Estrogen and Spermatogenesis

Abstract

Although it has been known for many years that estrogen administration has deleterious effects on male fertility, data from transgenic mice deficient in estrogen receptors or aromatase point to an essential physiological role for estrogen in male fertility. This review summarizes the current knowledge on the localization of estrogen receptors and aromatase in the testis in an effort to understand the likely sites of estrogen action. The review also discusses the many studies that have used models employing the administration of estrogenic substances to show that male fertility is responsive to estrogen, thus providing a mechanism by which inappropriate exposure to estrogenic substances may cause adverse effects on spermatogenesis and male fertility. The reproductive phenotypes of mice deficient in estrogen receptors alpha and/or beta and aromatase are also compared to evaluate the physiological role of estrogen in male fertility. The review focuses on the effects of estrogen administration or deprivation, primarily in rodents, on the hypothalamo-pituitary-testis axis, testicular function (including Leydig cell, Sertoli cell, and germ cell development and function), and in the development and function of the efferent ductules and epididymis. The requirement for estrogen in normal male sexual behavior is also reviewed, along with the somewhat limited data on the fertility of men who lack either the capacity to produce or respond to estrogen. This review highlights the ability of exogenous estrogen exposure to perturb spermatogenesis and male fertility, as well as the emerging physiological role of estrogens in male fertility, suggesting that, in this local context, estrogenic substances should also be considered "male hormones."

Effect of 17‐α‐ethynylestradiol on germ cell proliferation in organ and primary culture of medaka (Oryzias latipes) testis

“…Since the 1930s, estrogens have been known to be synthesized in male vertebrates (Zondek 1934), but with respect to male reproduction, this finding has been largely ignored for a long time because estrogens were considered to be exclusively female hormones with no role in spermatogenesis (reviewed by O'Donnell et al 2001). However, it has become quite clear now that E2 is an essential hormone in male reproduction (Hess et al 1997(Hess et al , 2001Sharpe 1998).…”

The faah gene is the first direct target of estrogen in the testis: role of histone demethylase LSD1

“…Spermatogenesis is controlled by gonadotrophins and testosterone and is modulated by a complex network of endocrine and paracrine factors, among which are estrogens [1]. The biological effects of 17b-estradiol (E 2 ) are mediated by the estrogen receptors a (ERa) and b (ERb), which belong to the nuclear receptor superfamily and function as ligand-induced transcriptional factors.…”

Breast cancer resistance protein (Bcrp) and the testis—an unexpected turn of events

“…In fact, recent studies have shown that steroids, such as oestradiol-17b, testosterone and progesterone, can inhibit the transport activity of Bcrp and upregulate Bcrp expression and its cellular localisation in cancer cells, endothelial cells of the brain and endocrine organs. 21,41,42 Steroids, particularly testosterone and oestrogens, are known to regulate BTB and testicular Bcrp and spermatogenesis XJ Qian et al 456 function, [43][44][45][46] and Bcrp plays a significant role in regulating the transport of steroids across the myoid cells and Sertoli cells at the apical ES (Table 1). Additionally, the activity, expression and cellular distribution of Bcrp are regulated by steroids.…”