CYP1 and AhR expression in 7,12-dimethylbenz[ a]anthracene-induced mammary carcinoma of rats prenatally exposed to 3,3′,4,4′,5-pentachlorobiphenyl
We previously reported the finding that prenatal exposure to a relatively low dose of 3,3′,4,4′,5-pentachlorobiphenyl (PCB126) acted as an enhancing agent for 17-beta-estradiol (E2)-dependent 7,12-dimethylbenz[ a]anthracene (DMBA)-induced rat mammary carcinoma, while a high dose decreased it. E2 is...
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| Veröffentlicht in: | Toxicology (Amsterdam) 2005-08, Vol.211 (3), p.231-241 |
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| creator | Wakui, Shin Yokoo, Kiyofumi Takahashi, Hiroyuki Muto, Tomoko Suzuki, Yoshihiko Kanai, Yoshikatsu Hano, Hiroshi Furusato, Masakuni Endou, Hitoshi |
| description | We previously reported the finding that prenatal exposure to a relatively low dose of 3,3′,4,4′,5-pentachlorobiphenyl (PCB126) acted as an enhancing agent for 17-beta-estradiol (E2)-dependent 7,12-dimethylbenz[
a]anthracene (DMBA)-induced rat mammary carcinoma, while a high dose decreased it. E2 is a known risk factor for mammary carcinoma, and CYP1A1 and 1B1 (CYP1) are the major enzymes catalyzing 2- and 4-hydroxylation of E2, respectively. We investigated the induction of CYP1 and aryl hydrocarbon receptor (AhR) in DMBA-induced mammary carcinoma using female Sprague–Dawley rats whose dams had been treated (i.g.) with 2.5
ng, 250
ng, 7.5
μg of PCB126/kg or the vehicle on days 13–19 post-conception. Immunohistochemical analysis revealed that the mammary carcinoma of the 250
ng group showed a significantly higher number of nuclei expressing estrogen receptor α (ER) and proliferating cell nuclear antigen (PCNA) compared to those of the other groups. Quantitative real-time RT-PCR analysis revealed that the 7.5
μg group showed a significantly higher level of CYP1A1 mRNA, and that the 250
ng group showed significantly higher levels of CYP1B1 mRNA. The level of AhR mRNA was significantly higher in both the 7.5
μg and 250
ng groups. Western blotting analysis was consistent with mRNA changes. It has been revealed that CYP1B1 catalyzes a step in the formation of 4-hydroxylated E2 metabolites, which show quite high mammary carcinogenicity. This study indicates that the enhancement of DMBA-induced mammary carcinogenicity in a relatively low PCB126 dose group might partially involve the higher expression of CYP1B1 and AhR in these carcinomas. |
| doi_str_mv | 10.1016/j.tox.2005.03.016 |
| format | Article |
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a]anthracene (DMBA)-induced rat mammary carcinoma, while a high dose decreased it. E2 is a known risk factor for mammary carcinoma, and CYP1A1 and 1B1 (CYP1) are the major enzymes catalyzing 2- and 4-hydroxylation of E2, respectively. We investigated the induction of CYP1 and aryl hydrocarbon receptor (AhR) in DMBA-induced mammary carcinoma using female Sprague–Dawley rats whose dams had been treated (i.g.) with 2.5
ng, 250
ng, 7.5
μg of PCB126/kg or the vehicle on days 13–19 post-conception. Immunohistochemical analysis revealed that the mammary carcinoma of the 250
ng group showed a significantly higher number of nuclei expressing estrogen receptor α (ER) and proliferating cell nuclear antigen (PCNA) compared to those of the other groups. Quantitative real-time RT-PCR analysis revealed that the 7.5
μg group showed a significantly higher level of CYP1A1 mRNA, and that the 250
ng group showed significantly higher levels of CYP1B1 mRNA. The level of AhR mRNA was significantly higher in both the 7.5
μg and 250
