Ultrastructural Study of the Effects of 17β-Oestradiol on the Lateral Prostate and Seminal Vesicle of the Castrated Guinea Pig

Abstract

Administration of oestradiol to castrated animals induced hypertrophy of the secretory cells in the lateral prostate and seminal vesicle. In the lateral prostate, increases in the number of small highly electron-dense granules, multivesicular bodies and intercellular spaces were the prevailing effects 2 weeks after oestradiol treatment. There was also an apparent increase in the amount of cytokeratin intermediate filaments. Prolonged oestradiol administration for 4 weeks showed no appreciable changes in the glandular epithelium when compared with 2-week treatment. However, an increase in the thickness of the fibromuscular layer was observed. In the seminal vesicle, basal cell hyperplasia was associated with a concurrent increase in the size of intercellular spaces 2 weeks after oestradiol administration. There were also apparent increases in the volume of the lamina propria and in the number of stromal cells. An apparent increase in the density of collagen fibres in the stroma was observed 2 and 4 weeks after oestradiol administration. In conclusion the responses of the epithelium of the lateral prostate and seminal vesicle to a pharmacological dose of oestradiol are different. Prolonged oestradiol administration exerts a more prominent effect on the smooth muscle in the lateral prostate but not in the seminal vesicle. The effects of oestradiol may be mediated directly or indirectly through the other hormones.

Developmental Exposure to Environmental Contaminants

“…In mice, slow-release implants of testosterone and estradiol drive an increase in voiding frequency, a reduction in voided volume, an increase in collagen deposition, and a change in velocity of urine flow through the prostatic urethra [124]. The mechanism by which changes in circulating testosterone and 17-beta-estradiol drive voiding dysfunction are not clear but may include direct actions on the bladder [134,135], changes in prostatic desmin and smooth muscle actin content or function [136][137][138][139].…”