A review was made to understand how plasma binding protein might influence sex-hormone action in target tissues. Steroids are predominately bound to plasma proteins and only unbound steroids enter the cells. Sex-hormone-binding globulin (SHBG) binds to both the main circulating steroid T and E2 but changes in SHBG concentrations exert significant results. Increased SHBG levels increase estrogen production and decreases T activity; whereas increased androgens increase T action and inhibit SHBG production. These disturbances in hormone maintenance may lead to abnormal adult sex differentiation such as hirsutism and forms of hynaecomastia. By developing SHBG concentration measurement methods-responses of hirsutism to glucocorticoid or estrogem may be assessed. In addition the effect of thyroid hormones on SHBG may also have therapeutic implications in endocrine disease.

https://onlinelibrary.wiley.com/doi/pdf/10.1111/j.1365-2265.1974.tb03298.x

Sex-hormone-binding globulin.

Sexual dimorphism in selected extragenital tissues is described with emphasis on the molecular basis of the differences. Testosterone rather than 5 alpha-dihydrotestosterone appears to be the major intracellular androgen in organs other than skin and reproductive tract, but other steroid metabolites and their receptors are required to produce the diverse tissue differences observed in males and females. There is also evidence that multiple hormones from several endocrine glands are required to act in concert with androgens to produce and maintain their effects. Although many of the consequences of sexual dimorphism, such as body size and strength, have been evident for centuries, other differences between males and females such as disease incidence, response to drugs and toxins, and the metabolism and assimilation of dietary constituents have only recently been discovered.

Testosterone: a major determinant of extragenital sexual dimorphism

Publisher Summary This chapter describes the hormonal effects on cell proliferation in rat prostate. The growth and function of male accessory sex glands are under the direct control of androgens, and consequently these tissues can potentially serve as an excellent model system for the study of the regulation of cell proliferation by steroid hormones. Three phases can be distinguished in the response of rat prostate to changes in the hormonal status of the animal, and these are summarized. It is found that treatment of castrated rats with testosterone propionate produced a massive but transitory increase in the incorporation of radioactive thymidine into DNA of prostate both in vitro and in vivo, which was paralleled by an elevation and decline in DNA polymerase activity. It is observed that a vital factor determining the magnitude of the proliferative response of prostate to androgens is the number of cells in the gland relative to normal. Tissues that contain fewer than the normal number of cells respond to hormone administration by proliferating rapidly, but once the number of cells has returned to normal the rate of proliferation declines sharply.

Hormonal effects on cell proliferation in rat prostate.

Publisher Summary This chapter discusses the epithelial-stromal interactions in development of the urogenital tract. The hormonal influences on urogenital morphogenesis, differentiation, and function are discussed. The hormone-dependent development of the urogenital tract occurs via an interaction between epithelium and stroma in which the stroma plays a decisive role in mediating the unique morphological response of epithelium to sex hormones by inducing specific patterns of epithelial morphogenesis. Through stromal induction, which has been demonstrated during pre and postnatal periods and even into adulthood, the developmental fate of the epithelium is usually determined during fetal or early neonatal periods. However, once determined, urogenital epithelia continue to require a relatively specific interaction with urogenital stroma for full expression of morphogenesis, cytodifferentiation, and function. The developmental properties of epithelium and stroma, which vary temporally, account for changes in hormonal responsiveness of the intact target organs. Thus the developmental responses of urogenital organs to sex hormones are not strictly epithelial phenomena, but are interactive processes dependent on both the epithelium and stroma.

Epithelial-stromal interactions in development of the urogenital tract.

Publisher Summary This chapter discusses androgen metabolism and the mechanism of action in male pseudohermaphroditism. It has been found that testosterone is the major androgen secreted into the blood of most mammals and that this steroid has biological actions on many tissues. As animals with testicular feminization cannot respond to androgens in utero, tissues, such as prostate, Wolffian duct derivatives, and external genitalia, do not differentiate, and the tfm animal develops as a male pseudohermaphrodite. Male pseudohermaphroditism resembling testicular feminization also develops in animals that are deprived of androgens in utero by one of the several mechanisms, including castration, defective testosterone synthesis, and exposure to pharmacologic agents that either block androgen biosynthesis in the testis or androgen action at the end organ. When the gonaducts and external genitalia fail to undergo androgen-dependent differentiation in utero, they do not develop into a normal reproductive tract when subsequently exposed to large doses of androgens. Thus, certain tissues may acquire insensitivity to androgens during differentiation. The chapter also discusses ultrastructural examination of the interstitial area of vet rat testes that demonstrates increased peritubular connective tissue. The interstitial tissue consisted predominantly of fibroblasts and a few peritubular sheath cells.

Etienne-Emile Bauliec

Papers

Hormone metabolism and action: Testosterone and metabolites in prostate organ culture