Dibutyl phthalate induced testicular dysgenesis originates after seminiferous cord formation in rats
| العنوان: | Dibutyl phthalate induced testicular dysgenesis originates after seminiferous cord formation in rats |
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| المؤلفون: | Sander van den Driesche, Nathália Lm Lara Lara, Luiz R. França, Richard M. Sharpe, Sheila Macpherson |
| المصدر: | 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 |
| بيانات النشر: | Nature Publishing Group UK, 2017. |
| سنة النشر: | 2017 |
| مصطلحات موضوعية: | 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 |
| الوصف: | 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. |
| اللغة: | English |
| تدمد: | 2045-2322 |
| الوصول الحر: | https://explore.openaire.eu/search/publication?articleId=doi_dedup___::1912609bceb6af8878e94de7094ed510Test http://europepmc.org/articles/PMC5451485Test |
| حقوق: | OPEN |
| رقم الانضمام: | edsair.doi.dedup.....1912609bceb6af8878e94de7094ed510 |
| قاعدة البيانات: | OpenAIRE |
| تدمد: | 20452322 |
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