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The role of DNA-repair processes in N-nitrosopyrrolidine-induced mutagenesis
The cytotoxic and mutagenic effects of increasing concentrations of N-nitrosopyrrolidine (NPYR) were studied using various DNA repair mutants of Escherichia coli together with rat-liver S9 activation system. Irrespective of which strain was used, the cytotoxic effects of NPYR were similar to those o...
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Published in: | Carcinogenesis (New York) 1985-01, Vol.6 (1), p.105-108 |
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container_title | Carcinogenesis (New York) |
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creator | Alldrick, A.J. Cottrell, R.C. Rowland, I.R. Gangolli, S.D. |
description | The cytotoxic and mutagenic effects of increasing concentrations of N-nitrosopyrrolidine (NPYR) were studied using various DNA repair mutants of Escherichia coli together with rat-liver S9 activation system. Irrespective of which strain was used, the cytotoxic effects of NPYR were similar to those observed in the parent strain. Mutagenicity studies revealed that the uvrA− derivative was more mutable than its repair proficient parent. These observations suggest that NPYR reacts with DNA to generate bulky lesions, which although potentially mutagenic, do not contribute significantly to cellkilling. Subsequent experiments with the metabolic inhibitor SKF 525A revealed that this compound only partially inhibited the mutagenic activity of NPYR, suggesting that although hepatic mixed function oxidase enzymes may participate in NPYR activation other pathways of metabolism are also involved. |
doi_str_mv | 10.1093/carcin/6.1.105 |
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Subsequent experiments with the metabolic inhibitor SKF 525A revealed that this compound only partially inhibited the mutagenic activity of NPYR, suggesting that although hepatic mixed function oxidase enzymes may participate in NPYR activation other pathways of metabolism are also involved.</description><identifier>ISSN: 0143-3334</identifier><identifier>EISSN: 1460-2180</identifier><identifier>DOI: 10.1093/carcin/6.1.105</identifier><identifier>PMID: 3967328</identifier><identifier>CODEN: CRNGDP</identifier><language>eng</language><publisher>Oxford: Oxford University Press</publisher><subject>Animals ; Biological and medical sciences ; Cell Survival - drug effects ; Chemical mutagenesis ; DNA Repair ; Escherichia coli ; Male ; Medical sciences ; Microsomes, Liver - metabolism ; Mutation ; N-Nitrosopyrrolidine - metabolism ; N-Nitrosopyrrolidine - toxicity ; Nitrosamines - toxicity ; Proadifen - pharmacology ; Rats ; Rats, Inbred Strains ; Toxicology</subject><ispartof>Carcinogenesis (New York), 1985-01, Vol.6 (1), p.105-108</ispartof><rights>1986 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c388t-dafcda9487fa9d7d5fa50c7725c192c2e3f2e6bd3ed8f4a4318e22678c1fb4573</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,4024,27923,27924,27925</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=8463271$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/3967328$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Alldrick, A.J.</creatorcontrib><creatorcontrib>Cottrell, R.C.</creatorcontrib><creatorcontrib>Rowland, I.R.</creatorcontrib><creatorcontrib>Gangolli, S.D.</creatorcontrib><title>The role of DNA-repair processes in N-nitrosopyrrolidine-induced mutagenesis</title><title>Carcinogenesis (New York)</title><addtitle>Carcinogenesis</addtitle><description>The cytotoxic and mutagenic effects of increasing concentrations of N-nitrosopyrrolidine (NPYR) were studied using various DNA repair mutants of Escherichia coli together with rat-liver S9 activation system. Irrespective of which strain was used, the cytotoxic effects of NPYR were similar to those observed in the parent strain. Mutagenicity studies revealed that the uvrA− derivative was more mutable than its repair proficient parent. These observations suggest that NPYR reacts with DNA to generate bulky lesions, which although potentially mutagenic, do not contribute significantly to cellkilling. Subsequent experiments with the metabolic inhibitor SKF 525A revealed that this compound only partially inhibited the mutagenic activity of NPYR, suggesting that although hepatic mixed function oxidase enzymes may participate in NPYR activation other pathways of metabolism are also involved.