Testosterone concentration in different functional compartments of the male reproductive tract

Adamopoulos, D. A.; Lawrence, Daphne M.; Vassilopoulos, P.; Kontogeorgos, L.; Ntounis, Athanassios; Swyer, G. I. M.

doi:10.3109/01485017908985042

Cited by 8 publications

(1 citation statement)

References 7 publications

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“…However, the concentrations of testosterone (10 Ϫ7 mol/L) required for this apoptosis inhibiting effect were 100-1000 times the effective concentrations of estradiol (10 Ϫ9 -10 Ϫ10 mol/L). Of note, the relative potencies of testosterone and estradiol are in the range of their relative physiological concentrations in the spermatic vein (43)(44)(45)(46)(47) and testis tissue (48,49). In vivo, testosterone can be metabolized to either estrogens or DHT.…”

Section: Discussionmentioning

confidence: 99%

Estradiol Acts as a Germ Cell Survival Factor in the Human Testis in Vitro*

Pentikäinen

Erkkilä

Suomalainen

et al. 2000

The Journal of Clinical Endocrinology &Amp; Metabolism

116

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The necessity of estrogens for male fertility was recently discovered in studies on both estrogen receptor ␣ knockout and aromatase (cyp 19 gene) knockout mice. However, direct testicular effects of estrogens in male reproduction have remained unclear. Here we studied the protein expression of ER␣ and the recently described estrogen receptor ␤ in the human seminiferous epithelium and evaluated the role of 17␤-estradiol, the main physiological estrogen, in male germ cell survival. Interestingly, both estrogen receptors ␣ and ␤ were found in early meiotic spermatocytes and elongating spermatids of the human testis. Furthermore, low concentrations of 17␤-estradiol (10 Ϫ9 and 10 Ϫ10 mol/L) effectively inhibited male germ cell apoptosis, which was induced in vitro by incubating segments of human seminiferous tubules without survival factors (i.e. serum and hormones). Dihydrotestosterone, which, in addition to estradiol, is an end metabolite of testosterone, was also capable of inhibiting testicular apoptosis, but at a far higher concentration (10 Ϫ7 mol/L) than estradiol. Thus, estradiol appears to be a potent germ cell survival factor in the human testis. The novel findings of the present study together with the previously reported indirect effects of estrogens on male germ cells indicate the importance of estrogens for the normal function of the testis. (J Clin Endocrinol Metab 85: 2057-2067, 2000 R ECENT CONCERN over the potentially harmful effects of environmental estrogen-like chemicals on male fertility (1, 2) has aroused growing interest in understanding the physiological effects of estrogens in the male. Although estrogens have been regarded as female steroid hormones, they are now known to have profound effects on both female and male reproductive systems. In males, estrogens are synthesized mainly in the testis, where they are formed from testosterone by the enzyme P450 aromatase. In the rat, there is an age-related change in the aromatization site from Sertoli cells in the immature testis to Leydig cells in the adult testis (3, 4). In various other species, including humans, P450 aromatase has been found to be present in the Leydig cells of the adult testis (5-9). In addition, in the mouse (6), rat (7), brown bear (9), and rooster (10), aromatase has been found in meiotic and postmeiotic germ cells of the testis, predominantly in spermatids.Estrogens exert their cellular effects through estrogen receptors (ER) that exist in at least two subtypes, ER␣ (11, 12) and the recently described ER␤ (13, 14), which differ in the C-terminal ligand-binding domain and in the N-terminal trans-activation domain. These two subtypes of ER have similar high affinities for 17␤-estradiol, but some synthetic and naturally occurring ligands have different relative affinities for ER␣ and ER␤ (15). In the male reproductive tract, ER␣ has been shown to be strongly expressed in the epididymis and efferent ductules (16 -20). It has also been found in the Leydig cells of the rat testis (16), whereas the seminiferous epitheliu...

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