Stimulation of aniline, p-nitrophenol and N-nitrosodimethylamine metabolism in kidney by pyridine pretreatment of rabbits
Pyridine has been shown to cause liver and kidney damage in animals and in humans. In a previous study we examined the effects of pyridine on rabbit liver and lung microsomal drug-metabolizing enzymes. In this study, in vivo i.p. administration of pyridine to rabbits caused a significant 3.4-fold in...
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| Veröffentlicht in: | Archives of toxicology 2000-11, Vol.74 (9), p.527-532 |
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| creator | ARINC, Emel ADALI, Orhan GENCLER-ÖZKAN, Ayse Mine |
| description | Pyridine has been shown to cause liver and kidney damage in animals and in humans. In a previous study we examined the effects of pyridine on rabbit liver and lung microsomal drug-metabolizing enzymes. In this study, in vivo i.p. administration of pyridine to rabbits caused a significant 3.4-fold increase in kidney N-nitrosodimethylamine (NDMA) N-demethylase activity as compared to the activity in control rabbits. The same treatment also significantly stimulated the activity of other cytochrome P4502E1-associated enzymes. The activities of p-nitrophenol hydroxylase and aniline 4-hydroxylase in kidney microsomes were increased 4.9-and 4.5-fold, respectively. Pyridine treatment increased the P450 content of the kidney 1.6-fold (P |
| doi_str_mv | 10.1007/s002040000164 |
| format | Article |
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In a previous study we examined the effects of pyridine on rabbit liver and lung microsomal drug-metabolizing enzymes. In this study, in vivo i.p. administration of pyridine to rabbits caused a significant 3.4-fold increase in kidney N-nitrosodimethylamine (NDMA) N-demethylase activity as compared to the activity in control rabbits. The same treatment also significantly stimulated the activity of other cytochrome P4502E1-associated enzymes. The activities of p-nitrophenol hydroxylase and aniline 4-hydroxylase in kidney microsomes were increased 4.9-and 4.5-fold, respectively. Pyridine treatment increased the P450 content of the kidney 1.6-fold (P<0.05). SDS-PAGE of both kidney and liver microsomes of pyridine-treated rabbits showed a protein band of enhanced intensity at 51,000 Mr migrating in the region of cytochrome P4502E1. p-Aminophenol, a 4-hydroxylation product of aniline, has been shown to be nephrotoxic and NDMA, a procarcinogen, has been shown to be carcinogenic following bioactivation by NDMA N-demethylase in a number of tissues including the kidney. Since pyridine was shown to be nephrotoxic, it is expected that pyridine potentiates the toxic and/or carcinogenic effects of aniline, p-nitrophenol and NDMA through induction of their metabolism by the cytochrome P450-dependent drug-metabolizing enzymes.</description><identifier>ISSN: 0340-5761</identifier><identifier>EISSN: 1432-0738</identifier><identifier>DOI: 10.1007/s002040000164</identifier><identifier>PMID: 11131032</identifier><identifier>CODEN: ARTODN</identifier><language>eng</language><publisher>Berlin: Springer</publisher><subject>Aniline Compounds - metabolism ; Aniline Hydroxylase - metabolism ; Animals ; Biological and medical sciences ; Chemical and industrial products toxicology. Toxic occupational diseases ; Cytochrome P-450 CYP2E1 - metabolism ; In Vitro Techniques ; Kidney - drug effects ; Kidney - metabolism ; Liver - drug effects ; Liver - metabolism ; Male ; Medical sciences ; Microsomes - drug effects ; Microsomes - metabolism ; Nitrophenols - metabolism ; Nitroso Compounds - metabolism ; Oxidoreductases, N-Demethylating - metabolism ; p-Nitrophenol ; Pyridines - pharmacology ; Rabbits ; Stimulation, Chemical ; Toxicology ; Various organic compounds</subject><ispartof>Archives of toxicology, 2000-11, Vol.74 (9), p.527-532</ispartof><rights>2001 