P38/TRHr-Dependent Regulation of TPO in Thyroid Cells Contributes to the Hypothyroidism of Triclosan-Treated Rats
Background/Aims: Triclosan, as an antimicrobial agent and a potential endocrine disruptor, has been used extensively in diverse products, resulting in widespread human exposure. In recent years, studies suggest that triclosan could disturb thyroid functions and decline thyroid hormones (THs). Method...
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| Veröffentlicht in: | Cellular physiology and biochemistry 2018-01, Vol.45 (4), p.1303-1315 |
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| description | Background/Aims: Triclosan, as an antimicrobial agent and a potential endocrine disruptor, has been used extensively in diverse products, resulting in widespread human exposure. In recent years, studies suggest that triclosan could disturb thyroid functions and decline thyroid hormones (THs). Methods: To verify our hypothesis that the MAPK pathway may function significantly in triclosan-induced hypothyroidism, Sprague-Dawley rats were gavaged with triclosan for 31 consecutive days; Nthy-ori 3-1 cells were treated with triclosan in the presence/absence of NAC, inhibitors (SB203580 and SB202474), or TRHr siRNA. Tissues and/or cells were analyzed by several techniques including transmission electron microscopy, confocal laser scanning microscopy, gene silencing, western blot, and real-time PCR. Results: Triclosan led to histopathologic changes in the thyroid and decreases in triiodothyronine (T3) and thyroxine (T4). Triclosan stimulated ROS production and oxidative stress occurrence, thereby activating the p38 pathway in vivo and in vitro. Thyrotropin releasing hormone receptor (TRHr) was induced when the p38 pathway was activated, and was suppressed when that pathway was inhibited. Moreover, thyroid peroxidase (TPO) was restrained and modulated by the p38/TRHr pathway after triclosan treatment. Furthermore, deiodinase 3 (D3) and hepatic enzymes (Ugt2b1, CYP1a1, CYP1a2, CYP2b1, CYP3a1, and Sult1e1) were also induced by triclosan. Conclusion: Taken together, p38/TRHr-dependent regulation of TPO in thyroid cells contributes to the hypothyroidism of triclosan-treated rats. |
| doi_str_mv | 10.1159/000487558 |
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In recent years, studies suggest that triclosan could disturb thyroid functions and decline thyroid hormones (THs). Methods: To verify our hypothesis that the MAPK pathway may function significantly in triclosan-induced hypothyroidism, Sprague-Dawley rats were gavaged with triclosan for 31 consecutive days; Nthy-ori 3-1 cells were treated with triclosan in the presence/absence of NAC, inhibitors (SB203580 and SB202474), or TRHr siRNA. Tissues and/or cells were analyzed by several techniques including transmission electron microscopy, confocal laser scanning microscopy, gene silencing, western blot, and real-time PCR. Results: Triclosan led to histopathologic changes in the thyroid and decreases in triiodothyronine (T3) and thyroxine (T4). Triclosan stimulated ROS production and oxidative stress occurrence, thereby activating the p38 pathway in vivo and in vitro. Thyrotropin releasing hormone receptor (TRHr) was induced when the p38 pathway was activated, and was suppressed when that pathway was inhibited. Moreover, thyroid peroxidase (TPO) was restrained and modulated by the p38/TRHr pathway after triclosan treatment. Furthermore, deiodinase 3 (D3) and hepatic enzymes (Ugt2b1, CYP1a1, CYP1a2, CYP2b1, CYP3a1, and Sult1e1) were also induced by triclosan. Conclusion: Taken together, p38/TRHr-dependent regulation of TPO in thyroid cells contributes to the hypothyroidism of triclosan-treated rats.