Lack of modification of 2-amino-3,8-dimethylimidazo[4,5- f]quinoxaline (MeIQx)-induced hepatocarcinogenesis in rats by fenbendazole – a CYP1A2 inducer
Fenbendazole (FBZ) is an anthelmintic drug known to be a potent CYP1A2 inducer. Combined effects of FBZ on 2-amino-3,8-dimethylimidazo[4,5- f]quinoxaline (MeIQx)-induced hepatocarcinogenesis in rats were investigated using a medium-term liver bioassay system. No modifying influence was found in term...
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| Veröffentlicht in: | Cancer letters 2002-11, Vol.185 (1), p.39-45 |
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| creator | Suzuki, Shugo Takahashi, Satoru Asamoto, Makoto Inaguma, Shingo Ogiso, Tadashi Hirose, Masao Shirai, Tomoyuki |
| description | Fenbendazole (FBZ) is an anthelmintic drug known to be a potent CYP1A2 inducer. Combined effects of FBZ on 2-amino-3,8-dimethylimidazo[4,5-
f]quinoxaline (MeIQx)-induced hepatocarcinogenesis in rats were investigated using a medium-term liver bioassay system. No modifying influence was found in terms of glutathione S-transferase placental-form positive foci development although CYP1A2 protein expression in the livers of rats that were given MeIQx and FBZ was 2.3-fold higher than with MeIQx alone. NAT2 mRNA expression did not differ among the groups as revealed by quantitative reverse transcriptase-polymerase chain reaction analysis. These results suggest that elevated CYP1A2 expression is not sufficient to enhance MeIQx-induced hepatocarcinogenesis. |
| doi_str_mv | 10.1016/S0304-3835(02)00243-4 |
| format | Article |
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f]quinoxaline (MeIQx)-induced hepatocarcinogenesis in rats were investigated using a medium-term liver bioassay system. No modifying influence was found in terms of glutathione S-transferase placental-form positive foci development although CYP1A2 protein expression in the livers of rats that were given MeIQx and FBZ was 2.3-fold higher than with MeIQx alone. NAT2 mRNA expression did not differ among the groups as revealed by quantitative reverse transcriptase-polymerase chain reaction analysis. These results suggest that elevated CYP1A2 expression is not sufficient to enhance MeIQx-induced hepatocarcinogenesis.</description><identifier>ISSN: 0304-3835</identifier><identifier>EISSN: 1872-7980</identifier><identifier>DOI: 10.1016/S0304-3835(02)00243-4</identifier><identifier>PMID: 12142077</identifier><identifier>CODEN: CALEDQ</identifier><language>eng</language><publisher>Shannon: Elsevier Ireland Ltd</publisher><subject>2-Amino-3,8-dimethylimidazo[4,5- f]quinoxaline ; Animals ; Antinematodal Agents - pharmacology ; Arylamine N-Acetyltransferase - genetics ; Arylamine N-Acetyltransferase - metabolism ; Bioassays ; Biological and medical sciences ; Blotting, Western ; Carcinogenesis, carcinogens and anticarcinogens ; Carcinogens - toxicity ; Carcinoma, Hepatocellular - chemically induced ; Carcinoma, Hepatocellular - enzymology ; Chemical agents ; CYP1A2 ; Cytochrome P-450 CYP1A2 - metabolism ; DNA Primers - chemistry ; Drug Combinations ; Drug Synergism ; Enzyme Induction ; Fenbendazole ; Fenbendazole - pharmacology ; Food ; Glutathione Transferase - metabolism ; Hepatocarcinogenesis ; Immunoenzyme Techniques ; Liver - drug effects ; Liver - enzymology ; Liver Neoplasms, Experimental - chemically induced ; Liver Neoplasms, Experimental - enzymology ; Male ; Medical sciences ; Microsomes, Liver - drug effects ; Microsomes, Liver - enzymology ; Quinoxalines - toxicity ; Rat ; Rats ; Rats, Inbred F344 ; Reverse