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Developmental estrogen exposures predispose to prostate carcinogenesis with aging.

Gail S Prins1, Lynn Birch, Wan-Yee Tang

  • 1Department of Urology, University of Illinois at Chicago, 820 South Wood Street, MC 955, Chicago, IL 60612, United States. gprins@uic.edu

Reproductive Toxicology (Elmsford, N.Y.)
|November 25, 2006
PubMed
Summary

Early life exposure to estrogens, including environmental chemicals like bisphenol A, permanently alters prostate development. This developmental estrogenization increases susceptibility to prostate lesions and cancer later in life.

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Area of Science:

  • Endocrinology
  • Developmental Biology
  • Oncology

Background:

  • Prostate development is influenced by hormones, primarily androgens, but estrogens also play a permanent role.
  • Abnormal estrogen exposure during critical developmental periods can lead to lasting changes in prostate morphology and function, a process known as developmental estrogenization.

Purpose of the Study:

  • To characterize developmental estrogenization in a rodent model.
  • To identify molecular pathways involved in mediating estrogen's effects on prostate development.
  • To investigate the impact of low-dose and environmentally relevant endocrine disruptor exposures on prostate cancer susceptibility.

Main Methods:

  • Neonatal rodent model exposed to varying doses of estradiol and bisphenol A.
  • Analysis of prostate morphology, lesion incidence (hyperplasia, inflammation, prostatic intraepithelial neoplasia - PIN), and aging effects.

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  • Gene methylation analysis to explore epigenetic mechanisms.

    • Main Results:

    • Early high-dose estradiol exposure increased the incidence of prostatic lesions, including PIN, with aging.
    • Low-dose estradiol and bisphenol A exposures during development increased susceptibility to PIN lesions after adult estradiol exposure.
    • Gene methylation analysis suggests an epigenetic basis for estrogen imprinting in the prostate.

    Conclusions:

    • Developmental estrogenization, from low-dose to high-dose exposures, increases the risk of prostate neoplastic transformation in aging males.
    • Environmental estrogens like bisphenol A contribute to this increased susceptibility.
    • These findings suggest a fetal origin for adult prostate diseases, highlighting the importance of endocrine disruptor regulation.