ArticleScientific reports2017
Dibutyl phthalate induced testicular dysgenesis originates after seminiferous cord formation in rats.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 42 citations in OpenAlex.
- Protective effects of 20(R) ginsenoside Rg3 on DBP-induced reproductive injury in mice through Nrf2/ARE pathway.Scientific reports · 2025Article
- Dose-response assessment of dipentyl phthalate effects on testosterone production and morphogenesis of late-gestation fetal rat testis.Environment international · 2025Article
- Prenatal Exposure to Dibutyl Phthalate and Its Negative Health Effects on Offspring: In Vivo and Epidemiological Studies.Journal of xenobiotics · 2024Review
- Environmentally relevant DEHP exposure during gestational and lactational period inhibits filamin a testicular expression.Journal of molecular histology · 2023Article
- Phthalate Toxicity in Rats and Its Relation to Testicular Dysgenesis Syndrome in Humans.Toxicologic pathology · 2021Article
- Pharmacophore based in silico study with laboratory verification-environmental explanation of prostate cancer recurrence.Environmental science and pollution research international · 2021Article
- Effects ofArchives of Razi Institute · 2021Article
- REPRODUCTIVE TOXICOLOGY: Environmental exposures, fetal testis development and function: phthalates and beyond.Reproduction (Cambridge, England) · 2021Review
- Reconstitution of rat fetal testis during the masculinisation programming window induces focal dysgenesis consistent with testicular dysgenesis syndrome.Scientific reports · 2020Article
- Intrauterine exposure to diethylhexyl phthalate disrupts gap junctions in the fetal rat testis.Current research in toxicology · 2020Article
- Mechanisms of Testicular Disruption from Exposure to Bisphenol A and Phtalates.Journal of clinical medicine · 2020Review
- Cross Sectional Study on Exposure to BPA and Phthalates and Semen Parameters in Men Attending a Fertility Center.International journal of environmental research and public health · 2020Article
- Proceedings of the 2019 National Toxicology Program Satellite Symposium.Toxicologic pathology · 2019Article
- Role of JNK and ERK1/2 MAPK signaling pathway in testicular injury of rats induced by di-N-butyl-phthalate (DBP).Biological research · 2019Article
- All-trans Retinoic Acid Disrupts Development in Ex Vivo Cultured Fetal Rat Testes. II: Modulation of Mono-(2-ethylhexyl) Phthalate Toxicity.Toxicological sciences : an official journal of the Society of Toxicology · 2019Article
- Phthalate-Induced Fetal Leydig Cell Dysfunction Mediates Male Reproductive Tract Anomalies.Frontiers in pharmacology · 2019Review
- Proceedings of the 2018 National Toxicology Program Satellite Symposium.Toxicologic pathology · 2018Article
- DMRT1 repression using a novel approach to genetic manipulation induces testicular dysgenesis in human fetal gonads.Human reproduction (Oxford, England) · 2018Article
Corrections and comments
- Erratum issued
Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
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.
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