Dichlorodiphenyltrichloroethane impairs follicle-stimulating hormone receptor-mediated signaling in rat Sertoli cells
Any toxicant that affects Sertoli cell development can potentially disturb male fertility. So far, the effects of organochlorine compounds have been poorly investigated in male. Here, we studied the effects of dichlorodiphenyltrichloroethane (DDT), an organochloride pesticide, on Sertoli cells. DDT...
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Veröffentlicht in: | Reproductive toxicology (Elmsford, N.Y.) N.Y.), 2007-02, Vol.23 (2), p.158-164 |
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creator | Bernard, Laure Martinat, Nadine Lécureuil, Charlotte Crépieux, Pascale Reiter, Eric Tilloy-Ellul, Anne Chevalier, Stéphane Guillou, Florian |
description | Any toxicant that affects Sertoli cell development can potentially disturb male fertility. So far, the effects of organochlorine compounds have been poorly investigated in male. Here, we studied the effects of dichlorodiphenyltrichloroethane (DDT), an organochloride pesticide, on Sertoli cells. DDT inhibited the cAMP response to follicle-stimulating hormone (FSH), the major endocrine control of Sertoli cell development, and to a β2-agonist, isoproterenol. DDT exposure decreased the level of FSH binding sites. Direct adenylyl cyclase activation by Forskolin was unaltered by DDT, while the activation of Gαs by cholera toxin was decreased by DDT. The DDT inhibitory effect on the FSH response was also observed in Ser W3 cells, a Sertoli cell-derived immortalized cell line. All these effects were reproduced by the lipophilic aromatic bisphenol A but not by structurally unrelated CisPlatin. In conclusion, these results are a first step in understanding the molecular basis of DDT deleterious effects in spermatogenesis. |
doi_str_mv | 10.1016/j.reprotox.2006.11.002 |
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So far, the effects of organochlorine compounds have been poorly investigated in male. Here, we studied the effects of dichlorodiphenyltrichloroethane (DDT), an organochloride pesticide, on Sertoli cells. DDT inhibited the cAMP response to follicle-stimulating hormone (FSH), the major endocrine control of Sertoli cell development, and to a β2-agonist, isoproterenol. DDT exposure decreased the level of FSH binding sites. Direct adenylyl cyclase activation by Forskolin was unaltered by DDT, while the activation of Gαs by cholera toxin was decreased by DDT. The DDT inhibitory effect on the FSH response was also observed in Ser W3 cells, a Sertoli cell-derived immortalized cell line. All these effects were reproduced by the lipophilic aromatic bisphenol A but not by structurally unrelated CisPlatin. In conclusion, these results are a first step in understanding the molecular basis of DDT deleterious effects in spermatogenesis.</description><identifier>ISSN: 0890-6238</identifier><identifier>EISSN: 1873-1708</identifier><identifier>DOI: 10.1016/j.reprotox.2006.11.002</identifier><identifier>PMID: 17157474</identifier><language>eng</language><publisher>New York, NY: Elsevier Inc</publisher><subject>Animals ; Benzhydryl Compounds ; Biological and medical sciences ; cAMP ; Cell Line, Transformed ; Cholera Toxin - pharmacology ; Cisplatin - pharmacology ; Computer Science ; Cyclic AMP - metabolism ; DDT ; DDT - toxicity ; Dose-Response Relationship, Drug ; Drug Antagonism ; Embryology: invertebrates and vertebrates. Teratology ; FSH ; FSH receptor ; Fundamental and applied biological sciences. Psychology ; Isoproterenol - pharmacology ; Life Sciences ; Male ; Medical sciences ; Pesticides - toxicity ; Pesticides, fertilizers and other agrochemicals toxicology ; Phenols - pharmacology ; Rats ; Receptors, FSH - drug effects ; Receptors, FSH - metabolism ; Sertoli cells ; Sertoli Cells - drug effects ; Sertoli Cells - metabolism ; Signal Transduction - drug effects ; Teratology. 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So far, the effects of organochlorine compounds have been poorly investigated in male. Here, we studied the effects of dichlorodiphenyltrichloroethane (DDT), an organochloride pesticide, on Sertoli cells. DDT inhibited the cAMP response to follicle-stimulating hormone (FSH), the major endocrine control of Sertoli cell development, and to a β2-agonist, isoproterenol. DDT exposure decreased the level of FSH binding sites. Direct adenylyl cyclase activation by Forskolin was unaltered by DDT, while the activation of Gαs by cholera toxin was decreased by DDT. The DDT inhibitory effect on the FSH response was also observed in Ser W3 cells, a Sertoli cell-derived immortalized cell line. All these effects were reproduced by the lipophilic aromatic bisphenol A but not by structurally unrelated CisPlatin. In conclusion, these results are a first step in understanding the molecular basis of DDT deleterious effects in spermatogenesis.