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c348t-5e947d13d4d4020d7db8677f4e7a34834f5551e6261f75ee2acd8762a5db212b3</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,778,782,27911,27912</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=797860$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/11131032$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>ARINC, Emel</creatorcontrib><creatorcontrib>ADALI, Orhan</creatorcontrib><creatorcontrib>GENCLER-ÖZKAN, Ayse Mine</creatorcontrib><title>Stimulation of aniline, p-nitrophenol and N-nitrosodimethylamine metabolism in kidney by pyridine pretreatment of rabbits</title><title>Archives of toxicology</title><addtitle>Arch Toxicol</addtitle><description>Pyridine has been shown to cause liver and kidney damage in animals and in humans. In a previous study we examined the effects of pyridine on rabbit liver and lung microsomal drug-metabolizing enzymes. In this study, in vivo i.p. administration of pyridine to rabbits caused a significant 3.4-fold increase in kidney N-nitrosodimethylamine (NDMA) N-demethylase activity as compared to the activity in control rabbits. The same treatment also significantly stimulated the activity of other cytochrome P4502E1-associated enzymes. The activities of p-nitrophenol hydroxylase and aniline 4-hydroxylase in kidney microsomes were increased 4.9-and 4.5-fold, respectively. Pyridine treatment increased the P450 content of the kidney 1.6-fold (P<0.05). SDS-PAGE of both kidney and liver microsomes of pyridine-treated rabbits showed a protein band of enhanced intensity at 51,000 Mr migrating in the region of cytochrome P4502E1. p-Aminophenol, a 4-hydroxylation product of aniline, has been shown to be nephrotoxic and NDMA, a procarcinogen, has been shown to be carcinogenic following bioactivation by NDMA N-demethylase in a number of tissues including the kidney. Since pyridine was shown to be nephrotoxic, it is expected that pyridine potentiates the toxic and/or carcinogenic effects of aniline, p-nitrophenol and NDMA through induction of their metabolism by the cytochrome P450-dependent drug-metabolizing enzymes.</description><subject>Aniline Compounds - metabolism</subject><subject>Aniline Hydroxylase - metabolism</subject><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Chemical and industrial products toxicology. Toxic occupational diseases</subject><subject>Cytochrome P-450 CYP2E1 - metabolism</subject><subject>In Vitro Techniques</subject><subject>Kidney - drug effects</subject><subject>Kidney - metabolism</subject><subject>Liver - drug effects</subject><subject>Liver - metabolism</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Microsomes - drug effects</subject><subject>Microsomes - metabolism</subject><subject>Nitrophenols - metabolism</subject><subject>Nitroso Compounds - metabolism</subject><subject>Oxidoreductases, N-Demethylating - metabolism</subject><subject>p-Nitrophenol</subject><subject>Pyridines - pharmacology</subject><subject>Rabbits</subject><subject>Stimulation, Chemical</subject><subject>Toxicology</subject><subject>Various organic compounds</subject><issn>0340-5761</issn><issn>1432-0738</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2000</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpV0E1LxDAQBuAgiruuHr1KQPBkNV9t2qMsfsGiB_Vc0mbKRtO0JtlD_71ZdlHMZcLwMMO8CJ1TckMJkbeBEEYESY8W4gDNqeAsI5KXh2hOuCBZLgs6QychfCbCyoofoxmllFPC2RxNb9H0G6uiGRweOqycscbBNR4zZ6IfxjW4waa2xi-7Thi06SGuJ6v6JHH6q2awJvTYOPxltIMJNxMeJ2_0FoweogcVe3Bxu8KrpjExnKKjTtkAZ_u6QB8P9-_Lp2z1-vi8vFtlLRdlzHKohNSUa6FFulRL3ZSFlJ0AqRLgosvznELBCtrJHICpVpeyYCrXDaOs4Qt0tZs7-uF7AyHWvQktWKscDJtQUylFVVU0wWwH23Rk8NDVoze98lNNSb3Nuv6XdfIX-8Gbpgf9p_fhJnC5Byq0ynZeudaEXycrWRaE_wARMIfB</recordid><startdate>20001101</startdate><enddate>20001101</enddate><creator>ARINC, Emel</creator><creator>ADALI, Orhan</creator><creator>GENCLER-ÖZKAN, Ayse Mine</creator><general>Springer</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>20001101</creationdate><title>Stimulation of aniline, p-nitrophenol and N-nitrosodimethylamine metabolism in kidney by pyridine pretreatment of rabbits</title><author>ARINC, Emel ; ADALI, Orhan ; GENCLER-ÖZKAN, Ayse Mine</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c348t-5e947d13d4d4020d7db8677f4e7a34834f5551e6261f75ee2acd8762a5db212b3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2000</creationdate><topic>Aniline