 1879-3169</identifier><identifier>DOI: 10.1016/0378-4274(84)90178-4</identifier><identifier>PMID: 6695393</identifier><identifier>CODEN: TOLED5</identifier><language>eng</language><publisher>Shannon: Elsevier Ireland Ltd</publisher><subject>Animals ; Benzoflavones - pharmacology ; beta-Naphthoflavone ; Biological and medical sciences ; Bromobenzene ; Bromobenzenes - metabolism ; Bromobenzenes - toxicity ; bromocatechol ; bromophenol ; Chemical and industrial products toxicology. Toxic occupational diseases ; Kidney - drug effects ; Liver - drug effects ; Male ; Maleates - pharmacology ; Medical sciences ; Mice ; Mice, Inbred ICR ; nephrotoxicity ; Sulfhydryl Compounds - analysis ; Toxicology ; Various organic compounds</subject><ispartof>Toxicology letters, 1984, Vol.20 (1), p.23-32</ispartof><rights>1984</rights><rights>1984 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c417t-ef9a2b7c3c786d034bc3c9cdf6d4f094cfe2fed89a751f2cbee775a1ec8ce0ef3</citedby><cites>FETCH-LOGICAL-c417t-ef9a2b7c3c786d034bc3c9cdf6d4f094cfe2fed89a751f2cbee775a1ec8ce0ef3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/0378-4274(84)90178-4$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,780,784,3550,4024,27923,27924,27925,45995</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=9527563$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/6695393$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Rush, Glenn F.</creatorcontrib><creatorcontrib>Kuo, Chao-Hen</creatorcontrib><creatorcontrib>Hook, Jerry B.</creatorcontrib><title>Nephrotoxicity of bromobenzene in mice</title><title>Toxicology letters</title><addtitle>Toxicol Lett</addtitle><description>I.p. administration of bromobenzene to male mice at doses ranging from 0 to 9.4
mmol
kg
resulted in a dose-dependent increase in blood urea nitrogen (BUN) and serum glutamic-pyruvic transaminase (SGPT) activity and a decrease in renal cortical accumulation of
para-aminohippurate (PAH) and tetraethylammonium (TEA). Induction of renal and hepatic mixed-function oxidases by β-naphthoflavone (BNF) did not result in any alterations in the hepatotoxic or nephrotoxic response to bromobenzene. Renal and hepatic non-protein sulfhydryl (NPSH) concentrations were decreased significantly 1 h after administration of bromobenzene (7.5
mmol
kg
) and were maximally depleted in both organs to 18% of control after 7 h. Depletion of renal NPSH by bromobenzene was dose-dependent up to 9.4
mmol
kg
. Treatment of mice with diethyl maleate (DEM) (0.6
ml
kg
) 60 min prior to bromobenzene administration resulted in greater hepatotoxicity, evidenced by increased SGPT, while renal toxicity was unchanged. These data demonstrate that large doses of bromobenzene produce functional alterations in the kidney.</description><subject>Animals</subject><subject>Benzoflavones - pharmacology</subject><subject>beta-Naphthoflavone</subject><subject>Biological and medical sciences</subject><subject>Bromobenzene</subject><subject>Bromobenzenes - metabolism</subject><subject>Bromobenzenes - toxicity</subject><subject>bromocatechol</subject><subject>bromophenol</subject><subject>Chemical and industrial products toxicology. Toxic occupational diseases</subject><subject>Kidney - drug effects</subject><subject>Liver - drug effects</subject><subject>Male</subject><subject>Maleates - pharmacology</subject><subject>Medical sciences</subject><subject>Mice</subject><subject>Mice, Inbred ICR</subject><subject>nephrotoxicity</subject><subject>Sulfhydryl Compounds - analysis</subject><subject>Toxicology</subject><subject>Various organic compounds</subject><issn>0378-4274</issn><issn>1879-3169</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1984</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kE9PwzAMxSMEGmPwDUDaAU1wKCRtmjQXJDTxT5rgAucodR0RtDYj6RDj09OyakdOtvV-tvweIaeMXjHKxDXNZJHwVPKLgl8qyvppj4xZIVWSMaH2yXiHHJKjGD8opYKLfERGQqg8U9mYzJ5x9R58678duHYz9XZaBl_7EpsfbHDqmmntAI_JgTXLiCdDnZC3-7vX-WOyeHl4mt8uEuBMtglaZdJSQgayEBXNeNm1CiorKm6p4mAxtVgVysic2RRKRClzwxAKQIo2m5DZ9u4q-M81xlbXLgIul6ZBv46adYZYkWYdyLcgBB9jQKtXwdUmbDSjuo9H9951710XXP_Fo3m3djbcX5c1VrulIY9OPx90E8EsbTANuLjDVJ7KXPTYzRbDLosvh0FHcNgAVi4gtLry7v8_fgE-1YFp</recordid><startdate>1984</startdate><enddate>1984</enddate><creator>Rush, Glenn F.