Transcriptase Polymerase Chain Reaction ; Rodents ; Tumors</subject><ispartof>Cancer letters, 2002-11, Vol.185 (1), p.39-45</ispartof><rights>2002 Elsevier Science Ireland Ltd</rights><rights>2003 INIST-CNRS</rights><rights>Copyright Elsevier Limited Nov 8, 2002</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c485t-dc546be6eecc36f9674a66242f35f0d5c4e6ada7b7ea1c7fe10798743023636d3</citedby><cites>FETCH-LOGICAL-c485t-dc546be6eecc36f9674a66242f35f0d5c4e6ada7b7ea1c7fe10798743023636d3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S0304383502002434$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,776,780,3537,27903,27904,65309</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=13910833$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/12142077$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Suzuki, Shugo</creatorcontrib><creatorcontrib>Takahashi, Satoru</creatorcontrib><creatorcontrib>Asamoto, Makoto</creatorcontrib><creatorcontrib>Inaguma, Shingo</creatorcontrib><creatorcontrib>Ogiso, Tadashi</creatorcontrib><creatorcontrib>Hirose, Masao</creatorcontrib><creatorcontrib>Shirai, Tomoyuki</creatorcontrib><title>Lack of modification of 2-amino-3,8-dimethylimidazo[4,5- f]quinoxaline (MeIQx)-induced hepatocarcinogenesis in rats by fenbendazole – a CYP1A2 inducer</title><title>Cancer letters</title><addtitle>Cancer Lett</addtitle><description>Fenbendazole (FBZ) is an anthelmintic drug known to be a potent CYP1A2 inducer. Combined effects of FBZ on 2-amino-3,8-dimethylimidazo[4,5-
f]quinoxaline (MeIQx)-induced hepatocarcinogenesis in rats were investigated using a medium-term liver bioassay system. No modifying influence was found in terms of glutathione S-transferase placental-form positive foci development although CYP1A2 protein expression in the livers of rats that were given MeIQx and FBZ was 2.3-fold higher than with MeIQx alone. NAT2 mRNA expression did not differ among the groups as revealed by quantitative reverse transcriptase-polymerase chain reaction analysis. These results suggest that elevated CYP1A2 expression is not sufficient to enhance MeIQx-induced hepatocarcinogenesis.</description><subject>2-Amino-3,8-dimethylimidazo[4,5- f]quinoxaline</subject><subject>Animals</subject><subject>Antinematodal Agents - pharmacology</subject><subject>Arylamine N-Acetyltransferase - genetics</subject><subject>Arylamine N-Acetyltransferase - metabolism</subject><subject>Bioassays</subject><subject>Biological and medical sciences</subject><subject>Blotting, Western</subject><subject>Carcinogenesis, carcinogens and anticarcinogens</subject><subject>Carcinogens - toxicity</subject><subject>Carcinoma, Hepatocellular - chemically induced</subject><subject>Carcinoma, Hepatocellular - enzymology</subject><subject>Chemical agents</subject><subject>CYP1A2</subject><subject>Cytochrome P-450 CYP1A2 - metabolism</subject><subject>DNA Primers - chemistry</subject><subject>Drug Combinations</subject><subject>Drug Synergism</subject><subject>Enzyme Induction</subject><subject>Fenbendazole</subject><subject>Fenbendazole - pharmacology</subject><subject>Food</subject><subject>Glutathione Transferase - metabolism</subject><subject>Hepatocarcinogenesis</subject><subject>Immunoenzyme Techniques</subject><subject>Liver - drug effects</subject><subject>Liver - enzymology</subject><subject>Liver Neoplasms, Experimental - chemically induced</subject><subject>Liver Neoplasms, Experimental - enzymology</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Microsomes, Liver - drug effects</subject><subject>Microsomes, Liver - enzymology</subject><subject>Quinoxalines - toxicity</subject><subject>Rat</subject><subject>Rats</subject><subject>Rats, Inbred F344</subject><subject>Reverse Transcriptase Polymerase Chain Reaction</subject><subject>Rodents</subject><subject>Tumors</subject><issn>0304-3835</issn><issn>1872-7980</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2002</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkd9qFDEUxgdR7Fp9BCUgQguN5v_MXpWy2FpYUVEvRCRkkhObOpPZJjPS9cp38Mbn80nMdhd76dXhwO_7zuH7quoxJc8poerFe8KJwLzh8oCwQ0KY4FjcqWa0qRmu5w25W83-IXvVg5wvCSFS1PJ-tUcZFYzU9az6vTT2Gxo86gcXfLBmDEPc7AybPsQB86MGu9DDeLHuQh-c-TF8FkcSI__lairAtelCBHTwGs7fXR_iEN1kwaELWJlxsCbZwnyFCDlkFCJKZsyoXSMPsYW4cesA_fn5Cxm0-PSWnjC0dUgPq3vedBke7eZ-9fH05YfFK7x8c3a-OFliKxo5YmelUC0oAGu58nNVC6MUE8xz6YmTVoAyztRtDYba2gMlJZxacMK44srx_erp1neVhqsJ8qgvhynFclJTSSRXdK5IoeSWsmnIOYHXqxR6k9aaEr3pQ9_0oTdha8L0TR9aFN2TnfvU9uBuVbsCCvBsB5hsTeeTiTbkW47PKWk4L9zxloOSxfcASWcbIJaoQwI7ajeE_7zyF8-8p4g</recordid><startdate>20021108</startdate><enddate>20021108</enddate><creator>Suzuki, Shugo</creator><creator>Takahashi, Satoru</creator><creator>Asamoto, Makoto</creator><creator>Inaguma, Shingo</creator><creator>Ogiso, Tadashi</creator><creator>Hirose, Masao</creator><creator>Shirai, Tomoyuki</creator><general>Elsevier Ireland Ltd</general><general>Elsevier</general><general>Elsevier Limited</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>7TO</scope><scope>7U9</scope><scope>H94</scope><scope>K9.</scope><scope>NAPCQ</scope></search><sort><creationdate>20021108</creationdate><title>Lack of modification of 2-amino-3,8-dimethylimidazo[4,5- f]quinoxaline (MeIQx)-induced hepatocarcinogenesis in rats by fenbendazole – a CYP1A2 inducer</title><author>Suzuki, Shugo ; Takahashi, Satoru ; Asamoto, Makoto ; Inaguma, Shingo ; Ogiso, Tadashi ; Hirose, Masao ; Shirai, Tomoyuki</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c485t-dc546be6eecc36f9674a66242f35f0d5c4e6ada7b7ea1c7fe10798743023636d3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2002</creationdate><topic>2-Amino-3,8-dimethylimidazo[4,5- f]quinoxaline</topic><topic>Animals</topic><topic>Antinematodal Agents - pharmacology</topic><topic>Arylamine N-Acetyltransferase - genetics</topic><topic>Arylamine N-Acetyltransferase - metabolism</topic><topic>Bioassays</topic><topic>Biological and medical sciences</topic><topic>Blotting, Western</topic><topic>Carcinogenesis, carcinogens and anticarcinogens</topic><topic>Carcinogens - toxicity</topic><topic>Carcinoma, Hepatocellular - chemically induced</topic><topic>Carcinoma, Hepatocellular - enzymology</topic><topic>Chemical agents</topic><topic>CYP1A2</topic><topic>Cytochrome P-450 CYP1A2 - metabolism</topic><topic>DNA Primers - chemistry</topic><topic>Drug Combinations</topic><topic>Drug Synergism</topic><topic>Enzyme Induction</topic><topic>Fenbendazole</topic><topic>Fenbendazole - pharmacology</topic><topic>Food</topic><topic>Glutathione Transferase - metabolism</topic><topic>Hepatocarcinogenesis</topic><topic>Immunoenzyme Techniques</topic><topic>Liver - drug effects</topic><topic>Liver - enzymology</topic><topic>Liver Neoplasms, Experimental - chemically induced</topic><topic>Liver Neoplasms, Experimental - enzymology</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Microsomes, Liver - drug effects</topic><topic>Microsomes, Liver - enzymology</topic><topic>Quinoxalines - toxicity</topic><topic>Rat</topic><topic>Rats</topic><topic>Rats, Inbred F344</topic><topic>Reverse Transcriptase Polymerase Chain