Altered thyroxin and retinoid metabolic response to 2,3,7,8-tetrachlorodibenzo-p-dioxin in aryl hydrocarbon receptor-null mice
To determine whether the disruption of thyroid hormone and retinoid homeostasis that occurs after exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) can be mediated by the arylhydrocarbon receptor (AhR), pregnant AhR-heterozygous (AhR+/-) mice were administered a single oral dose of 10 microg kg...
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description | To determine whether the disruption of thyroid hormone and retinoid homeostasis that occurs after exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) can be mediated by the arylhydrocarbon receptor (AhR), pregnant AhR-heterozygous (AhR+/-) mice were administered a single oral dose of 10 microg kg(-1) TCDD at gestation day 12.5. Serum and liver were collected on postnatal day 21 from vehicle-treated control or TCDD-treated AhR+/- and AhR-null (AhR-/-) mouse pups. Whereas TCDD exposure resulted in a marked reduction of total thyroxin (TT4) and free T4 (FT4) levels in the serum of AhR+/- mice, TCDD had no effects on AhR-/- mice. Gene expression of UDP-glucuronosyltransferase (UGT)1A6, cytochrome P450 (CYP)1A1, and CYP1A2 in the liver was induced markedly by TCDD in AhR+/- but not AhR-/- mice. Induction of CYP1A1 in response to TCDD was confirmed by immunohistochemical evidence in that CYP1A1 protein was conspicuously localized in the cytoplasm of hepatocytes in the centrilobular region. Levels of retinyl palmitate were greatly reduced in the liver of TCDD-exposed AhR+/- mice, but not in vehicle-treated AhR+/- mice. No effects of TCDD on retinoid levels in the liver were found in AhR-/- mice. We conclude that disruption of thyroid hormone and retinoid homeostasis is mediated entirely via AhR. Induction of UGT1A6 is thought to be responsible at least partly for reduced serum thyroid hormone levels in TCDD-exposed mice. |
doi_str_mv | 10.1007/s00204-004-0626-4 |
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Serum and liver were collected on postnatal day 21 from vehicle-treated control or TCDD-treated AhR+/- and AhR-null (AhR-/-) mouse pups. Whereas TCDD exposure resulted in a marked reduction of total thyroxin (TT4) and free T4 (FT4) levels in the serum of AhR+/- mice, TCDD had no effects on AhR-/- mice. Gene expression of UDP-glucuronosyltransferase (UGT)1A6, cytochrome P450 (CYP)1A1, and CYP1A2 in the liver was induced markedly by TCDD in AhR+/- but not AhR-/- mice. Induction of CYP1A1 in response to TCDD was confirmed by immunohistochemical evidence in that CYP1A1 protein was conspicuously localized in the cytoplasm of hepatocytes in the centrilobular region. Levels of retinyl palmitate were greatly reduced in the liver of TCDD-exposed AhR+/- mice, but not in vehicle-treated AhR+/- mice. No effects of TCDD on retinoid levels in the liver were found in AhR-/- mice. We conclude that disruption of thyroid hormone and retinoid homeostasis is mediated entirely via AhR. Induction of UGT1A6 is thought to be responsible at least partly for reduced serum thyroid hormone levels in TCDD-exposed mice.</description><identifier>ISSN: 0340-5761</identifier><identifier>EISSN: 1432-0738</identifier><identifier>DOI: 10.1007/s00204-004-0626-4</identifier><identifier>PMID: 15902423</identifier><identifier>CODEN: ARTODN</identifier><language>eng</language><publisher>Berlin: Springer</publisher><subject>Administration, Oral ; Animals ; Animals, Newborn ; Biological and medical sciences ; Cytochrome P-450 CYP1A1 - biosynthesis ; Cytochrome P-450 CYP1A1 - genetics ; Cytochrome P-450 CYP1A2 - biosynthesis ; Cytochrome P-450 CYP1A2 - genetics ; Environmental Pollutants - toxicity ; Enzyme Induction ; Female ; Fluorescent Antibody Technique, Indirect ; Gene Expression Regulation, Enzymologic - drug effects ; Glucuronosyltransferase - biosynthesis ; Glucuronosyltransferase - genetics ; Homeostasis ; Immunoenzyme Techniques ; Liver - drug effects ; Liver - enzymology ; Male ; Maternal Exposure ; Medical sciences ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Polychlorinated