ArticleJournal of molecular histology2025
Prenatal and pubertal exposure to ethinylestradiol induces Long-Term stromal and epithelial changes in the gerbil dorsal prostate.
Article in Journal of molecular histology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
17α-Ethinylestradiol (EE2) is a synthetic estrogen derived from 17β-estradiol and widely used in oral contraceptives. It interferes with the endocrine system and disrupts hormonal balance. This study investigated the long-term effects of prenatal and pubertal EE2 exposure on the dorsal prostate of aging gerbils. Adult female gerbils (90–120 days old) received EE2 (15 µg/kg/day) and were assigned to three groups (n = 5): Control (untreated), EE2/PRE (exposed during gestational days 18–22), and EE2/PUB (exposed during postnatal days 42–49). After 12 months, the animals were euthanized, and dorsal prostates were collected for biometric, histopathological (including quantification of prostatic acini/section and lesion multiplicity), and Morphometric analyses (epithelial height and muscle thickness), with stereological evaluation of the epithelium, lumen, muscle, stroma, blood vessels, and collagen fibers. Tissue sections were stained with Hematoxylin–Eosin, Gömori’s Trichrome, and Picrosirius Red. Results showed increased muscular thickness and decreased vascular volume in the EE2/PRE group, while the EE2/PUB group exhibited reduced volumes of the epithelium, lumen, and collagen fibers. Lesion analysis revealed a reduction in prostatic intraepithelial neoplasia (PIN) and an increase in luminal inflammation in the EE2/PUB group. These findings indicate that the biological effects of EE2 vary according to the timing of exposure, with both prenatal and pubertal periods representing critical developmental windows. EE2 exposure during these stages can induce alterations in epithelial-stromal interactions in a lobe-specific manner. Hormonal imbalance triggered ERα/ERβ signaling, influencing cellular differentiation and promoting inflammation. These distinct outcomes highlight how endocrine-disrupting chemicals (EDCs) compromise prostate homeostasis through hormone reprogramming and receptor-mediated pathways.
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Registered trials
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