Reaction</topic><topic>Rodents</topic><topic>Tumors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Suzuki, Shugo</creatorcontrib><creatorcontrib>Takahashi, Satoru</creatorcontrib><creatorcontrib>Asamoto, Makoto</creatorcontrib><creatorcontrib>Inaguma, Shingo</creatorcontrib><creatorcontrib>Ogiso, Tadashi</creatorcontrib><creatorcontrib>Hirose, Masao</creatorcontrib><creatorcontrib>Shirai, Tomoyuki</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>Oncogenes and Growth Factors Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Premium</collection><jtitle>Cancer letters</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Suzuki, Shugo</au><au>Takahashi, Satoru</au><au>Asamoto, Makoto</au><au>Inaguma, Shingo</au><au>Ogiso, Tadashi</au><au>Hirose, Masao</au><au>Shirai, Tomoyuki</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Lack of modification of 2-amino-3,8-dimethylimidazo[4,5- f]quinoxaline (MeIQx)-induced hepatocarcinogenesis in rats by fenbendazole – a CYP1A2 inducer</atitle><jtitle>Cancer letters</jtitle><addtitle>Cancer Lett</addtitle><date>2002-11-08</date><risdate>2002</risdate><volume>185</volume><issue>1</issue><spage>39</spage><epage>45</epage><pages>39-45</pages><issn>0304-3835</issn><eissn>1872-7980</eissn><coden>CALEDQ</coden><abstract>Fenbendazole (FBZ) is an anthelmintic drug known to be a potent CYP1A2 inducer. Combined effects of FBZ on 2-amino-3,8-dimethylimidazo[4,5-
f]quinoxaline (MeIQx)-induced hepatocarcinogenesis in rats were investigated using a medium-term liver bioassay system. No modifying influence was found in terms of glutathione S-transferase placental-form positive foci development although CYP1A2 protein expression in the livers of rats that were given MeIQx and FBZ was 2.3-fold higher than with MeIQx alone. NAT2 mRNA expression did not differ among the groups as revealed by quantitative reverse transcriptase-polymerase chain reaction analysis. These results suggest that elevated CYP1A2 expression is not sufficient to enhance MeIQx-induced hepatocarcinogenesis.</abstract><cop>Shannon</cop><pub>Elsevier Ireland Ltd</pub><pmid>12142077</pmid><doi>10.1016/S0304-3835(02)00243-4</doi><tpages>7</tpages></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0304-3835 |
| ispartof | Cancer letters, 2002-11, Vol.185 (1), p.39-45 |
| issn | 0304-3835 1872-7980 |
| language | eng |
| recordid | cdi_proquest_journals_1505361960 |
| source | MEDLINE; Elsevier ScienceDirect Journals Complete |
| subjects | 2-Amino-3,8-dimethylimidazo[4,5- f]quinoxaline Animals Antinematodal Agents - pharmacology Arylamine N-Acetyltransferase - genetics Arylamine N-Acetyltransferase - metabolism Bioassays Biological and medical sciences Blotting, Western Carcinogenesis, carcinogens and anticarcinogens Carcinogens - toxicity Carcinoma, Hepatocellular - chemically induced Carcinoma, Hepatocellular - enzymology Chemical agents CYP1A2 Cytochrome P-450 CYP1A2 - metabolism DNA Primers - chemistry Drug Combinations Drug Synergism Enzyme Induction Fenbendazole Fenbendazole - pharmacology Food Glutathione Transferase - metabolism Hepatocarcinogenesis Immunoenzyme Techniques Liver - drug effects Liver - enzymology Liver Neoplasms, Experimental - chemically induced Liver Neoplasms, Experimental - enzymology Male Medical sciences Microsomes, Liver - drug effects Microsomes, Liver - enzymology Quinoxalines - toxicity Rat Rats Rats, Inbred F344 Reverse Transcriptase Polymerase Chain Reaction Rodents Tumors |
| title | Lack of modification of 2-amino-3,8-dimethylimidazo[4,5- f]quinoxaline (MeIQx)-induced hepatocarcinogenesis in rats by fenbendazole – a CYP1A2 inducer |
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