Dibutyl phthalate induced testicular dysgenesis originates after seminiferous cord formation in rats
Autor(a) principal: | |
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Data de Publicação: | 2017 |
Outros Autores: | , , , |
Tipo de documento: | Artigo |
Idioma: | eng |
Título da fonte: | Repositório Institucional do INPA |
Texto Completo: | https://repositorio.inpa.gov.br/handle/1/15217 |
Resumo: | Administration of dibutyl phthalate (DBP) to pregnant rats causes reproductive disorders in male offspring, resulting from suppression of intratesticular testosterone, and is used as a model for human testicular dysgenesis syndrome (TDS). DBP exposure in pregnancy induces focal dysgenetic areas in fetal testes that appear between e19.5-e21.5, manifesting as focal aggregation of Leydig cells and ectopic Sertoli cells (SC). Our aim was to identify the origins of the ectopic SC. Time-mated female rats were administered 750 mg/kg/day DBP in three different time windows: full window (FW; e13.5-e20.5), masculinisation programming window (MPW; e15.5-e18.5), late window (LW; e19.5-e20.5). We show that DBP-MPW treatment produces more extensive and severe dysgenetic areas, with more ectopic SC and germ cells (GC) than DBP-FW treatment; DBP-LW induces no dysgenesis. Our findings demonstrate that ectopic SC do not differentiate de novo, but result from rupture of normally formed seminiferous cords beyond e20.5. The more severe testis dysgenesis in DBP-MPW animals may result from the presence of basally migrating GC and a weakened basal lamina, whereas GC migration was minimal in DBP-FW animals. Our findings provide the first evidence for how testicular dysgenesis can result after normal testis differentiation/development and may be relevant to understanding TDS in human patients. © 2017 The Author(s). |
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Lara, Nathália L.M.van den Driesche, SanderMacPherson, Sheila A.França, Luiz Renato deSharpe, Richard M.2020-05-07T14:14:46Z2020-05-07T14:14:46Z2017https://repositorio.inpa.gov.br/handle/1/1521710.1038/s41598-017-02684-2Administration of dibutyl phthalate (DBP) to pregnant rats causes reproductive disorders in male offspring, resulting from suppression of intratesticular testosterone, and is used as a model for human testicular dysgenesis syndrome (TDS). DBP exposure in pregnancy induces focal dysgenetic areas in fetal testes that appear between e19.5-e21.5, manifesting as focal aggregation of Leydig cells and ectopic Sertoli cells (SC). Our aim was to identify the origins of the ectopic SC. Time-mated female rats were administered 750 mg/kg/day DBP in three different time windows: full window (FW; e13.5-e20.5), masculinisation programming window (MPW; e15.5-e18.5), late window (LW; e19.5-e20.5). We show that DBP-MPW treatment produces more extensive and severe dysgenetic areas, with more ectopic SC and germ cells (GC) than DBP-FW treatment; DBP-LW induces no dysgenesis. Our findings demonstrate that ectopic SC do not differentiate de novo, but result from rupture of normally formed seminiferous cords beyond e20.5. The more severe testis dysgenesis in DBP-MPW animals may result from the presence of basally migrating GC and a weakened basal lamina, whereas GC migration was minimal in DBP-FW animals. Our findings provide the first evidence for how testicular dysgenesis can result after normal testis differentiation/development and may be relevant to understanding TDS in human patients. © 2017 The Author(s).Volume 7, Número 1Attribution-NonCommercial-NoDerivs 