Dibutyl phthalate induced testicular dysgenesis originates after seminiferous cord formation in rats

Abstract 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 a...

Descripción completa

Guardado en:

Detalles Bibliográficos
Autores principales:	Nathália L. M. Lara, Sander van den Driesche, Sheila Macpherson, Luiz R. França, Richard M. Sharpe
Formato:	article
Lenguaje:	EN
Publicado:	Nature Portfolio 2017
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/bc7abd18dbdd4aa5af0452f8df7c3a72
Etiquetas:	Agregar Etiqueta Sin Etiquetas, Sea el primero en etiquetar este registro!

id	oai:doaj.org-article:bc7abd18dbdd4aa5af0452f8df7c3a72
record_format	dspace
spelling	oai:doaj.org-article:bc7abd18dbdd4aa5af0452f8df7c3a722021-12-02T12:32:16ZDibutyl phthalate induced testicular dysgenesis originates after seminiferous cord formation in rats10.1038/s41598-017-02684-22045-2322https://doaj.org/article/bc7abd18dbdd4aa5af0452f8df7c3a722017-05-01T00:00:00Zhttps://doi.org/10.1038/s41598-017-02684-2https://doaj.org/toc/2045-2322Abstract 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.Nathália L. M. LaraSander van den DriescheSheila MacphersonLuiz R. FrançaRichard M. SharpeNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 7, Iss 1, Pp 1-13 (2017)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Nathália L. M. Lara Sander van den Driesche Sheila Macpherson Luiz R. França Richard M. Sharpe Dibutyl phthalate induced testicular dysgenesis originates after seminiferous cord formation in rats
description	Abstract 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.
format	article
author	Nathália L. M. Lara Sander van den Driesche Sheila Macpherson Luiz R. França Richard M. Sharpe
author_facet	Nathália L. M. Lara Sander van den Driesche Sheila Macpherson Luiz R. França Richard M. Sharpe
author_sort	Nathália L. M. Lara
title	Dibutyl phthalate induced testicular dysgenesis originates after seminiferous cord formation in rats
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
publisher	Nature Portfolio
publishDate	2017
url	https://doaj.org/article/bc7abd18dbdd4aa5af0452f8df7c3a72
work_keys_str_mv	AT nathalialmlara dibutylphthalateinducedtesticulardysgenesisoriginatesafterseminiferouscordformationinrats AT sandervandendriesche dibutylphthalateinducedtesticulardysgenesisoriginatesafterseminiferouscordformationinrats AT sheilamacpherson dibutylphthalateinducedtesticulardysgenesisoriginatesafterseminiferouscordformationinrats AT luizrfranca dibutylphthalateinducedtesticulardysgenesisoriginatesafterseminiferouscordformationinrats AT richardmsharpe dibutylphthalateinducedtesticulardysgenesisoriginatesafterseminiferouscordformationinrats
_version_	1718394116998430720

Dibutyl phthalate induced testicular dysgenesis originates after seminiferous cord formation in rats

Ejemplares similares