</creator><creator>Kuo, Chao-Hen</creator><creator>Hook, Jerry B.</creator><general>Elsevier Ireland Ltd</general><general>Elsevier Science</general><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>7U7</scope><scope>C1K</scope></search><sort><creationdate>1984</creationdate><title>Nephrotoxicity of bromobenzene in mice</title><author>Rush, Glenn F. ; Kuo, Chao-Hen ; Hook, Jerry B.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c417t-ef9a2b7c3c786d034bc3c9cdf6d4f094cfe2fed89a751f2cbee775a1ec8ce0ef3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1984</creationdate><topic>Animals</topic><topic>Benzoflavones - pharmacology</topic><topic>beta-Naphthoflavone</topic><topic>Biological and medical sciences</topic><topic>Bromobenzene</topic><topic>Bromobenzenes - metabolism</topic><topic>Bromobenzenes - toxicity</topic><topic>bromocatechol</topic><topic>bromophenol</topic><topic>Chemical and industrial products toxicology. Toxic occupational diseases</topic><topic>Kidney - drug effects</topic><topic>Liver - drug effects</topic><topic>Male</topic><topic>Maleates - pharmacology</topic><topic>Medical sciences</topic><topic>Mice</topic><topic>Mice, Inbred ICR</topic><topic>nephrotoxicity</topic><topic>Sulfhydryl Compounds - analysis</topic><topic>Toxicology</topic><topic>Various organic compounds</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Rush, Glenn F.</creatorcontrib><creatorcontrib>Kuo, Chao-Hen</creatorcontrib><creatorcontrib>Hook, Jerry B.</creatorcontrib><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>Toxicology Abstracts</collection><collection>Environmental Sciences and Pollution Management</collection><jtitle>Toxicology letters</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Rush, Glenn F.</au><au>Kuo, Chao-Hen</au><au>Hook, Jerry B.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Nephrotoxicity of bromobenzene in mice</atitle><jtitle>Toxicology letters</jtitle><addtitle>Toxicol Lett</addtitle><date>1984</date><risdate>1984</risdate><volume>20</volume><issue>1</issue><spage>23</spage><epage>32</epage><pages>23-32</pages><issn>0378-4274</issn><eissn>1879-3169</eissn><coden>TOLED5</coden><abstract>I.p. administration of bromobenzene to male mice at doses ranging from 0 to 9.4
mmol
kg
resulted in a dose-dependent increase in blood urea nitrogen (BUN) and serum glutamic-pyruvic transaminase (SGPT) activity and a decrease in renal cortical accumulation of
para-aminohippurate (PAH) and tetraethylammonium (TEA). Induction of renal and hepatic mixed-function oxidases by β-naphthoflavone (BNF) did not result in any alterations in the hepatotoxic or nephrotoxic response to bromobenzene. Renal and hepatic non-protein sulfhydryl (NPSH) concentrations were decreased significantly 1 h after administration of bromobenzene (7.5
mmol
kg
) and were maximally depleted in both organs to 18% of control after 7 h. Depletion of renal NPSH by bromobenzene was dose-dependent up to 9.4
mmol
kg
. Treatment of mice with diethyl maleate (DEM) (0.6
ml
kg
) 60 min prior to bromobenzene administration resulted in greater hepatotoxicity, evidenced by increased SGPT, while renal toxicity was unchanged. These data demonstrate that large doses of bromobenzene produce functional alterations in the kidney.</abstract><cop>Shannon</cop><cop>Amsterdam</cop><pub>Elsevier Ireland Ltd</pub><pmid>6695393</pmid><doi>10.1016/0378-4274(84)90178-4</doi><tpages>10</tpages></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0378-4274 |
| ispartof | Toxicology letters, 1984, Vol.20 (1), p.23-32 |
| issn | 0378-4274 1879-3169 |
| language | eng |
| recordid | cdi_proquest_miscellaneous_13781823 |
| source | MEDLINE; Elsevier ScienceDirect Journals Complete |
| subjects | Animals Benzoflavones - pharmacology beta-Naphthoflavone Biological and medical sciences Bromobenzene Bromobenzenes - metabolism Bromobenzenes - toxicity bromocatechol bromophenol Chemical and industrial products toxicology. Toxic occupational diseases Kidney - drug effects Liver - drug effects Male Maleates - pharmacology Medical sciences Mice Mice, Inbred ICR nephrotoxicity Sulfhydryl Compounds - analysis Toxicology Various organic compounds |
| title | Nephrotoxicity of bromobenzene in mice |
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