3.0 Brazilhttp://creativecommons.org/licenses/by-nc-nd/3.0/br/info:eu-repo/semantics/openAccessPhthalic Acid Dibutyl EsterAnimalsChemically InducedDisease ModelDrug EffectFemaleFetusGonadal DysgenesisGrowth, Development And AgingHumanLeydig CellMalePathologyPathophysiologyPregnancyPrenatal ExposureRatSeminiferous TubuleSex DifferentiationTestisTestis DiseaseWistar RatAnimalDibutyl PhthalateDisease Models, AnimalsFemaleFetusGonadal DysgenesisHumansLeydig CellsMalePregnancyPrenatal Exposure Delayed EffectsRatsRats, WistarSeminiferous TubulesSex DifferentiationTesticular DiseasesTestisDibutyl phthalate induced testicular dysgenesis originates after seminiferous cord formation in ratsinfo:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/articleScientific Reportsengreponame:Repositório Institucional do INPAinstname:Instituto Nacional de Pesquisas da Amazônia (INPA)instacron:INPAORIGINALartigo-inpa.pdfapplication/pdf3912518https://repositorio.inpa.gov.br/bitstream/1/15217/1/artigo-inpa.pdf8e39653e0245f9c425d860a0344f6aa4MD51CC-LICENSElicense_rdfapplication/octet-stream914https://repositorio.inpa.gov.br/bitstream/1/15217/2/license_rdf4d2950bda3d176f570a9f8b328dfbbefMD521/152172020-07-14 10:59:00.594oai:repositorio:1/15217Repositório de PublicaçõesPUBhttps://repositorio.inpa.gov.br/oai/requestopendoar:2020-07-14T14:59Repositório Institucional do INPA - Instituto Nacional de Pesquisas da Amazônia (INPA)false |
dc.title.en.fl_str_mv |
Dibutyl phthalate induced testicular dysgenesis originates after seminiferous cord formation in rats |
title |
Dibutyl phthalate induced testicular dysgenesis originates after seminiferous cord formation in rats |
spellingShingle |
Dibutyl phthalate induced testicular dysgenesis originates after seminiferous cord formation in rats Lara, Nathália L.M. Phthalic Acid Dibutyl Ester Animals Chemically Induced Disease Model Drug Effect Female Fetus Gonadal Dysgenesis Growth, Development And Aging Human Leydig Cell Male Pathology Pathophysiology Pregnancy Prenatal Exposure Rat Seminiferous Tubule Sex Differentiation Testis Testis Disease Wistar Rat Animal Dibutyl Phthalate Disease Models, Animals Female Fetus Gonadal Dysgenesis Humans Leydig Cells Male Pregnancy Prenatal Exposure Delayed Effects Rats Rats, Wistar Seminiferous Tubules Sex Differentiation Testicular Diseases Testis |
title_short |
Dibutyl phthalate induced testicular dysgenesis originates after seminiferous cord formation in rats |
title_full |
Dibutyl phthalate induced testicular dysgenesis originates after seminiferous cord formation in rats |
title_fullStr |
Dibutyl phthalate induced testicular dysgenesis originates after seminiferous cord formation in rats |
title_full_unstemmed |
Dibutyl phthalate induced testicular dysgenesis originates after seminiferous cord formation in rats |
title_sort |
Dibutyl phthalate induced testicular dysgenesis originates after seminiferous cord formation in rats |
author |
Lara, Nathália L.M. |
author_facet |
Lara, Nathália L.M. van den Driesche, Sander MacPherson, Sheila A. França, Luiz Renato de Sharpe, Richard M. |
author_role |
author |
author2 |
van den Driesche, Sander MacPherson, Sheila A. França, Luiz Renato de Sharpe, Richard M. |
author2_role |
author author author author |
dc.contributor.author.fl_str_mv |
Lara, Nathália L.M. van den Driesche, Sander MacPherson, Sheila A. França, Luiz Renato de Sharpe, Richard M. |
dc.subject.eng.fl_str_mv |