</description><identifier>ISSN: 1015-8987</identifier><identifier>EISSN: 1421-9778</identifier><identifier>DOI: 10.1159/000487558</identifier><identifier>PMID: 29462796</identifier><language>eng</language><publisher>Basel, Switzerland: S. Karger AG</publisher><subject>Acetylcysteine - pharmacology ; Animals ; Cell cycle ; Cell Line ; Cell Survival - drug effects ; Deiodinase 3 ; Enzymes ; Gene expression ; Hepatic enzymes ; Homeostasis ; Hormones ; Hypothyroidism ; Hypothyroidism - chemically induced ; Hypothyroidism - metabolism ; Hypothyroidism - pathology ; Imidazoles - pharmacology ; Iodide Peroxidase - metabolism ; Kinases ; Laboratories ; Liver - enzymology ; Male ; Original Paper ; Oxidative Stress - drug effects ; p38 Mitogen-Activated Protein Kinases - antagonists & inhibitors ; p38 Mitogen-Activated Protein Kinases - metabolism ; P38/TRHr ; Pyridines - pharmacology ; Rats ; Rats, Sprague-Dawley ; Reactive Oxygen Species - metabolism ; Receptors, Thyrotropin-Releasing Hormone - antagonists & inhibitors ; Receptors, Thyrotropin-Releasing Hormone - genetics ; Receptors, Thyrotropin-Releasing Hormone - metabolism ; RNA Interference ; Rodents ; Signal Transduction - drug effects ; Thyroid gland ; Thyroid Gland - metabolism ; Thyroid Hormones - blood ; Thyroxine - blood ; TPO ; Triclosan ; Triclosan - toxicity ; Triiodothyronine - blood ; Up-Regulation - drug effects</subject><ispartof>Cellular physiology and biochemistry, 2018-01, Vol.45 (4), p.1303-1315</ispartof><rights>2018 The Author(s). Published by S. Karger AG, Basel</rights><rights>2018 The Author(s). Published by S. Karger AG, Basel.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c529t-8bc8c82a555ddac2d5b5311f650f56ca5ecb4b72fc22e4afddcfae088d6424ad3</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,864,2102,27635,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/29462796$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Zhang, Pei</creatorcontrib><creatorcontrib>Yang, Min</creatorcontrib><creatorcontrib>Zeng, Li</creatorcontrib><creatorcontrib>Liu, Changjiang</creatorcontrib><title>P38/TRHr-Dependent Regulation of TPO in Thyroid Cells Contributes to the Hypothyroidism of Triclosan-Treated Rats</title><title>Cellular physiology and biochemistry</title><addtitle>Cell Physiol Biochem</addtitle><description>Background/Aims: Triclosan, as an antimicrobial agent and a potential endocrine disruptor, has been used extensively in diverse products, resulting in widespread human exposure. In recent years, studies suggest that triclosan could disturb thyroid functions and decline thyroid hormones (THs). Methods: To verify our hypothesis that the MAPK pathway may function significantly in triclosan-induced hypothyroidism, Sprague-Dawley rats were gavaged with triclosan for 31 consecutive days; Nthy-ori 3-1 cells were treated with triclosan in the presence/absence of NAC, inhibitors (SB203580 and SB202474), or TRHr siRNA. Tissues and/or cells were analyzed by several techniques including transmission electron microscopy, confocal laser scanning microscopy, gene silencing, western blot, and real-time PCR. Results: Triclosan led to histopathologic changes in the thyroid and decreases in triiodothyronine (T3) and thyroxine (T4). Triclosan stimulated ROS production and oxidative stress occurrence, thereby activating the p38 pathway in vivo and in vitro. Thyrotropin releasing hormone receptor (TRHr) was induced when the p38 pathway was activated, and was suppressed when that pathway was inhibited. Moreover, thyroid peroxidase (TPO) was restrained and modulated by the p38/TRHr pathway after triclosan treatment. Furthermore, deiodinase 3 (D3) and hepatic enzymes (Ugt2b1, CYP1a1, CYP1a2, CYP2b1, CYP3a1, and Sult1e1) were also induced by triclosan. Conclusion: Taken together, p38/TRHr-dependent regulation of TPO in thyroid cells contributes to the hypothyroidism of triclosan-treated rats.</description><subject>Acetylcysteine - pharmacology</subject><subject>Animals</subject><subject>Cell cycle</subject><subject>Cell Line</subject><subject>Cell Survival - drug effects</subject><subject>Deiodinase 3</subject><subject>Enzymes</subject><subject>Gene expression</subject><subject>Hepatic enzymes</subject><subject>Homeostasis</subject><subject>Hormones</subject><subject>Hypothyroidism</subject><subject>Hypothyroidism - chemically induced</subject><subject>Hypothyroidism - metabolism</subject><subject>Hypothyroidism - pathology</subject><subject>Imidazoles - pharmacology</subject><subject>Iodide Peroxidase - metabolism</subject><subject>Kinases</subject><subject>Laboratories</subject><subject>Liver - enzymology</subject><subject>Male</subject><subject>Original Paper</subject><subject>Oxidative