AI Article Synopsis

  • Erectile dysfunction (ED) is a common condition that adversely affects quality of life, and its rising prevalence suggests potential environmental risk factors.
  • The study investigates the impact of Endocrine Disrupting Chemicals (EDCs), particularly diethylstilbestrol (DES), on erectile function by using male mice as a model.
  • Findings reveal that chronic exposure to DES leads to abnormal erectile tissue function and increased expression of estrogen receptors, indicating that both long-term and short-term exposure to estrogenic EDCs may play a significant role in causing ED.

Article Abstract

Erectile dysfunction (ED) is an extremely prevalent condition which significantly impacts quality of life. The rapid increase of ED in recent decades suggests the existence of unidentified environmental risk factors contributing to this condition. Endocrine Disrupting Chemicals (EDCs) are one likely candidate, given that development and function of the erectile tissues are hormonally dependent. We use the estrogenic-EDC diethylstilbestrol (DES) to model how widespread estrogenic-EDC exposure may impact erectile function in humans. Here we show that male mice chronically exposed to DES exhibit abnormal contractility of the erectile tissue, indicative of ED. The treatment did not affect systemic testosterone production yet significantly increased estrogen receptor α (Esr1) expression in the primary erectile tissue, suggesting EDCs directly impact erectile function. In response, we isolated the erectile tissue from mice and briefly incubated them with the estrogenic-EDCs DES or genistein (a phytoestrogen). These acute-direct exposures similarly caused a significant reduction in erectile tissue contractility, again indicative of ED. Overall, these findings demonstrate a direct link between estrogenic EDCs and erectile dysfunction and show that both chronic and acute estrogenic exposures are likely risk factors for this condition.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC10987563PMC
http://dx.doi.org/10.1038/s42003-024-06048-1DOI Listing

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