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

Autor: Sander van den Driesche, Nathália Lm Lara Lara, Luiz R. França, Richard M. Sharpe, Sheila Macpherson
Jazyk: angličtina
Rok vydání: 2017
Předmět:
Male
0301 basic medicine
Sex Differentiation
Phthalic Acid Dibutyl Ester
Gonadal dysgenesis
Gonadal Dysgenesis
chemistry.chemical_compound
0302 clinical medicine
Pregnancy
Testis
Pathology
030219 obstetrics & reproductive medicine
Multidisciplinary
Disease Models
Animals
Leydig Cells
Wistar Rat
Seminiferous Tubules
Sertoli cell
Dibutyl Phthalate
3. Good health
medicine.anatomical_structure
Prenatal Exposure Delayed Effects
Medicine
Female
Basal lamina
Human
circulatory and respiratory physiology
Leydig Cell
medicine.medical_specialty
Dibutyl phthalate
Offspring
Science
Disease Model
Chemically Induced
Biology
Pathophysiology
Testicular Diseases
Article
03 medical and health sciences
Dysgenesis
Fetus
Internal medicine
medicine
Animals
Humans
Seminiferous Tubule
Rats
Wistar
Sexual differentiation
Animal
medicine.disease
Prenatal Exposure
Rats
Testis Disease
030104 developmental biology
Endocrinology
chemistry
Drug Effect
Growth
Development And Aging
Rat
Zdroj: Scientific Reports
Scientific Reports, Vol 7, Iss 1, Pp 1-13 (2017)
Repositório Institucional do INPA
Instituto Nacional de Pesquisas da Amazônia (INPA)
instacron:INPA
ISSN: 2045-2322
Popis: 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.
Databáze: OpenAIRE
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