Ho S M, Yu M
Department of Biology, Tufts University, Medford, MA 02155.
J Steroid Biochem Mol Biol. 1995 Mar;52(3):233-8. doi: 10.1016/0960-0760(94)00170-q.
We previously demonstrated that simultaneous treatment of Noble (NBL) rats with estradiol (E2) and testosterone (T) for 16 weeks induces a proliferative response selectively in the dorsolateral prostates (DLP) of all treated animals [1, 2]. The unique sensitivity of rat DLP to the conjoint androgen-estrogen-induced mitogenic action may be attributable to the presence of a moderate affinity, high capacity, nuclear estrogen binder (type II sites) found exclusively in this prostatic lobe [2, 3]. Little is known about whether prostatic type II site levels are under hormonal regulation. The aim of this study is to determine whether testicular steroids play a role in regulating the basal and/or induced levels of type II site expression in rat DLP. In the first experiment, rats were castrated and immediately treated with 5 alpha-dihydrotestosterone (DHT) and/or E2 for 6 weeks to determine whether these steroids, separately or jointly, could sustain DLP type II site levels in castrates. Treatments of castrated rats with DHT and DHT+E2 were found to be effective in maintaining DLP type II site levels and gland wet weights at values close to those found in intact untreated controls, while treatments with E2 failed to maintain these parameters at levels observed in intact animals. In the second experiment, intact rats were treated with an androgen (T or DHT) or E2, alone or in combination, for 16 weeks to ascertain which hormonal regimen could induce a higher level of type II site expression in the DLP. Treatments of rats with an androgen (T or DHT) or E2 alone did not change DLP type II site levels even though T treatment caused a slight increase in gland weight, while E2 treatment induced prostatic atrophy. Contrary to single hormone treatments, combined T + E2 and DHT+E2 treatments were effective in inducing a doubling of type II sites and increases in wet weight of the DLPs. These data indicate that testicular androgen is the primary factor responsible for maintaining a basal level of type II site expression in rat DLP, while conjoint androgenic-estrogenic action is needed for the induction of a higher level of type II site expression in the tissue.
我们之前证明，对诺布尔（NBL）大鼠同时给予雌二醇（E2）和睾酮（T）处理16周，可在所有接受处理的动物的背外侧前列腺（DLP）中选择性地诱导增殖反应[1,2]。大鼠DLP对联合雄激素 - 雌激素诱导的促有丝分裂作用具有独特的敏感性，这可能归因于仅在该前列腺叶中发现的中等亲和力、高容量的核雌激素结合蛋白（II型位点）的存在[2,3]。关于前列腺II型位点水平是否受激素调节知之甚少。本研究的目的是确定睾丸类固醇是否在调节大鼠DLP中II型位点表达的基础水平和/或诱导水平中起作用。在第一个实验中，对大鼠进行去势，并立即用5α - 双氢睾酮（DHT）和/或E2处理6周，以确定这些类固醇单独或联合使用是否能维持去势大鼠的DLP II型位点水平。发现用DHT和DHT + E2处理去势大鼠可有效维持DLP II型位点水平和腺体湿重，使其接近未处理的完整对照动物中的值，而用E2处理未能将这些参数维持在完整动物中观察到的水平。在第二个实验中，对完整大鼠单独或联合给予雄激素（T或DHT）或E2处理16周，以确定哪种激素方案可在DLP中诱导更高水平的II型位点表达。单独用雄激素（T或DHT）或E2处理大鼠并没有改变DLP II型位点水平，尽管T处理导致腺体重量略有增加，而E2处理诱导前列腺萎缩。与单一激素处理相反，联合T + E2和DHT + E2处理可有效诱导II型位点增加一倍，并使DLP的湿重增加。这些数据表明，睾丸雄激素是维持大鼠DLP中II型位点表达基础水平的主要因素，而联合雄激素 - 雌激素作用是在组织中诱导更高水平II型位点表达所必需的。
