Prenatal exposure to estrogenic compounds increases urinary disease susceptibility and heritability in mouse models

Document Type

Poster Presentation

Publication Date

4-17-2026

Keywords

fsc2026

Abstract

Objective: To evaluate the durability and susceptibility of prenatal estrogen exposure mediated urinary disease in mouse models across three generations.

Methods: Pregnant female CD1 mice were implanted with either an endogenous (17β-estradiol; E2) or endocrine disrupting (bisphenol S; BPS) estrogen at gestational day nine. Male offspring were then randomized into control (n=10-15) and experimental (n=15-20) groups or saved for breeding for the next generation. Three generations of male mice were collected, with only the first generation having been directly exposed to prenatal estrogens. Adult male mice were surgically implanted with steroid hormones to examine the susceptibility to increased urinary frequency by void spot assays. Anterior prostate tissues were collected from animals following euthanasia, and steroid hormone receptor expression assessed by immunohistochemistry.

Results: Prenatal exposure to high levels of endogenous E2 showed an increased urinary frequency, particularly in animals from generations two (p< .05) and three (p< .001). In these same animals, there is a decrease in expression of estrogen receptor beta (p< .01). For the animals exposed to BPS, they exhibited an increase in expression of estrogen receptor alpha (p< .001) and androgen receptor (p< .01) even though there is no change in urinary frequency in these animals.

Conclusions: Prenatal exposure to estrogenic compounds does in fact increase susceptibility to urinary frequency with expression changes in steroid hormone receptors, and this susceptibility is heritable over at least three generations in male mice.

Comments

Poster presented at the 2026 Fisher Showcase, St. John Fisher University, April 17, 2026.

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