Dibenzodioxins - toxicity ; Pregnancy ; Receptors, Aryl Hydrocarbon - deficiency ; Receptors, Aryl Hydrocarbon - genetics ; Reverse Transcriptase Polymerase Chain Reaction ; RNA, Messenger - metabolism ; Rodents ; Thyroid gland ; Thyroxine - blood ; Toxicology ; Vitamin A - metabolism</subject><ispartof>Archives of toxicology, 2005-05, Vol.79 (5), p.260-267</ispartof><rights>2005 INIST-CNRS</rights><rights>Springer-Verlag 2005</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c494t-9ff82bde9c7837294769b16a3076c4a235964782bb6796059e401bcada49595f3</citedby><cites>FETCH-LOGICAL-c494t-9ff82bde9c7837294769b16a3076c4a235964782bb6796059e401bcada49595f3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27922,27923</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=16824812$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/15902423$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>NISHIMURA, Noriko</creatorcontrib><creatorcontrib>YONEMOTO, Junzo</creatorcontrib><creatorcontrib>MIYABARA, Yuichi</creatorcontrib><creatorcontrib>FUJII-KURIYAMA, Yoshiaki</creatorcontrib><creatorcontrib>TOHYAMA, Chiharu</creatorcontrib><title>Altered thyroxin and retinoid metabolic response to 2,3,7,8-tetrachlorodibenzo-p-dioxin in aryl hydrocarbon receptor-null mice</title><title>Archives of toxicology</title><addtitle>Arch Toxicol</addtitle><description>To determine whether the disruption of thyroid hormone and retinoid homeostasis that occurs after exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) can be mediated by the arylhydrocarbon receptor (AhR), pregnant AhR-heterozygous (AhR+/-) mice were administered a single oral dose of 10 microg kg(-1) TCDD at gestation day 12.5. Serum and liver were collected on postnatal day 21 from vehicle-treated control or TCDD-treated AhR+/- and AhR-null (AhR-/-) mouse pups. Whereas TCDD exposure resulted in a marked reduction of total thyroxin (TT4) and free T4 (FT4) levels in the serum of AhR+/- mice, TCDD had no effects on AhR-/- mice. Gene expression of UDP-glucuronosyltransferase (UGT)1A6, cytochrome P450 (CYP)1A1, and CYP1A2 in the liver was induced markedly by TCDD in AhR+/- but not AhR-/- mice. Induction of CYP1A1 in response to TCDD was confirmed by immunohistochemical evidence in that CYP1A1 protein was conspicuously localized in the cytoplasm of hepatocytes in the centrilobular region. Levels of retinyl palmitate were greatly reduced in the liver of TCDD-exposed AhR+/- mice, but not in vehicle-treated AhR+/- mice. No effects of TCDD on retinoid levels in the liver were found in AhR-/- mice. We conclude that disruption of thyroid hormone and retinoid homeostasis is mediated entirely via AhR. Induction of UGT1A6 is thought to be responsible at least partly for reduced serum thyroid hormone levels in TCDD-exposed mice.</description><subject>Administration, Oral</subject><subject>Animals</subject><subject>Animals, Newborn</subject><subject>Biological and medical sciences</subject><subject>Cytochrome P-450 CYP1A1 - biosynthesis</subject><subject>Cytochrome P-450 CYP1A1 - genetics</subject><subject>Cytochrome P-450 CYP1A2 - biosynthesis</subject><subject>Cytochrome P-450 CYP1A2 - genetics</subject><subject>Environmental Pollutants - toxicity</subject><subject>Enzyme Induction</subject><subject>Female</subject><subject>Fluorescent Antibody Technique, Indirect</subject><subject>Gene Expression Regulation, Enzymologic - drug effects</subject><subject>Glucuronosyltransferase - biosynthesis</subject><subject>Glucuronosyltransferase - genetics</subject><subject>Homeostasis</subject><subject>Immunoenzyme Techniques</subject><subject>Liver - drug effects</subject><subject>Liver - enzymology</subject><subject>Male</subject><subject>Maternal Exposure</subject><subject>Medical sciences</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Mice, Knockout</subject><subject>Polychlorinated Dibenzodioxins - toxicity</subject><subject>Pregnancy</subject><subject>Receptors, Aryl Hydrocarbon - deficiency</subject><subject>Receptors, Aryl Hydrocarbon - genetics</subject><subject>Reverse Transcriptase Polymerase Chain