Compounds - metabolism</topic><topic>Aniline Hydroxylase - metabolism</topic><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Chemical and industrial products toxicology. Toxic occupational diseases</topic><topic>Cytochrome P-450 CYP2E1 - metabolism</topic><topic>In Vitro Techniques</topic><topic>Kidney - drug effects</topic><topic>Kidney - metabolism</topic><topic>Liver - drug effects</topic><topic>Liver - metabolism</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Microsomes - drug effects</topic><topic>Microsomes - metabolism</topic><topic>Nitrophenols - metabolism</topic><topic>Nitroso Compounds - metabolism</topic><topic>Oxidoreductases, N-Demethylating - metabolism</topic><topic>p-Nitrophenol</topic><topic>Pyridines - pharmacology</topic><topic>Rabbits</topic><topic>Stimulation, Chemical</topic><topic>Toxicology</topic><topic>Various organic compounds</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>ARINC, Emel</creatorcontrib><creatorcontrib>ADALI, Orhan</creatorcontrib><creatorcontrib>GENCLER-ÖZKAN, Ayse Mine</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>Archives of toxicology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>ARINC, Emel</au><au>ADALI, Orhan</au><au>GENCLER-ÖZKAN, Ayse Mine</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Stimulation of aniline, p-nitrophenol and N-nitrosodimethylamine metabolism in kidney by pyridine pretreatment of rabbits</atitle><jtitle>Archives of toxicology</jtitle><addtitle>Arch Toxicol</addtitle><date>2000-11-01</date><risdate>2000</risdate><volume>74</volume><issue>9</issue><spage>527</spage><epage>532</epage><pages>527-532</pages><issn>0340-5761</issn><eissn>1432-0738</eissn><coden>ARTODN</coden><abstract>Pyridine has been shown to cause liver and kidney damage in animals and in humans. In a previous study we examined the effects of pyridine on rabbit liver and lung microsomal drug-metabolizing enzymes. In this study, in vivo i.p. administration of pyridine to rabbits caused a significant 3.4-fold increase in kidney N-nitrosodimethylamine (NDMA) N-demethylase activity as compared to the activity in control rabbits. The same treatment also significantly stimulated the activity of other cytochrome P4502E1-associated enzymes. The activities of p-nitrophenol hydroxylase and aniline 4-hydroxylase in kidney microsomes were increased 4.9-and 4.5-fold, respectively. Pyridine treatment increased the P450 content of the kidney 1.6-fold (P<0.05). SDS-PAGE of both kidney and liver microsomes of pyridine-treated rabbits showed a protein band of enhanced intensity at 51,000 Mr migrating in the region of cytochrome P4502E1. p-Aminophenol, a 4-hydroxylation product of aniline, has been shown to be nephrotoxic and NDMA, a procarcinogen, has been shown to be carcinogenic following bioactivation by NDMA N-demethylase in a number of tissues including the kidney. Since pyridine was shown to be nephrotoxic, it is expected that pyridine potentiates the toxic and/or carcinogenic effects of aniline, p-nitrophenol and NDMA through induction of their metabolism by the cytochrome P450-dependent drug-metabolizing enzymes.</abstract><cop>Berlin</cop><pub>Springer</pub><pmid>11131032</pmid><doi>10.1007/s002040000164</doi><tpages>6</tpages></addata></record> |
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| subjects | Aniline Compounds - metabolism Aniline Hydroxylase - metabolism Animals Biological and medical sciences Chemical and industrial products toxicology. Toxic occupational diseases Cytochrome P-450 CYP2E1 - metabolism In Vitro Techniques Kidney - drug effects Kidney - metabolism Liver - drug effects Liver - metabolism Male Medical sciences Microsomes - drug effects Microsomes - metabolism Nitrophenols - metabolism Nitroso Compounds - metabolism Oxidoreductases, N-Demethylating - metabolism p-Nitrophenol Pyridines - pharmacology Rabbits Stimulation, Chemical Toxicology Various organic compounds |
| title | Stimulation of aniline, p-nitrophenol and N-nitrosodimethylamine metabolism in kidney by pyridine pretreatment of rabbits |
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