</description><subject>Animals</subject><subject>Benzhydryl Compounds</subject><subject>Biological and medical sciences</subject><subject>cAMP</subject><subject>Cell Line, Transformed</subject><subject>Cholera Toxin - pharmacology</subject><subject>Cisplatin - pharmacology</subject><subject>Computer Science</subject><subject>Cyclic AMP - metabolism</subject><subject>DDT</subject><subject>DDT - toxicity</subject><subject>Dose-Response Relationship, Drug</subject><subject>Drug Antagonism</subject><subject>Embryology: invertebrates and vertebrates. Teratology</subject><subject>FSH</subject><subject>FSH receptor</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Isoproterenol - pharmacology</subject><subject>Life Sciences</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Pesticides - toxicity</subject><subject>Pesticides, fertilizers and other agrochemicals toxicology</subject><subject>Phenols - pharmacology</subject><subject>Rats</subject><subject>Receptors, FSH - drug effects</subject><subject>Receptors, FSH - metabolism</subject><subject>Sertoli cells</subject><subject>Sertoli Cells - drug effects</subject><subject>Sertoli Cells - metabolism</subject><subject>Signal Transduction - drug effects</subject><subject>Teratology. Teratogens</subject><subject>Toxicology</subject><issn>0890-6238</issn><issn>1873-1708</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2007</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkUtP3DAURq2Kqkyn_QsomyKxSOpHYic7EFCoNFIXhbXleG6IR04cbAfBv6-jScuyK0tX5z78HYTOCC4IJvz7ofAweRfda0Ex5gUhBcb0A9qQWrCcCFyfoA2uG5xzyupT9DmEA8a4FI34hE6JIJUoRblB843RvXXe7c3Uw_hmo18LEHs1QmaGSRkfss5Za7SFPEQzzFZFMz5lvfODS5AHDVN0Ph9gb1SEfRbM06jswpgx8ypmv8FHZ02mwdrwBX3slA3wdX236PHH7cP1fb77dffz-mqX65KTmFOuhOCk1RpYQxkoWrbpswJ3iguuBZQl1prWvG5YV5Kua4HzttHQMgqaErZFF8e5vbJy8mZQ_k06ZeT91U4uNUx5xXHFXhb2_MimWJ9nCFEOJizXphTcHCRpeMNJ2rRF_Ahq70Lw0P2bTLBc5MiD_CtHLnIkITLJSY1n64a5TUG9t602EvBtBVTQynZejdqEd66uWCUYTtzlkYOU3YsBL4M2MOoUfjIR5d6Z_93yBxVBtDg</recordid><startdate>20070201</startdate><enddate>20070201</enddate><creator>Bernard, Laure</creator><creator>Martinat, Nadine</creator><creator>Lécureuil, Charlotte</creator><creator>Crépieux, Pascale</creator><creator>Reiter, Eric</creator><creator>Tilloy-Ellul, Anne</creator><creator>Chevalier, Stéphane</creator><creator>Guillou, Florian</creator><general>Elsevier Inc</general><general>Elsevier</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>7QL</scope><scope>7U7</scope><scope>C1K</scope><scope>1XC</scope><orcidid>https://orcid.org/0000-0002-7339-9185</orcidid><orcidid>https://orcid.org/0000-0002-2712-5271</orcidid><orcidid>https://orcid.org/0000-0001-9092-3623</orcidid><orcidid>https://orcid.org/0000-0001-6489-438X</orcidid><orcidid>https://orcid.org/0000-0002-4631-7439</orcidid><orcidid>https://orcid.org/0000-0002-7325-5317</orcidid></search><sort><creationdate>20070201</creationdate><title>Dichlorodiphenyltrichloroethane impairs follicle-stimulating hormone receptor-mediated signaling in rat Sertoli cells</title><author>Bernard, Laure ; Martinat, Nadine ; Lécureuil, Charlotte ; Crépieux, Pascale ; Reiter, Eric ; Tilloy-Ellul, Anne ; Chevalier, Stéphane ; Guillou, Florian</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c461t-26a7761bcce3923ea24b00670fa676c7e440cc286893f41ffbe66b9ceb32ec213</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2007</creationdate><topic>Animals</topic><topic>Benzhydryl Compounds</topic><topic>Biological and medical sciences</topic><topic>cAMP</topic><topic>Cell Line, Transformed</topic><topic>Cholera Toxin - pharmacology</topic><topic>Cisplatin - pharmacology</topic><topic>Computer Science</topic><topic>Cyclic AMP - metabolism</topic><topic>DDT</topic><topic>DDT - toxicity</topic><topic>Dose-Response Relationship, Drug</topic><topic>Drug Antagonism</topic><topic>Embryology: invertebrates and vertebrates. Teratology</topic><topic>FSH</topic><topic>FSH receptor</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Isoproterenol - pharmacology</topic><topic>Life