Possible involvement of oxidative stress in piperonyl butoxide induced hepatocarcinogenesis in rats
Abstract To clarify the possible mechanism of non-genotoxic hepatocarcinogenesis induced by piperonyl butoxide (PBO), male F344 rats were administered an i.p. injection of N -diethylnitrosamine (DEN) to initiate hepatocarcinogenesis. Two weeks later, the rats were administered a PBO-containing (0, 1...
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| Veröffentlicht in: | Toxicology (Amsterdam) 2007-07, Vol.236 (1), p.61-75 |
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| creator | Muguruma, Masako Unami, Akira Kanki, Masayuki Kuroiwa, Yuichi Nishimura, Jihei Dewa, Yasuaki Umemura, Takashi Oishi, Yuji Mitsumori, Kunitoshi |
| description | Abstract To clarify the possible mechanism of non-genotoxic hepatocarcinogenesis induced by piperonyl butoxide (PBO), male F344 rats were administered an i.p. injection of N -diethylnitrosamine (DEN) to initiate hepatocarcinogenesis. Two weeks later, the rats were administered a PBO-containing (0, 1, or 2%) diet for 6 weeks and subjected to a two-third partial hepatectomy 1 week later. After sacrificing them on week 8, their livers were histopathologically examined and analyzed for gene expression using a microarray and real-time RT-PCR. Reactive oxygen species (ROS) products were also measured using liver microsomes. Hepatocytes exhibited centrilobular hypertrophy and increased glutathione S -transferase placental form (GST-P) positive foci formation. ROS products increased significantly in liver microsomes. In the microarray analysis, the expressions of genes related to metabolism and oxidative stress – NAD(P)H dehydrogenase, quinone 1 ( Nqo1 ), UDP-glucuronosyltransferase ( UDPGTR-2 ), glutathione peroxidase 2 ( Gpx2 ), glutathione reductase ( GRx ) – multidrug resistance associated protein 3 ( Abcc3 ), and solute carrier family 7 (cationic amino acid transporter, y+ system) member 5 ( Slc7a5 ) were up-regulated in the PBO group in comparison to the 0% PBO group; this was confirmed by real-time RT-PCR. Additionally, a significant up-regulation of stress response related genes such as CYP1A1 was observed in PBO-treated groups in real-time RT-PCR. HPLC analysis revealed that the level of 8-OHdG in the 2% PBO group was significantly higher than that in the 0% PBO group. This suggests that PBO has the potential to generate ROS via metabolic pathways and induce oxidative stress, including oxidative DNA damage, resulting in the induction of hepatocellular tumors in rats. |
| doi_str_mv | 10.1016/j.tox.2007.03.025 |
| format | Article |
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Two weeks later, the rats were administered a PBO-containing (0, 1, or 2%) diet for 6 weeks and subjected to a two-third partial hepatectomy 1 week later. After sacrificing them on week 8, their livers were histopathologically examined and analyzed for gene expression using a microarray and real-time RT-PCR. Reactive oxygen species (ROS) products were also measured using liver microsomes. Hepatocytes exhibited centrilobular hypertrophy and increased glutathione S -transferase placental form (GST-P) positive foci formation. ROS products increased significantly in liver microsomes. In the microarray analysis, the expressions of genes related to metabolism and oxidative stress – NAD(P)H dehydrogenase, quinone 1 ( Nqo1 ), UDP-glucuronosyltransferase ( UDPGTR-2 ), glutathione peroxidase 2 ( Gpx2 ), glutathione reductase ( GRx ) – multidrug resistance associated protein 3 ( Abcc3 ), and solute carrier family 7 (cationic amino acid transporter, y+ system) member 5 ( Slc7a5 ) were up-regulated in the PBO group in comparison to the 0% PBO group; this was confirmed by real-time RT-PCR. Additionally, a significant up-regulation of stress response related genes such as CYP1A1 was observed in PBO-treated groups in real-time RT-PCR. HPLC analysis revealed that the level of 8-OHdG in the 2% PBO group was significantly higher than that in the 0% PBO group. This suggests that PBO has the potential to generate ROS via metabolic pathways and induce oxidative stress, including oxidative DNA damage, resulting in the induction of hepatocellular tumors in rats.