ng groups. Western blotting analysis was consistent with mRNA changes. It has been revealed that CYP1B1 catalyzes a step in the formation of 4-hydroxylated E2 metabolites, which show quite high mammary carcinogenicity. This study indicates that the enhancement of DMBA-induced mammary carcinogenicity in a relatively low PCB126 dose group might partially involve the higher expression of CYP1B1 and AhR in these carcinomas.</description><identifier>ISSN: 0300-483X</identifier><identifier>EISSN: 1879-3185</identifier><identifier>DOI: 10.1016/j.tox.2005.03.016</identifier><identifier>PMID: 15908097</identifier><identifier>CODEN: TXICDD</identifier><language>eng</language><publisher>Shannon: Elsevier Ireland Ltd</publisher><subject>9,10-Dimethyl-1,2-benzanthracene ; Adenocarcinoma - chemically induced ; Adenocarcinoma - enzymology ; Adenocarcinoma - metabolism ; Adenocarcinoma - pathology ; AhR ; Animals ; Aryl Hydrocarbon Hydroxylases - biosynthesis ; Aryl Hydrocarbon Hydroxylases - genetics ; Biological and medical sciences ; Blotting, Western ; Body Weight - drug effects ; Carcinogens, Environmental - toxicity ; CYP1 ; Cytochrome P-450 CYP1A1 - biosynthesis ; Cytochrome P-450 CYP1A1 - genetics ; Cytochrome P-450 CYP1B1 ; DMBA ; Female ; Immunohistochemistry ; Male ; Mammary carcinoma ; Mammary Neoplasms, Experimental - chemically induced ; Mammary Neoplasms, Experimental - enzymology ; Mammary Neoplasms, Experimental - metabolism ; Mammary Neoplasms, Experimental - pathology ; Medical sciences ; Organ Size - drug effects ; PCB126 ; Polychlorinated Biphenyls - toxicity ; Pregnancy ; Prenatal Exposure Delayed Effects ; Rat ; Rats ; Receptors, Aryl Hydrocarbon - biosynthesis ; Receptors, Aryl Hydrocarbon - genetics ; Receptors, Aryl Hydrocarbon - metabolism ; Reverse Transcriptase Polymerase Chain Reaction ; RNA, Messenger - biosynthesis ; RNA, Messenger - genetics ; Toxicology</subject><ispartof>Toxicology (Amsterdam), 2005-08, Vol.211 (3), p.231-241</ispartof><rights>2005 Elsevier Ireland Ltd</rights><rights>2005 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c443t-530375c87e1b8d35be55e2f9c9ab2a0f7499314f640b84f63762eeb99602f2c73</citedby><cites>FETCH-LOGICAL-c443t-530375c87e1b8d35be55e2f9c9ab2a0f7499314f640b84f63762eeb99602f2c73</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S0300483X05001691$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,776,780,3537,27901,27902,65306</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=16829503$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/15908097$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Wakui, Shin</creatorcontrib><creatorcontrib>Yokoo, Kiyofumi</creatorcontrib><creatorcontrib>Takahashi, Hiroyuki</creatorcontrib><creatorcontrib>Muto, Tomoko</creatorcontrib><creatorcontrib>Suzuki, Yoshihiko</creatorcontrib><creatorcontrib>Kanai, Yoshikatsu</creatorcontrib><creatorcontrib>Hano, Hiroshi</creatorcontrib><creatorcontrib>Furusato, Masakuni</creatorcontrib><creatorcontrib>Endou, Hitoshi</creatorcontrib><title>CYP1 and AhR expression in 7,12-dimethylbenz[ a]anthracene-induced mammary carcinoma of rats prenatally exposed to 3,3′,4,4′,5-pentachlorobiphenyl</title><title>Toxicology (Amsterdam)</title><addtitle>Toxicology</addtitle><description>We previously reported the finding that prenatal exposure to a relatively low dose of 3,3′,4,4′,5-pentachlorobiphenyl (PCB126) acted as an enhancing agent for 17-beta-estradiol (E2)-dependent 7,12-dimethylbenz[
a]anthracene (DMBA)-induced rat mammary carcinoma, while a high dose decreased it. E2 is a known risk factor for mammary carcinoma, and CYP1A1 and 1B1 (CYP1) are the major enzymes catalyzing 2- and 4-hydroxylation of E2, respectively. We investigated the induction of CYP1 and aryl hydrocarbon receptor (AhR) in DMBA-induced mammary carcinoma using female Sprague–Dawley rats whose dams had been treated (i.g.) with 2.5
