Moger W H
Can J Physiol Pharmacol. 1980 Sep;58(9):1011-22. doi: 10.1139/y80-154.
This article reviews literature relevant to the view that estradiol (E2) synthesized in the testis acts locally to modify testosterone secretion. Despite a lack of convincing evidence from in vitro experiments, in vivo experiments with intact and hypophysectomized animals have demonstrated that estrogens can inhibit testosterone secretion by acting directly on the testis. Reduced testosterone production in estrogen-treated animals probably results from reduced 17 alpha-hydroxylase and (or) C17-C20 lyase activity. Estrogen-inhibited steroidogenesis may result from estrogen binding to high affinity--low capacity estrogen receptors. Besides being an estrogen target tissue, the testis produces E2; the cellular site of testicular E2 synthesis remains controversial. Recent studies indicate that E2 is synthesized primarily in the Sertoli cells of neonatal rats and in the Leydig cells of older rats. Follicle-stimulating hormone and human chorionic gonadotropin (hCG) increase testicular aromatase activity and E2 concentrations in neonatal and older rats, respectively. An increase in testicular E2 concentrations, following hCG administration, may be one mechanism by which testosterone synthesis becomes desensitized to subsequent hCG stimulation. However, whether gonadotropin-stimulated testicular E2 synthesis is part of a physiologically relevant "short" feedback loop that participates in the regulation of testosterone synthesis remains to be determined.
本文综述了与睾丸中合成的雌二醇（E2）在局部作用以调节睾酮分泌这一观点相关的文献。尽管体外实验缺乏令人信服的证据，但对完整动物和垂体切除动物的体内实验表明，雌激素可通过直接作用于睾丸来抑制睾酮分泌。雌激素处理的动物中睾酮生成减少可能是由于17α-羟化酶和（或）C17-C20裂解酶活性降低所致。雌激素抑制的类固醇生成可能是由于雌激素与高亲和力——低容量的雌激素受体结合。睾丸除了是雌激素的靶组织外，还产生E2；睾丸E2合成的细胞位点仍存在争议。最近的研究表明，E2主要在新生大鼠的支持细胞和成年大鼠的睾丸间质细胞中合成。促卵泡激素和人绒毛膜促性腺激素（hCG）分别增加新生大鼠和成年大鼠的睾丸芳香化酶活性和E2浓度。给予hCG后睾丸E2浓度的增加可能是睾酮合成对随后hCG刺激产生脱敏的一种机制。然而，促性腺激素刺激的睾丸E2合成是否是参与睾酮合成调节的生理相关“短”反馈回路的一部分，仍有待确定。