</description><identifier>ISSN: 0300-483X</identifier><identifier>EISSN: 1879-3185</identifier><identifier>DOI: 10.1016/j.tox.2007.03.025</identifier><identifier>PMID: 17498859</identifier><identifier>CODEN: TXICDD</identifier><language>eng</language><publisher>Shannon: Elsevier Ireland Ltd</publisher><subject>Animals ; Biological and medical sciences ; Deoxyadenosines - metabolism ; DNA - metabolism ; Emergency ; Gastroenterology. Liver. Pancreas. Abdomen ; Gene Expression - drug effects ; Gene Expression Profiling ; Liver - drug effects ; Liver - metabolism ; Liver - pathology ; Liver Neoplasms, Experimental - chemically induced ; Liver Neoplasms, Experimental - metabolism ; Liver Neoplasms, Experimental - pathology ; Liver. Biliary tract. Portal circulation. Exocrine pancreas ; Male ; Medical sciences ; Microsomes, Liver - drug effects ; Microsomes, Liver - metabolism ; Oligonucleotide Array Sequence Analysis ; Oxidative Stress ; Pesticide Synergists ; Piperonyl Butoxide ; Rat ; Rats ; Rats, Inbred F344 ; Reactive oxygen species ; Reactive Oxygen Species - metabolism ; Reverse Transcriptase Polymerase Chain Reaction ; RNA, Messenger - metabolism ; Toxicology ; Tumors ; Two-stage liver carcinogenesis model</subject><ispartof>Toxicology (Amsterdam), 2007-07, Vol.236 (1), p.61-75</ispartof><rights>Elsevier Ireland Ltd</rights><rights>2007 Elsevier Ireland Ltd</rights><rights>2007 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c467t-f95d3ba73a2ed204c1ddeb19e2f94da2a65ea13b9a028e412052e6ecf7981ed33</citedby><cites>FETCH-LOGICAL-c467t-f95d3ba73a2ed204c1ddeb19e2f94da2a65ea13b9a028e412052e6ecf7981ed33</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.tox.2007.03.025$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,780,784,3550,27924,27925,45995</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=18804082$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/17498859$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Muguruma, Masako</creatorcontrib><creatorcontrib>Unami, Akira</creatorcontrib><creatorcontrib>Kanki, Masayuki</creatorcontrib><creatorcontrib>Kuroiwa, Yuichi</creatorcontrib><creatorcontrib>Nishimura, Jihei</creatorcontrib><creatorcontrib>Dewa, Yasuaki</creatorcontrib><creatorcontrib>Umemura, Takashi</creatorcontrib><creatorcontrib>Oishi, Yuji</creatorcontrib><creatorcontrib>Mitsumori, Kunitoshi</creatorcontrib><title>Possible involvement of oxidative stress in piperonyl butoxide induced hepatocarcinogenesis in rats</title><title>Toxicology (Amsterdam)</title><addtitle>Toxicology</addtitle><description>Abstract To clarify the possible mechanism of non-genotoxic hepatocarcinogenesis induced by piperonyl butoxide (PBO), male F344 rats were administered an i.p. injection of N -diethylnitrosamine (DEN) to initiate hepatocarcinogenesis. Two weeks later, the rats were administered a PBO-containing (0, 1, or 2%) diet for 6 weeks and subjected to a two-third partial hepatectomy 1 week later. After sacrificing them on week 8, their livers were histopathologically examined and analyzed for gene expression using a microarray and real-time RT-PCR. Reactive oxygen species (ROS) products were also measured using liver microsomes. Hepatocytes exhibited centrilobular hypertrophy and increased glutathione S -transferase placental form (GST-P) positive foci formation. ROS products increased significantly in liver microsomes. In the microarray analysis, the expressions of genes related to metabolism and oxidative stress – NAD(P)H dehydrogenase, quinone 1 ( Nqo1 ), UDP-glucuronosyltransferase ( UDPGTR-2 ), glutathione peroxidase 2 ( Gpx2 ), glutathione reductase ( GRx ) – multidrug resistance associated protein 3 ( Abcc3 ), and solute carrier family 7 (cationic amino acid transporter, y+ system) member 5 ( Slc7a5 ) were up-regulated in the PBO group in comparison to the 0% PBO group; this was confirmed by real-time RT-PCR. Additionally, a significant up-regulation of stress response related genes such as CYP1A1 was observed in PBO-treated groups in real-time RT-PCR. HPLC analysis revealed that the level of 8-OHdG in the 2% PBO group was significantly higher than that in the 0% PBO group. This suggests that PBO has the potential to generate ROS via metabolic pathways and induce oxidative stress, including oxidative DNA damage, resulting in the induction of hepatocellular tumors in rats.