ng, 250
ng, 7.5
μg of PCB126/kg or the vehicle on days 13–19 post-conception. Immunohistochemical analysis revealed that the mammary carcinoma of the 250
ng group showed a significantly higher number of nuclei expressing estrogen receptor α (ER) and proliferating cell nuclear antigen (PCNA) compared to those of the other groups. Quantitative real-time RT-PCR analysis revealed that the 7.5
μg group showed a significantly higher level of CYP1A1 mRNA, and that the 250
ng group showed significantly higher levels of CYP1B1 mRNA. The level of AhR mRNA was significantly higher in both the 7.5
μg and 250
ng groups. Western blotting analysis was consistent with mRNA changes. It has been revealed that CYP1B1 catalyzes a step in the formation of 4-hydroxylated E2 metabolites, which show quite high mammary carcinogenicity. This study indicates that the enhancement of DMBA-induced mammary carcinogenicity in a relatively low PCB126 dose group might partially involve the higher expression of CYP1B1 and AhR in these carcinomas.</description><subject>9,10-Dimethyl-1,2-benzanthracene</subject><subject>Adenocarcinoma - chemically induced</subject><subject>Adenocarcinoma - enzymology</subject><subject>Adenocarcinoma - metabolism</subject><subject>Adenocarcinoma - pathology</subject><subject>AhR</subject><subject>Animals</subject><subject>Aryl Hydrocarbon Hydroxylases - biosynthesis</subject><subject>Aryl Hydrocarbon Hydroxylases - genetics</subject><subject>Biological and medical sciences</subject><subject>Blotting, Western</subject><subject>Body Weight - drug effects</subject><subject>Carcinogens, Environmental - toxicity</subject><subject>CYP1</subject><subject>Cytochrome P-450 CYP1A1 - biosynthesis</subject><subject>Cytochrome P-450 CYP1A1 - genetics</subject><subject>Cytochrome P-450 CYP1B1</subject><subject>DMBA</subject><subject>Female</subject><subject>Immunohistochemistry</subject><subject>Male</subject><subject>Mammary carcinoma</subject><subject>Mammary Neoplasms, Experimental - chemically induced</subject><subject>Mammary Neoplasms, Experimental - enzymology</subject><subject>Mammary Neoplasms, Experimental - metabolism</subject><subject>Mammary Neoplasms, Experimental - pathology</subject><subject>Medical sciences</subject><subject>Organ Size - drug effects</subject><subject>PCB126</subject><subject>Polychlorinated Biphenyls - toxicity</subject><subject>Pregnancy</subject><subject>Prenatal Exposure Delayed Effects</subject><subject>Rat</subject><subject>Rats</subject><subject>Receptors, Aryl Hydrocarbon - biosynthesis</subject><subject>Receptors, Aryl Hydrocarbon - genetics</subject><subject>Receptors, Aryl Hydrocarbon - metabolism</subject><subject>Reverse Transcriptase Polymerase Chain Reaction</subject><subject>RNA, Messenger - biosynthesis</subject><subject>RNA, Messenger - genetics</subject><subject>Toxicology</subject><issn>0300-483X</issn><issn>1879-3185</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2005</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkcuK1EAUhoMoTs_oA7iR2uiqE0_dcsHV0DgqDCiioIgUlcoJqSapaqvSMu3Kp_BBfCSfxIrdMDtd_XD4zs_hfFn2iEJBgZbPtsXsbwoGIAvgRZrcyVa0rpqc01rezVbAAXJR849n2XmMWwBgXJT3szMqG6ihqVbZz82nt5Ro15HL4R3Bm13AGK13xDpSrSnLOzvhPBzGFt33z0R_0W4egjboMLeu2xvsyKSnSYcDMToY6_ykie9J0HMkqc3pWY_jYan2McGzJ3zNf__4tRZrsYTMd-hmbYbRB9_a3YDuMD7I7vV6jPjwlBfZh6sX7zev8us3L19vLq9zIwSfc8mBV9LUFdK27rhsUUpkfWMa3TINfSWahlPRlwLaOgWvSobYNk0JrGem4hfZ02PvLvive4yzmmw0OI7aod9HRatScgH8_6CoRMkkJJAeQRN8jAF7tQt2eY-ioBZraquSNbVYU8BVmqSdx6fyfTthd7tx0pSAJydAR6PHPmhnbLzlypo18u-Vz48cpp99sxhUNBZdkmQDmll13v7jjD_WKrcC</recordid><startdate>20050801</startdate><enddate>20050801</enddate><creator>Wakui, Shin</creator><creator>Yokoo, Kiyofumi</creator><creator>Takahashi, Hiroyuki</creator><creator>Muto, Tomoko</creator><creator>Suzuki, Yoshihiko</creator><creator>Kanai, Yoshikatsu</creator><creator>Hano, Hiroshi</creator><creator>Furusato, Masakuni</creator><creator>Endou, Hitoshi</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>7ST</scope><scope>C1K</scope><scope>SOI</scope><scope>7U7</scope></search><sort><creationdate>20050801</creationdate><title>CYP1 