Sciences</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Pesticides - toxicity</topic><topic>Pesticides, fertilizers and other agrochemicals toxicology</topic><topic>Phenols - pharmacology</topic><topic>Rats</topic><topic>Receptors, FSH - drug effects</topic><topic>Receptors, FSH - metabolism</topic><topic>Sertoli cells</topic><topic>Sertoli Cells - drug effects</topic><topic>Sertoli Cells - metabolism</topic><topic>Signal Transduction - drug effects</topic><topic>Teratology. Teratogens</topic><topic>Toxicology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Bernard, Laure</creatorcontrib><creatorcontrib>Martinat, Nadine</creatorcontrib><creatorcontrib>Lécureuil, Charlotte</creatorcontrib><creatorcontrib>Crépieux, Pascale</creatorcontrib><creatorcontrib>Reiter, Eric</creatorcontrib><creatorcontrib>Tilloy-Ellul, Anne</creatorcontrib><creatorcontrib>Chevalier, Stéphane</creatorcontrib><creatorcontrib>Guillou, Florian</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>Bacteriology Abstracts (Microbiology B)</collection><collection>Toxicology Abstracts</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Hyper Article en Ligne (HAL)</collection><jtitle>Reproductive toxicology (Elmsford, N.Y.)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Bernard, Laure</au><au>Martinat, Nadine</au><au>Lécureuil, Charlotte</au><au>Crépieux, Pascale</au><au>Reiter, Eric</au><au>Tilloy-Ellul, Anne</au><au>Chevalier, Stéphane</au><au>Guillou, Florian</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Dichlorodiphenyltrichloroethane impairs follicle-stimulating hormone receptor-mediated signaling in rat Sertoli cells</atitle><jtitle>Reproductive toxicology (Elmsford, N.Y.)</jtitle><addtitle>Reprod Toxicol</addtitle><date>2007-02-01</date><risdate>2007</risdate><volume>23</volume><issue>2</issue><spage>158</spage><epage>164</epage><pages>158-164</pages><issn>0890-6238</issn><eissn>1873-1708</eissn><abstract>Any toxicant that affects Sertoli cell development can potentially disturb male fertility. So far, the effects of organochlorine compounds have been poorly investigated in male. Here, we studied the effects of dichlorodiphenyltrichloroethane (DDT), an organochloride pesticide, on Sertoli cells. DDT inhibited the cAMP response to follicle-stimulating hormone (FSH), the major endocrine control of Sertoli cell development, and to a β2-agonist, isoproterenol. DDT exposure decreased the level of FSH binding sites. Direct adenylyl cyclase activation by Forskolin was unaltered by DDT, while the activation of Gαs by cholera toxin was decreased by DDT. The DDT inhibitory effect on the FSH response was also observed in Ser W3 cells, a Sertoli cell-derived immortalized cell line. All these effects were reproduced by the lipophilic aromatic bisphenol A but not by structurally unrelated CisPlatin. In conclusion, these results are a first step in understanding the molecular basis of DDT deleterious effects in spermatogenesis.</abstract><cop>New York, NY</cop><pub>Elsevier Inc</pub><pmid>17157474</pmid><doi>10.1016/j.reprotox.2006.11.002</doi><tpages>7</tpages><orcidid>https://orcid.org/0000-0002-7339-9185</orcidid><orcidid>https://orcid.org/0000-0002-2712-5271</orcidid><orcidid>https://orcid.org/0000-0001-9092-3623</orcidid><orcidid>https://orcid.org/0000-0001-6489-438X</orcidid><orcidid>https://orcid.org/0000-0002-4631-7439</orcidid><orcidid>https://orcid.org/0000-0002-7325-5317</orcidid></addata></record> |
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subjects | Animals Benzhydryl Compounds Biological and medical sciences cAMP Cell Line, Transformed Cholera Toxin - pharmacology Cisplatin - pharmacology Computer Science Cyclic AMP - metabolism DDT DDT - toxicity Dose-Response Relationship, Drug Drug Antagonism Embryology: invertebrates and vertebrates. Teratology FSH FSH receptor Fundamental and applied biological sciences. Psychology Isoproterenol - pharmacology Life Sciences Male Medical sciences Pesticides - toxicity Pesticides, fertilizers and other agrochemicals toxicology Phenols - pharmacology Rats Receptors, FSH - drug effects Receptors, FSH - metabolism Sertoli cells Sertoli Cells - drug effects Sertoli Cells - metabolism Signal Transduction - drug effects Teratology. Teratogens Toxicology |
title | Dichlorodiphenyltrichloroethane impairs follicle-stimulating hormone receptor-mediated signaling in rat Sertoli cells |
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