</description><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Deoxyadenosines - metabolism</subject><subject>DNA - metabolism</subject><subject>Emergency</subject><subject>Gastroenterology. Liver. Pancreas. Abdomen</subject><subject>Gene Expression - drug effects</subject><subject>Gene Expression Profiling</subject><subject>Liver - drug effects</subject><subject>Liver - metabolism</subject><subject>Liver - pathology</subject><subject>Liver Neoplasms, Experimental - chemically induced</subject><subject>Liver Neoplasms, Experimental - metabolism</subject><subject>Liver Neoplasms, Experimental - pathology</subject><subject>Liver. Biliary tract. Portal circulation. Exocrine pancreas</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Microsomes, Liver - drug effects</subject><subject>Microsomes, Liver - metabolism</subject><subject>Oligonucleotide Array Sequence Analysis</subject><subject>Oxidative Stress</subject><subject>Pesticide Synergists</subject><subject>Piperonyl Butoxide</subject><subject>Rat</subject><subject>Rats</subject><subject>Rats, Inbred F344</subject><subject>Reactive oxygen species</subject><subject>Reactive Oxygen Species - metabolism</subject><subject>Reverse Transcriptase Polymerase Chain Reaction</subject><subject>RNA, Messenger - metabolism</subject><subject>Toxicology</subject><subject>Tumors</subject><subject>Two-stage liver carcinogenesis model</subject><issn>0300-483X</issn><issn>1879-3185</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2007</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kk2LFDEQhoMo7uzqD_AifdFbt5WkPxIEQRZXhQUFFbyFdFKtGXuSMUkPO__etDOw4MFTDnneqtSTIuQZhYYC7V9tmxzuGgYwNMAbYN0DsqFikDWnontINsAB6lbw7xfkMqUtADDe9o_JBR1aKUQnN8R8Dim5ccbK-UOYD7hDn6swVeHOWZ3dAauUI6ZU7qu922MM_jhX45JXYE3ZxaCtfuJe52B0NM6HH-gxub-RqHN6Qh5Nek749HxekW83775ef6hvP73_eP32tjZtP-R6kp3lox64ZmgZtIZaiyOVyCbZWs1036GmfJQamMCWMugY9mimQQqKlvMr8vJUdx_D7wVTVjuXDM6z9hiWpKgU0Eo5FJCeQBPL9BEntY9up-NRUVCrWbVVZT61mlXAVTFbMs_PxZdxh_Y-cVZZgBdnQCej5ylqb1y650RpDoIV7vWJw6Li4DCqZBz6ItFFNFnZ4P77jDf_pM3svCsNf-ER0zYs0RfHiqrEFKgv6wqsGwBD-XwQkv8BglyuYw</recordid><startdate>20070701</startdate><enddate>20070701</enddate><creator>Muguruma, Masako</creator><creator>Unami, Akira</creator><creator>Kanki, Masayuki</creator><creator>Kuroiwa, Yuichi</creator><creator>Nishimura, Jihei</creator><creator>Dewa, Yasuaki</creator><creator>Umemura, Takashi</creator><creator>Oishi, Yuji</creator><creator>Mitsumori, Kunitoshi</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>7TM</scope><scope>7U7</scope><scope>C1K</scope></search><sort><creationdate>20070701</creationdate><title>Possible involvement of oxidative stress in piperonyl butoxide induced hepatocarcinogenesis in rats</title><author>Muguruma, Masako ; Unami, Akira ; Kanki, Masayuki ; Kuroiwa, Yuichi ; Nishimura, Jihei ; Dewa, Yasuaki ; Umemura, Takashi ; Oishi, Yuji ; Mitsumori, Kunitoshi</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c467t-f95d3ba73a2ed204c1ddeb19e2f94da2a65ea13b9a028e412052e6ecf7981ed33</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2007</creationdate><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Deoxyadenosines - metabolism</topic><topic>DNA - metabolism</topic><topic>Emergency</topic><topic>Gastroenterology. 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Exocrine pancreas</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Microsomes, Liver - drug effects</topic><topic>Microsomes, Liver - metabolism</topic><topic>Oligonucleotide Array Sequence Analysis</topic><topic>Oxidative Stress</topic><topic>Pesticide Synergists</topic><topic>Piperonyl Butoxide</topic><topic>Rat</topic><topic>Rats</topic><topic>Rats, Inbred F344</topic><topic>Reactive oxygen species</topic><topic>Reactive Oxygen Species - metabolism</topic><topic>Reverse Transcriptase Polymerase Chain Reaction</topic><topic>RNA, Messenger - metabolism</topic><topic>Toxicology</topic><topic>Tumors</topic><topic>Two-stage liver carcinogenesis