Please use this identifier to cite or link to this item: https://repositorio.inpa.gov.br/handle/1/15217
Title: Dibutyl phthalate induced testicular dysgenesis originates after seminiferous cord formation in rats
Authors: Lara, Nathália L.M.
van den Driesche, Sander
MacPherson, Sheila A.
França, Luiz Renato de
Sharpe, Richard M.
Keywords: 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
Issue Date: 2017
metadata.dc.publisher.journal: Scientific Reports
metadata.dc.relation.ispartof: Volume 7, Número 1
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. © 2017 The Author(s).
metadata.dc.identifier.doi: 10.1038/s41598-017-02684-2
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