Reaction</subject><subject>RNA, Messenger - metabolism</subject><subject>Rodents</subject><subject>Thyroid gland</subject><subject>Thyroxine - blood</subject><subject>Toxicology</subject><subject>Vitamin A - metabolism</subject><issn>0340-5761</issn><issn>1432-0738</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2005</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>8G5</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNpdkU2LFDEQhoMo7rj6A7xII-hpopWPTjrHZfELFrzoOaTTaSZLOmmTNDh78LebcQYWPBQFxVMPVbwIvSbwgQDIjwWAAsdwKkEF5k_QjnBGMUg2PEU7YBxwLwW5Qi9KuQcgdFDsOboivQLKKduhPzehuuymrh6OOf32sTNx6rKrPiY_dYurZkzB2zYqa4rFdTV1dM_2cj_g6mo29hBSTpMfXXxIeMWT_6c5mfIxdIfjlJM1eUyxOaxba8o4biF0i7fuJXo2m1Dcq0u_Rj8_f_px-xXfff_y7fbmDluueMVqngc6Tk5ZOTBJFZdCjUQYBlJYbijrleCyIaOQSkCvHAcyWjMZrnrVz-wavT9715x-ba5UvfhiXQgmurQVTSTvuVKsgW__A-_TlmO7TQs2AJUcVIPIGbI5lZLdrNfsl_auJqBPyehzMhpO1ZLRvO28uYi3cXHT48Yliga8uwCmWBPmbKL15ZETA-UDoewvMsSWGA</recordid><startdate>20050501</startdate><enddate>20050501</enddate><creator>NISHIMURA, Noriko</creator><creator>YONEMOTO, Junzo</creator><creator>MIYABARA, Yuichi</creator><creator>FUJII-KURIYAMA, Yoshiaki</creator><creator>TOHYAMA, Chiharu</creator><general>Springer</general><general>Springer Nature B.V</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>3V.</scope><scope>7T2</scope><scope>7TK</scope><scope>7U7</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>88I</scope><scope>8AO</scope><scope>8C1</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>ATCPS</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>M2O</scope><scope>M2P</scope><scope>MBDVC</scope><scope>PATMY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PYCSY</scope><scope>Q9U</scope></search><sort><creationdate>20050501</creationdate><title>Altered thyroxin and retinoid metabolic response to 2,3,7,8-tetrachlorodibenzo-p-dioxin in aryl hydrocarbon receptor-null mice</title><author>NISHIMURA, Noriko ; YONEMOTO, Junzo ; MIYABARA, Yuichi ; FUJII-KURIYAMA, Yoshiaki ; TOHYAMA, Chiharu</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c494t-9ff82bde9c7837294769b16a3076c4a235964782bb6796059e401bcada49595f3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2005</creationdate><topic>Administration, Oral</topic><topic>Animals</topic><topic>Animals, Newborn</topic><topic>Biological and medical sciences</topic><topic>Cytochrome P-450 CYP1A1 - biosynthesis</topic><topic>Cytochrome P-450 CYP1A1 - genetics</topic><topic>Cytochrome P-450 CYP1A2 - biosynthesis</topic><topic>Cytochrome P-450 CYP1A2 - genetics</topic><topic>Environmental Pollutants - toxicity</topic><topic>Enzyme Induction</topic><topic>Female</topic><topic>Fluorescent Antibody Technique, Indirect</topic><topic>Gene Expression Regulation, Enzymologic - drug effects</topic><topic>Glucuronosyltransferase - biosynthesis</topic><topic>Glucuronosyltransferase - genetics</topic><topic>Homeostasis</topic><topic>Immunoenzyme Techniques</topic><topic>Liver - drug effects</topic><topic>Liver - enzymology</topic><topic>Male</topic><topic>Maternal Exposure</topic><topic>Medical sciences</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Mice, Knockout</topic><topic>Polychlorinated Dibenzodioxins - toxicity</topic><topic>Pregnancy</topic><topic>Receptors, Aryl Hydrocarbon - deficiency</topic><topic>Receptors, Aryl Hydrocarbon - genetics</topic><topic>Reverse Transcriptase Polymerase Chain Reaction</topic><topic>RNA, Messenger - metabolism</topic><topic>Rodents</topic><topic>Thyroid gland</topic><topic>Thyroxine - blood</topic><topic>Toxicology</topic><topic>Vitamin A - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>NISHIMURA, Noriko</creatorcontrib><creatorcontrib>YONEMOTO, Junzo</creatorcontrib><creatorcontrib>MIYABARA, Yuichi</creatorcontrib><creatorcontrib>FUJII-KURIYAMA, Yoshiaki</creatorcontrib><creatorcontrib>TOHYAMA, Chiharu</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>ProQuest Central (Corporate)</collection><collection>Health and Safety Science Abstracts (Full archive)</collection><collection>Neurosciences Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Science Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Public