model</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Muguruma, Masako</creatorcontrib><creatorcontrib>Unami, Akira</creatorcontrib><creatorcontrib>Kanki, Masayuki</creatorcontrib><creatorcontrib>Kuroiwa, Yuichi</creatorcontrib><creatorcontrib>Nishimura, Jihei</creatorcontrib><creatorcontrib>Dewa, Yasuaki</creatorcontrib><creatorcontrib>Umemura, Takashi</creatorcontrib><creatorcontrib>Oishi, Yuji</creatorcontrib><creatorcontrib>Mitsumori, Kunitoshi</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>Nucleic Acids Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Environmental Sciences and Pollution Management</collection><jtitle>Toxicology (Amsterdam)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Muguruma, Masako</au><au>Unami, Akira</au><au>Kanki, Masayuki</au><au>Kuroiwa, Yuichi</au><au>Nishimura, Jihei</au><au>Dewa, Yasuaki</au><au>Umemura, Takashi</au><au>Oishi, Yuji</au><au>Mitsumori, Kunitoshi</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Possible involvement of oxidative stress in piperonyl butoxide induced hepatocarcinogenesis in rats</atitle><jtitle>Toxicology (Amsterdam)</jtitle><addtitle>Toxicology</addtitle><date>2007-07-01</date><risdate>2007</risdate><volume>236</volume><issue>1</issue><spage>61</spage><epage>75</epage><pages>61-75</pages><issn>0300-483X</issn><eissn>1879-3185</eissn><coden>TXICDD</coden><abstract>Abstract To clarify the possible mechanism of non-genotoxic hepatocarcinogenesis induced by piperonyl butoxide (PBO), male F344 rats were administered an i.p. injection of N -diethylnitrosamine (DEN) to initiate hepatocarcinogenesis. Two weeks later, the rats were administered a PBO-containing (0, 1, or 2%) diet for 6 weeks and subjected to a two-third partial hepatectomy 1 week later. After sacrificing them on week 8, their livers were histopathologically examined and analyzed for gene expression using a microarray and real-time RT-PCR. Reactive oxygen species (ROS) products were also measured using liver microsomes. Hepatocytes exhibited centrilobular hypertrophy and increased glutathione S -transferase placental form (GST-P) positive foci formation. ROS products increased significantly in liver microsomes. In the microarray analysis, the expressions of genes related to metabolism and oxidative stress – NAD(P)H dehydrogenase, quinone 1 ( Nqo1 ), UDP-glucuronosyltransferase ( UDPGTR-2 ), glutathione peroxidase 2 ( Gpx2 ), glutathione reductase ( GRx ) – multidrug resistance associated protein 3 ( Abcc3 ), and solute carrier family 7 (cationic amino acid transporter, y+ system) member 5 ( Slc7a5 ) were up-regulated in the PBO group in comparison to the 0% PBO group; this was confirmed by real-time RT-PCR. Additionally, a significant up-regulation of stress response related genes such as CYP1A1 was observed in PBO-treated groups in real-time RT-PCR. HPLC analysis revealed that the level of 8-OHdG in the 2% PBO group was significantly higher than that in the 0% PBO group. This suggests that PBO has the potential to generate ROS via metabolic pathways and induce oxidative stress, including oxidative DNA damage, resulting in the induction of hepatocellular tumors in rats.</abstract><cop>Shannon</cop><cop>Amsterdam</cop><pub>Elsevier Ireland Ltd</pub><pmid>17498859</pmid><doi>10.1016/j.tox.2007.03.025</doi><tpages>15</tpages></addata></record> |
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| subjects | Animals Biological and medical sciences Deoxyadenosines - metabolism DNA - metabolism Emergency Gastroenterology. Liver. Pancreas. Abdomen Gene Expression - drug effects Gene Expression Profiling Liver - drug effects Liver - metabolism Liver - pathology Liver Neoplasms, Experimental - chemically induced Liver Neoplasms, Experimental - metabolism Liver Neoplasms, Experimental - pathology Liver. Biliary tract. Portal circulation. Exocrine pancreas Male Medical sciences Microsomes, Liver - drug effects Microsomes, Liver - metabolism Oligonucleotide Array Sequence Analysis Oxidative Stress Pesticide Synergists Piperonyl Butoxide Rat Rats Rats, Inbred F344 Reactive oxygen species Reactive Oxygen Species - metabolism Reverse Transcriptase Polymerase Chain Reaction RNA, Messenger - metabolism Toxicology Tumors Two-stage liver carcinogenesis model |
| title | Possible involvement of oxidative stress in piperonyl butoxide induced hepatocarcinogenesis in rats |
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