Stress - drug effects</subject><subject>p38 Mitogen-Activated Protein Kinases - antagonists & inhibitors</subject><subject>p38 Mitogen-Activated Protein Kinases - metabolism</subject><subject>P38/TRHr</subject><subject>Pyridines - pharmacology</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Reactive Oxygen Species - metabolism</subject><subject>Receptors, Thyrotropin-Releasing Hormone - antagonists & inhibitors</subject><subject>Receptors, Thyrotropin-Releasing Hormone - genetics</subject><subject>Receptors, Thyrotropin-Releasing Hormone - metabolism</subject><subject>RNA Interference</subject><subject>Rodents</subject><subject>Signal Transduction - drug effects</subject><subject>Thyroid gland</subject><subject>Thyroid Gland - metabolism</subject><subject>Thyroid Hormones - blood</subject><subject>Thyroxine - blood</subject><subject>TPO</subject><subject>Triclosan</subject><subject>Triclosan - toxicity</subject><subject>Triiodothyronine - blood</subject><subject>Up-Regulation - drug effects</subject><issn>1015-8987</issn><issn>1421-9778</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2018</creationdate><recordtype>article</recordtype><sourceid>M--</sourceid><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DOA</sourceid><recordid>eNptkc1v1DAQxSMEoqVw4I6QJS5wCPU4cewcIXxspUpdrcLZcuzJNks23trOYf97TLMsEuJke_TzezPzsuw10I8AvL6mlJZScC6fZJdQMshrIeTTdKfAc1lLcZG9CGFH01PU7Hl2weqyYqKuLrOHdSGv283K51_wgJPFKZINbudRx8FNxPWkXd-RYSLt_dG7wZIGxzGQxk3RD90cMZDoSLxHsjoeXFygIewff_rBjC7oKW896oiWbHQML7NnvR4DvjqdV9mPb1_bZpXf3n2_aT7d5oazOuayM9JIpjnn1mrDLO94AdBXnPa8Mpqj6cpOsN4whqXurTW9RiqlrUpWaltcZTeLrnV6pw5-2Gt_VE4P6rHg_FZpH1OHqEDrglIsOPSyTPZdVcsaCkaNgE4WImm9X7QO3j3MGKLaD8GkTegJ3RwUo1QAA1HJhL77B9252U9pUsUABFRSACTqw0IZ70Lw2J8bBKp-Z6rOmSb27Ulx7vZoz-SfEP9a_tR-i_4MNOvPi4Q62D5Rb_5LnVx-Ad4nr8Y</recordid><startdate>20180101</startdate><enddate>20180101</enddate><creator>Zhang, Pei</creator><creator>Yang, Min</creator><creator>Zeng, Li</creator><creator>Liu, Changjiang</creator><general>S. Karger AG</general><general>Cell Physiol Biochem Press GmbH & Co KG</general><scope>M--</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>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>DOA</scope></search><sort><creationdate>20180101</creationdate><title>P38/TRHr-Dependent Regulation of TPO in Thyroid Cells Contributes to the Hypothyroidism of Triclosan-Treated Rats</title><author>Zhang, Pei ; Yang, Min ; Zeng, Li ; Liu, Changjiang</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c529t-8bc8c82a555ddac2d5b5311f650f56ca5ecb4b72fc22e4afddcfae088d6424ad3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2018</creationdate><topic>Acetylcysteine - pharmacology</topic><topic>Animals</topic><topic>Cell cycle</topic><topic>Cell Line</topic><topic>Cell Survival - drug effects</topic><topic>Deiodinase 3</topic><topic>Enzymes</topic><topic>Gene expression</topic><topic>Hepatic enzymes</topic><topic>Homeostasis</topic><topic>Hormones</topic><topic>Hypothyroidism</topic><topic>Hypothyroidism - chemically induced</topic><topic>Hypothyroidism - metabolism</topic><topic>Hypothyroidism - pathology</topic><topic>Imidazoles - pharmacology</topic><topic>Iodide Peroxidase - metabolism</topic><topic>Kinases</topic><topic>Laboratories</topic><topic>Liver - enzymology</topic><topic>Male</topic><topic>Original Paper</topic><topic>Oxidative Stress - drug effects</topic><topic>p38 Mitogen-Activated Protein Kinases - antagonists & inhibitors</topic><topic>p38 Mitogen-Activated Protein Kinases - metabolism</topic><topic>P38/TRHr</topic><topic>Pyridines - pharmacology</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Reactive Oxygen Species - metabolism</topic><topic>Receptors, Thyrotropin-Releasing Hormone - antagonists & inhibitors</topic><topic>Receptors, Thyrotropin-Releasing Hormone - genetics</topic><topic>Receptors, Thyrotropin-Releasing Hormone - metabolism</topic><topic>RNA Interference</topic><topic>Rodents</topic><topic>Signal Transduction - drug effects</topic><topic>Thyroid gland</topic><topic>Thyroid Gland - metabolism</topic><topic>Thyroid Hormones - blood</topic><topic>Thyroxine - blood</topic><topic>TPO</topic><topic>Triclosan</topic><topic>Triclosan - toxicity</topic><topic>Triiodothyronine - blood</topic><topic>Up-Regulation - drug effects</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Zhang, Pei</creatorcontrib><creatorcontrib>Yang, Min</creatorcontrib><creatorcontrib>Zeng, Li</creatorcontrib><creatorcontrib>Liu, Changjiang</creatorcontrib><collection>Karger Open Access</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 & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical 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>ProQuest Central China</collection><collection>MEDLINE - Academic</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>Cellular physiology and biochemistry</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Zhang, Pei</au><au>Yang, Min</au><au>Zeng, Li</au><au>Liu, Changjiang</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>P38/TRHr-Dependent Regulation of TPO in Thyroid Cells Contributes to the Hypothyroidism of Triclosan-Treated Rats</atitle><jtitle>Cellular physiology and biochemistry</jtitle><addtitle>Cell Physiol Biochem</addtitle><date>2018-01-01</date><risdate>2018</risdate><volume>45</volume><issue>4</issue><spage>1303</spage><epage>1315</epage><pages>1303-1315</pages><issn>1015-8987</issn><eissn>1421-9778</eissn><abstract>Background/Aims: Triclosan, as an antimicrobial agent and a potential endocrine disruptor, has been used extensively in diverse products, resulting in widespread human exposure. In recent years, studies suggest that triclosan could disturb thyroid functions and decline thyroid hormones (THs). Methods: To verify our hypothesis that the MAPK pathway may function significantly in triclosan-induced hypothyroidism, Sprague-Dawley rats were gavaged with triclosan for 31 consecutive days; Nthy-ori 3-1 cells were treated with triclosan in the presence/absence of NAC, inhibitors (SB203580 and SB202474), or TRHr siRNA. Tissues and/or cells were analyzed by several techniques including transmission electron microscopy, confocal laser scanning microscopy, gene silencing, western blot, and real-time PCR. Results: Triclosan led to histopathologic changes in the thyroid and decreases in triiodothyronine (T3) and thyroxine (T4). Triclosan stimulated ROS production and oxidative stress occurrence, thereby activating the p38 pathway in vivo and in vitro. Thyrotropin releasing hormone receptor (TRHr) was induced when the p38 pathway was activated, and was suppressed when that pathway was inhibited. Moreover, thyroid peroxidase (TPO) was restrained and modulated by the p38/TRHr pathway after triclosan treatment. Furthermore, deiodinase 3 (D3) and hepatic enzymes (Ugt2b1, CYP1a1, CYP1a2, CYP2b1, CYP3a1, and Sult1e1) were also induced by triclosan. Conclusion: Taken together, p38/TRHr-dependent regulation of TPO in thyroid cells contributes to the hypothyroidism of triclosan-treated rats.</abstract><cop>Basel, Switzerland</cop><pub>S. Karger AG</pub><pmid>29462796</pmid><doi>10.1159/000487558</doi><tpages>13</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Acetylcysteine - pharmacology Animals Cell cycle Cell Line Cell Survival - drug effects Deiodinase 3 Enzymes Gene expression Hepatic enzymes Homeostasis Hormones Hypothyroidism Hypothyroidism - chemically induced Hypothyroidism - metabolism Hypothyroidism - pathology Imidazoles - pharmacology Iodide Peroxidase - metabolism Kinases Laboratories Liver - enzymology Male Original Paper Oxidative Stress - drug effects p38 Mitogen-Activated Protein Kinases - antagonists & inhibitors p38 Mitogen-Activated Protein Kinases - metabolism P38/TRHr Pyridines - pharmacology Rats Rats, Sprague-Dawley Reactive Oxygen Species - metabolism Receptors, Thyrotropin-Releasing Hormone - antagonists & inhibitors Receptors, Thyrotropin-Releasing Hormone - genetics Receptors, Thyrotropin-Releasing Hormone - metabolism RNA Interference Rodents Signal Transduction - drug effects Thyroid gland Thyroid Gland - metabolism Thyroid Hormones - blood Thyroxine - blood TPO Triclosan Triclosan - toxicity Triiodothyronine - blood Up-Regulation - drug effects |
| title | P38/TRHr-Dependent Regulation of TPO in Thyroid Cells Contributes to the Hypothyroidism of Triclosan-Treated Rats |
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