Health Database</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>Research Library (Alumni Edition)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>Agricultural & Environmental Science Collection</collection><collection>ProQuest Central Essentials</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>Research Library Prep</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Research Library</collection><collection>Science Database</collection><collection>Research Library (Corporate)</collection><collection>Environmental Science Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>Environmental Science Collection</collection><collection>ProQuest Central Basic</collection><jtitle>Archives of toxicology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>NISHIMURA, Noriko</au><au>YONEMOTO, Junzo</au><au>MIYABARA, Yuichi</au><au>FUJII-KURIYAMA, Yoshiaki</au><au>TOHYAMA, Chiharu</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Altered thyroxin and retinoid metabolic response to 2,3,7,8-tetrachlorodibenzo-p-dioxin in aryl hydrocarbon receptor-null mice</atitle><jtitle>Archives of toxicology</jtitle><addtitle>Arch Toxicol</addtitle><date>2005-05-01</date><risdate>2005</risdate><volume>79</volume><issue>5</issue><spage>260</spage><epage>267</epage><pages>260-267</pages><issn>0340-5761</issn><eissn>1432-0738</eissn><coden>ARTODN</coden><abstract>To determine whether the disruption of thyroid hormone and retinoid homeostasis that occurs after exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) can be mediated by the arylhydrocarbon receptor (AhR), pregnant AhR-heterozygous (AhR+/-) mice were administered a single oral dose of 10 microg kg(-1) TCDD at gestation day 12.5. Serum and liver were collected on postnatal day 21 from vehicle-treated control or TCDD-treated AhR+/- and AhR-null (AhR-/-) mouse pups. Whereas TCDD exposure resulted in a marked reduction of total thyroxin (TT4) and free T4 (FT4) levels in the serum of AhR+/- mice, TCDD had no effects on AhR-/- mice. Gene expression of UDP-glucuronosyltransferase (UGT)1A6, cytochrome P450 (CYP)1A1, and CYP1A2 in the liver was induced markedly by TCDD in AhR+/- but not AhR-/- mice. Induction of CYP1A1 in response to TCDD was confirmed by immunohistochemical evidence in that CYP1A1 protein was conspicuously localized in the cytoplasm of hepatocytes in the centrilobular region. Levels of retinyl palmitate were greatly reduced in the liver of TCDD-exposed AhR+/- mice, but not in vehicle-treated AhR+/- mice. No effects of TCDD on retinoid levels in the liver were found in AhR-/- mice. We conclude that disruption of thyroid hormone and retinoid homeostasis is mediated entirely via AhR. Induction of UGT1A6 is thought to be responsible at least partly for reduced serum thyroid hormone levels in TCDD-exposed mice.</abstract><cop>Berlin</cop><pub>Springer</pub><pmid>15902423</pmid><doi>10.1007/s00204-004-0626-4</doi><tpages>8</tpages></addata></record> |
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subjects | Administration, Oral Animals Animals, Newborn Biological and medical sciences Cytochrome P-450 CYP1A1 - biosynthesis Cytochrome P-450 CYP1A1 - genetics Cytochrome P-450 CYP1A2 - biosynthesis Cytochrome P-450 CYP1A2 - genetics Environmental Pollutants - toxicity Enzyme Induction Female Fluorescent Antibody Technique, Indirect Gene Expression Regulation, Enzymologic - drug effects Glucuronosyltransferase - biosynthesis Glucuronosyltransferase - genetics Homeostasis Immunoenzyme Techniques Liver - drug effects Liver - enzymology Male Maternal Exposure Medical sciences Mice Mice, Inbred C57BL Mice, Knockout Polychlorinated Dibenzodioxins - toxicity Pregnancy Receptors, Aryl Hydrocarbon - deficiency Receptors, Aryl Hydrocarbon - genetics Reverse Transcriptase Polymerase Chain Reaction RNA, Messenger - metabolism Rodents Thyroid gland Thyroxine - blood Toxicology Vitamin A - metabolism |
title | Altered thyroxin and retinoid metabolic response to 2,3,7,8-tetrachlorodibenzo-p-dioxin in aryl hydrocarbon receptor-null mice |
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