and AhR expression in 7,12-dimethylbenz[ a]anthracene-induced mammary carcinoma of rats prenatally exposed to 3,3′,4,4′,5-pentachlorobiphenyl</title><author>Wakui, Shin ; Yokoo, Kiyofumi ; Takahashi, Hiroyuki ; Muto, Tomoko ; Suzuki, Yoshihiko ; Kanai, Yoshikatsu ; Hano, Hiroshi ; Furusato, Masakuni ; Endou, Hitoshi</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c443t-530375c87e1b8d35be55e2f9c9ab2a0f7499314f640b84f63762eeb99602f2c73</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2005</creationdate><topic>9,10-Dimethyl-1,2-benzanthracene</topic><topic>Adenocarcinoma - chemically induced</topic><topic>Adenocarcinoma - enzymology</topic><topic>Adenocarcinoma - metabolism</topic><topic>Adenocarcinoma - pathology</topic><topic>AhR</topic><topic>Animals</topic><topic>Aryl Hydrocarbon Hydroxylases - biosynthesis</topic><topic>Aryl Hydrocarbon Hydroxylases - genetics</topic><topic>Biological and medical sciences</topic><topic>Blotting, Western</topic><topic>Body Weight - drug effects</topic><topic>Carcinogens, Environmental - toxicity</topic><topic>CYP1</topic><topic>Cytochrome P-450 CYP1A1 - biosynthesis</topic><topic>Cytochrome P-450 CYP1A1 - genetics</topic><topic>Cytochrome P-450 CYP1B1</topic><topic>DMBA</topic><topic>Female</topic><topic>Immunohistochemistry</topic><topic>Male</topic><topic>Mammary carcinoma</topic><topic>Mammary Neoplasms, Experimental - chemically induced</topic><topic>Mammary Neoplasms, Experimental - enzymology</topic><topic>Mammary Neoplasms, Experimental - metabolism</topic><topic>Mammary Neoplasms, Experimental - pathology</topic><topic>Medical sciences</topic><topic>Organ Size - drug effects</topic><topic>PCB126</topic><topic>Polychlorinated Biphenyls - toxicity</topic><topic>Pregnancy</topic><topic>Prenatal Exposure Delayed Effects</topic><topic>Rat</topic><topic>Rats</topic><topic>Receptors, Aryl Hydrocarbon - biosynthesis</topic><topic>Receptors, Aryl Hydrocarbon - genetics</topic><topic>Receptors, Aryl Hydrocarbon - metabolism</topic><topic>Reverse Transcriptase Polymerase Chain Reaction</topic><topic>RNA, Messenger - biosynthesis</topic><topic>RNA, Messenger - genetics</topic><topic>Toxicology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Wakui, Shin</creatorcontrib><creatorcontrib>Yokoo, Kiyofumi</creatorcontrib><creatorcontrib>Takahashi, Hiroyuki</creatorcontrib><creatorcontrib>Muto, Tomoko</creatorcontrib><creatorcontrib>Suzuki, Yoshihiko</creatorcontrib><creatorcontrib>Kanai, Yoshikatsu</creatorcontrib><creatorcontrib>Hano, Hiroshi</creatorcontrib><creatorcontrib>Furusato, Masakuni</creatorcontrib><creatorcontrib>Endou, Hitoshi</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>Environment Abstracts</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Environment Abstracts</collection><collection>Toxicology Abstracts</collection><jtitle>Toxicology (Amsterdam)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Wakui, Shin</au><au>Yokoo, Kiyofumi</au><au>Takahashi, Hiroyuki</au><au>Muto, Tomoko</au><au>Suzuki, Yoshihiko</au><au>Kanai, Yoshikatsu</au><au>Hano, Hiroshi</au><au>Furusato, Masakuni</au><au>Endou, Hitoshi</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>CYP1 and AhR expression in 7,12-dimethylbenz[ a]anthracene-induced mammary carcinoma of rats prenatally exposed to 3,3′,4,4′,5-pentachlorobiphenyl</atitle><jtitle>Toxicology (Amsterdam)</jtitle><addtitle>Toxicology</addtitle><date>2005-08-01</date><risdate>2005</risdate><volume>211</volume><issue>3</issue><spage>231</spage><epage>241</epage><pages>231-241</pages><issn>0300-483X</issn><eissn>1879-3185</eissn><coden>TXICDD</coden><abstract>We previously reported the finding that prenatal exposure to a relatively low dose of 3,3′,4,4′,5-pentachlorobiphenyl (PCB126) acted as an enhancing agent for 17-beta-estradiol (E2)-dependent 7,12-dimethylbenz[