</description><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Cell Survival - drug effects</subject><subject>Chemical mutagenesis</subject><subject>DNA Repair</subject><subject>Escherichia coli</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Microsomes, Liver - metabolism</subject><subject>Mutation</subject><subject>N-Nitrosopyrrolidine - metabolism</subject><subject>N-Nitrosopyrrolidine - toxicity</subject><subject>Nitrosamines - toxicity</subject><subject>Proadifen - pharmacology</subject><subject>Rats</subject><subject>Rats, Inbred Strains</subject><subject>Toxicology</subject><issn>0143-3334</issn><issn>1460-2180</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1985</creationdate><recordtype>article</recordtype><recordid>eNo9kEFvEzEUhC1EVULplRvSHhA3p7afvfYeq0BbRBouRUK9WI79DIbNbmrvSvTf1yhRTk-j-d5oNIS852zJWQdX3mWfhqt2yatWr8iCy5ZRwQ17TRaMS6AAIN-Qt6X8YYy3oLpzcg5dq0GYBVk__MYmjz02Y2w-b65pxr1Ludnn0WMpWJo0NBs6pCmPZdw_58qmkAakaQizx9Ds5sn9wgFLKu_IWXR9wcvjvSA_br48rO7o-vvt19X1mnowZqLBRR9cJ42Orgs6qOgU81oL5XknvECIAtttAAwmSieBGxSi1cbzuJVKwwX5dMitLZ9mLJPdpeKx792A41wslxwUKFnB5QH0tX3JGO0-p53Lz5Yz-38-e5jPtpZXrerDh2PyvN1hOOHHvar_8ei74l0fsxt8KifMyBaE5hWjByyVCf-dbJf_2pqjlb37-WjNSt98U-zebuAFpquJDQ</recordid><startdate>198501</startdate><enddate>198501</enddate><creator>Alldrick, A.J.</creator><creator>Cottrell, R.C.</creator><creator>Rowland, I.R.</creator><creator>Gangolli, S.D.</creator><general>Oxford University Press</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>7TM</scope><scope>7U7</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>P64</scope><scope>RC3</scope></search><sort><creationdate>198501</creationdate><title>The role of DNA-repair processes in N-nitrosopyrrolidine-induced mutagenesis</title><author>Alldrick, A.J. ; Cottrell, R.C. ; Rowland, I.R. ; Gangolli, S.D.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c388t-dafcda9487fa9d7d5fa50c7725c192c2e3f2e6bd3ed8f4a4318e22678c1fb4573</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1985</creationdate><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Cell Survival - drug effects</topic><topic>Chemical mutagenesis</topic><topic>DNA Repair</topic><topic>Escherichia coli</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Microsomes, Liver - metabolism</topic><topic>Mutation</topic><topic>N-Nitrosopyrrolidine - metabolism</topic><topic>N-Nitrosopyrrolidine - toxicity</topic><topic>Nitrosamines - toxicity</topic><topic>Proadifen - pharmacology</topic><topic>Rats</topic><topic>Rats, Inbred Strains</topic><topic>Toxicology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Alldrick, A.J.</creatorcontrib><creatorcontrib>Cottrell, R.C.</creatorcontrib><creatorcontrib>Rowland, I.R.</creatorcontrib><creatorcontrib>Gangolli, S.D.</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>Nucleic Acids Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Technology Research Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Engineering Research Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><jtitle>Carcinogenesis (New York)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Alldrick, A.J.</au><au>Cottrell, R.C.</au><au>Rowland, I.R.</au><au>Gangolli, S.D.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The role of DNA-repair processes in N-nitrosopyrrolidine-induced mutagenesis</atitle><jtitle>Carcinogenesis (New York)</jtitle><addtitle>Carcinogenesis</addtitle><date>1985-01</date><risdate>1985</risdate><volume>6</volume><issue>1</issue><spage>105</spage><epage>108</epage><pages>105-108</pages><issn>0143-3334</issn><eissn>1460-2180</eissn><coden>CRNGDP</coden><abstract>The cytotoxic and mutagenic effects of increasing concentrations of N-nitrosopyrrolidine (NPYR) were studied using various DNA repair mutants of Escherichia coli together with rat-liver S9 activation system. Irrespective of which strain was used, the cytotoxic effects of NPYR were similar to those observed in the parent strain. Mutagenicity studies revealed that the uvrA− derivative was more mutable than its repair proficient parent. These observations suggest that NPYR reacts with DNA to generate bulky lesions, which although potentially mutagenic, do not contribute significantly to cellkilling. Subsequent experiments with the metabolic inhibitor SKF 525A revealed that this compound only partially inhibited the mutagenic activity of NPYR, suggesting that although hepatic mixed function oxidase enzymes may participate in NPYR activation other pathways of metabolism are also involved.</abstract><cop>Oxford</cop><pub>Oxford University Press</pub><pmid>3967328</pmid><doi>10.1093/carcin/6.1.105</doi><tpages>4</tpages></addata></record> |
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source | Oxford University Press:Jisc Collections:Oxford Journal Archive: Access period 2024-2025 |
subjects | Animals Biological and medical sciences Cell Survival - drug effects Chemical mutagenesis DNA Repair Escherichia coli Male Medical sciences Microsomes, Liver - metabolism Mutation N-Nitrosopyrrolidine - metabolism N-Nitrosopyrrolidine - toxicity Nitrosamines - toxicity Proadifen - pharmacology Rats Rats, Inbred Strains Toxicology |
title | The role of DNA-repair processes in N-nitrosopyrrolidine-induced mutagenesis |
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