In utero and lactational 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) exposure exacerbates urinary dysfunction in hormone-treated C57BL/6J mice through a non-malignant mechanism involving proteomic changes in the prostate that differ from those elicited by testosterone and estradiol.

ABSTRACT: A recent study directed new focus on the fetal and neonatal environment as a risk factor for urinary dysfunction in aging males. Male mice were exposed in utero and via lactation (IUL) to the persistent environmental contaminant 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) and then administered slow-release, subcutaneous implants of testosterone and estradiol (T+E2) as adults to mimic the hormonal environment of aging men. IUL TCDD exposure worsened T+E2-induced voiding dysfunction. Mice in the previous study were genetically prone to prostatic neoplasia and it was therefore unclear whether TCDD exacerbates voiding dysfunction through a malignant or non-malignant mechanism. We demonstrate here that IUL TCDD exposure acts via a non-malignant mechanism to exacerbate T+E2-mediated

SUBMITTER: Turco AE 

PROVIDER: S-EPMC7076297 | biostudies-literature | 2020

REPOSITORIES: biostudies-literature