Phthalic Acid Dibutyl Ester Animals Chemically Induced Disease Model Drug Effect Female Fetus Gonadal Dysgenesis Growth, Development And Aging Human Leydig Cell Male Pathology Pathophysiology Pregnancy Prenatal Exposure Rat Seminiferous Tubule Sex Differentiation Testis Testis Disease Wistar Rat Animal Dibutyl Phthalate Disease Models, Animals Female Fetus Gonadal Dysgenesis Humans Leydig Cells Male Pregnancy Prenatal Exposure Delayed Effects Rats Rats, Wistar Seminiferous Tubules Sex Differentiation Testicular Diseases Testis |
topic |
Phthalic Acid Dibutyl Ester Animals Chemically Induced Disease Model Drug Effect Female Fetus Gonadal Dysgenesis Growth, Development And Aging Human Leydig Cell Male Pathology Pathophysiology Pregnancy Prenatal Exposure Rat Seminiferous Tubule Sex Differentiation Testis Testis Disease Wistar Rat Animal Dibutyl Phthalate Disease Models, Animals Female Fetus Gonadal Dysgenesis Humans Leydig Cells Male Pregnancy Prenatal Exposure Delayed Effects Rats Rats, Wistar Seminiferous Tubules Sex Differentiation Testicular Diseases Testis |
description |
Administration of dibutyl phthalate (DBP) to pregnant rats causes reproductive disorders in male offspring, resulting from suppression of intratesticular testosterone, and is used as a model for human testicular dysgenesis syndrome (TDS). DBP exposure in pregnancy induces focal dysgenetic areas in fetal testes that appear between e19.5-e21.5, manifesting as focal aggregation of Leydig cells and ectopic Sertoli cells (SC). Our aim was to identify the origins of the ectopic SC. Time-mated female rats were administered 750 mg/kg/day DBP in three different time windows: full window (FW; e13.5-e20.5), masculinisation programming window (MPW; e15.5-e18.5), late window (LW; e19.5-e20.5). We show that DBP-MPW treatment produces more extensive and severe dysgenetic areas, with more ectopic SC and germ cells (GC) than DBP-FW treatment; DBP-LW induces no dysgenesis. Our findings demonstrate that ectopic SC do not differentiate de novo, but result from rupture of normally formed seminiferous cords beyond e20.5. The more severe testis dysgenesis in DBP-MPW animals may result from the presence of basally migrating GC and a weakened basal lamina, whereas GC migration was minimal in DBP-FW animals. Our findings provide the first evidence for how testicular dysgenesis can result after normal testis differentiation/development and may be relevant to understanding TDS in human patients. © 2017 The Author(s). |
publishDate |
2017 |
dc.date.issued.fl_str_mv |
2017 |
dc.date.accessioned.fl_str_mv |
2020-05-07T14:14:46Z |
dc.date.available.fl_str_mv |
2020-05-07T14:14:46Z |
dc.type.status.fl_str_mv |
info:eu-repo/semantics/publishedVersion |
dc.type.driver.fl_str_mv |
info:eu-repo/semantics/article |
format |
article |
status_str |
publishedVersion |
dc.identifier.uri.fl_str_mv |
https://repositorio.inpa.gov.br/handle/1/15217 |
dc.identifier.doi.none.fl_str_mv |
10.1038/s41598-017-02684-2 |
url |
https://repositorio.inpa.gov.br/handle/1/15217 |
identifier_str_mv |
10.1038/s41598-017-02684-2 |
dc.language.iso.fl_str_mv |
eng |
language |
eng |
dc.relation.ispartof.pt_BR.fl_str_mv |
Volume 7, Número 1 |
dc.rights.driver.fl_str_mv |
Attribution-NonCommercial-NoDerivs 3.0 Brazil http://creativecommons.org/licenses/by-nc-nd/3.0/br/ info:eu-repo/semantics/openAccess |
rights_invalid_str_mv |
Attribution-NonCommercial-NoDerivs 3.0 Brazil http://creativecommons.org/licenses/by-nc-nd/3.0/br/ |
eu_rights_str_mv |
openAccess |
dc.publisher.none.fl_str_mv |
Scientific Reports |
publisher.none.fl_str_mv |
Scientific Reports |
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