Proliferative Response of Mouse Seminal Vesicle Epithelium to Androgen and Estrogen, Assayed by Incorporation of [¹²⁵I]Iododeoxyuridine*

Abstract

The proliferation and death of androgen- and estrogen-responsive cells in the seminal vesicles of mice were investigated. Since 5-[125I]iodo-2'-deoxyuridine ([125I]IdUrd) was incorporated into seminal vesicle DNA, and since the steroid-induced change in [125I]IdUrd uptake by whole seminal vesicles paralleled the change in the mitotic index in epithelial cells, [125I]IdUrd uptake was used as an index in epithelial cells, [125I]IdUrd uptake was used as an index for the proliferation of epithelial cells. Injections of testosterone propionate (TP) in castrated mice induced a 50-fold increase in [125I]IdUrd uptake. When androgen-induced cell proliferation was labeled with [125I]IdUrd, the incorporated radioactivity was retained in mice given continuous TP injections but not in mice given continuous TP injections but not in mice given 17 beta-estradiol (E2) or vehicle. Although the injection of E2 into castrated mice induced a 10-fold increase in [125I]IdUrd uptake, E2 did not increase seminal vesicle weight, and when estrogen-induced cell proliferation was labeled with [125I]IdUrd, the incorporated radioactivity was not retained in mice given continuous E2 injections. The simultaneous injections of E2 and TP showed no significant additive effect on [125I]IdUrd uptake. The present results suggest that 1) androgen induces proliferation and differentiation of the seminal vesicle epithelium and maintains the differentiated cells; 2) estrogen induces epithelial cell proliferation without further differentiation or maintenance of the resulting cells. The seminal vesicle epithelial cells responsive to estrogen may be the same cells that are responsive to androgen.