a]anthracene (DMBA)-induced rat mammary carcinoma, while a high dose decreased it. E2 is a known risk factor for mammary carcinoma, and CYP1A1 and 1B1 (CYP1) are the major enzymes catalyzing 2- and 4-hydroxylation of E2, respectively. We investigated the induction of CYP1 and aryl hydrocarbon receptor (AhR) in DMBA-induced mammary carcinoma using female Sprague–Dawley rats whose dams had been treated (i.g.) with 2.5
ng, 250
ng, 7.5
μg of PCB126/kg or the vehicle on days 13–19 post-conception. Immunohistochemical analysis revealed that the mammary carcinoma of the 250
ng group showed a significantly higher number of nuclei expressing estrogen receptor α (ER) and proliferating cell nuclear antigen (PCNA) compared to those of the other groups. Quantitative real-time RT-PCR analysis revealed that the 7.5
μg group showed a significantly higher level of CYP1A1 mRNA, and that the 250
ng group showed significantly higher levels of CYP1B1 mRNA. The level of AhR mRNA was significantly higher in both the 7.5
μg and 250
ng groups. Western blotting analysis was consistent with mRNA changes. It has been revealed that CYP1B1 catalyzes a step in the formation of 4-hydroxylated E2 metabolites, which show quite high mammary carcinogenicity. This study indicates that the enhancement of DMBA-induced mammary carcinogenicity in a relatively low PCB126 dose group might partially involve the higher expression of CYP1B1 and AhR in these carcinomas.</abstract><cop>Shannon</cop><cop>Amsterdam</cop><pub>Elsevier Ireland Ltd</pub><pmid>15908097</pmid><doi>10.1016/j.tox.2005.03.016</doi><tpages>11</tpages></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0300-483X |
| ispartof | Toxicology (Amsterdam), 2005-08, Vol.211 (3), p.231-241 |
| issn | 0300-483X 1879-3185 |
| language | eng |
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| source | MEDLINE; Elsevier ScienceDirect Journals |
| subjects | 9,10-Dimethyl-1,2-benzanthracene Adenocarcinoma - chemically induced Adenocarcinoma - enzymology Adenocarcinoma - metabolism Adenocarcinoma - pathology AhR Animals Aryl Hydrocarbon Hydroxylases - biosynthesis Aryl Hydrocarbon Hydroxylases - genetics Biological and medical sciences Blotting, Western Body Weight - drug effects Carcinogens, Environmental - toxicity CYP1 Cytochrome P-450 CYP1A1 - biosynthesis Cytochrome P-450 CYP1A1 - genetics Cytochrome P-450 CYP1B1 DMBA Female Immunohistochemistry Male Mammary carcinoma Mammary Neoplasms, Experimental - chemically induced Mammary Neoplasms, Experimental - enzymology Mammary Neoplasms, Experimental - metabolism Mammary Neoplasms, Experimental - pathology Medical sciences Organ Size - drug effects PCB126 Polychlorinated Biphenyls - toxicity Pregnancy Prenatal Exposure Delayed Effects Rat Rats Receptors, Aryl Hydrocarbon - biosynthesis Receptors, Aryl Hydrocarbon - genetics Receptors, Aryl Hydrocarbon - metabolism Reverse Transcriptase Polymerase Chain Reaction RNA, Messenger - biosynthesis RNA, Messenger - genetics Toxicology |
| title | CYP1 and AhR expression in 7,12-dimethylbenz[ a]anthracene-induced mammary carcinoma of rats prenatally exposed to 3,3′,4,4′,5-pentachlorobiphenyl |
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