Effects of hormones on the prostate in adult and aging men and animals

Abstract

Literature on the effect of steroid hormones (androgens, estrogens, and other steroids), of peptide hormones (e.g., prolactin), and growth factors (e.g., EGF, FGF, TGF-beta), on the effect of castration and of experimental hormone application on the prostate is reviewed. Androgens have inductive, repressive, and interactive effects. They counterbalance an agonistic effect on proliferation and an antagonistic effect on cell death; they may influence DNA synthesis and induce the synthesis of substances with mitogenic effects on the prostate. Estrogens exert direct and indirect effects on the prostate. They suppress the secretion of gonatropins, thus repressing testicular androgen secretion. They stimulate the fibromuscular stroma and induce squamous metaplasia of the epithelium. Estrogens may also be involved in the onset of benign prostatic hyperplasia. Prolactin is preferentially bound in the diseased human prostate. An abundance of information has been gained on EGF, FGF, TGF-beta, and other growth factors. They may be involved in the development of prostatic hyperplasia. Castration leads to a striking reduction in prostatic size in a short period of time due to autophagic and heterophagic processes. In castrated individuals, the prostate is enriched in androgen-independent cells. Experimental hormone application involves the substitution of androgens as well as anti-androgens, long-term application of different hormones, and application of combinations of drugs. The results of several studies are described. Further directions in the field of prostate research should concentrate on the role of growth factors in prostate development and pathology and on the effect of certain lectins on prostate diseases. We think that the investigation of interactions between steroid hormones and growth factors in normal and pathological neovascularization of the prostate is important.

Hormonal control of programmed cell death/apoptosis

“…This occurrence has been observed in the prostate after castration (25,26) and in the adrenal cortex after suppression of secretion of adrenocorticotrophic hormone (ACTH) by administration of glucocorticoid (27). Various forms of cancer therapy, such as a variety of cancer-chemotherapeutic agents and moderate doses of radiation, induce or enhance extensive apoptosis in rapidly proliferating cell populations (5,28).…”

“…They counterbalance these agonistic effects on proliferation with an antagonistic effect on programmed cell death. Conversely, oestrogens exert direct and indirect opposing effects on cell death in the prostate (26).…”

Effects of pituitary hormones on the prostate

“…Numerous growth factors have also been identified in prostate secretions: nerve growth factor, insulin-like growth factors, epidermisderived growth factor, ␣ and ␤ transforming growth factors, acid and basic fibroblast growth factors, and platelet-derived growth factor [7][8][9]. These growth factors play an important role in the regulation of prostatic growth through autocrine or paracrine control mechanisms.…”

Benign prostatic hyperplasia: dietary and metabolic risk factors

“…Previous studies have implicated family history [5], race/ethnicity [3], immunological [6], and endocrinal factors as existing risk factors. Among endocrine factors, the role of hormones like androgen [7], estrogen [8], growth hormone [9], prolactin [10], and growth factors such as insulin-like growth factors [11], fibroblast growth factor [12], and transforming growth factors [13] have already been established.…”