Specific cultures were used to detect growth of Neisseria Gonorrhoeae (NG) in 90 ejaculates of partners of childless marriages. Although no gonococcal growth was observed in undiluted semen, 9 out of 68 subjects with silent infection presented growth of NG in seminal plasma after dilution 1:2 with saline. It is concluded that semen dilution increases the chances of detection of NG in semen samples of asymptomatic gonococci carriers.
Leydig cells, purified on two sequential Percoll gradients to purities of 89 ± 1%, were used to study the binding of 17‐β‐hydroxy‐17α‐memyl‐estra‐4,9,11‐triene‐3‐one(3H‐R1881). The accumulation of 3H‐R1881 in the nuclear fraction of these cells was time‐ and temperature‐dependent. Specific binding was saturable with an apparent Ka of 0.14 nM−1 and a single class of binding sites at a concentration of 721 fmol/mg DNA. A fraction of the bound radioactivity in the nuclear pellet could be extracted with 0.4 M KCl, and a portion of this extracted steroid was associated with macromolecular species. The nuclear accumulation was androgen‐specific. These data are consistent with the presence of androgen receptors in rat Leydig cells.
Abstract. In six healthy subjects serum oestradiol was selectively decreased by administering an aromatase activity inhibitor, hydrotestolactone (HT). After HT administration serum oestradiol (Oe2) decreased from 18.7 ± 2.3 (sem) to 6.7 ± 0.6 pg/ml whereas testosterone (T) and dihydrotestosterone (DHT) blood levels were not modified. These oestradiol changes were associated with a significant increase in serum LH and FSH concentrations (P < 0.001). The administration of tamoxifen, an oestrogen antagonist, to 5 subjects caused a sharp increase in LH and FSH levels (P < 0.001). Oe2 was unchanged after the treatment with tamoxifen, whereas T levels were significantly higher. The sum of these data suggests that oestradiol under physiological conditions plays a specific role in the feedback mechanism of gonadotrophin release.
In order to determine the effect of dihydrotestosterone on the feed-back mechanism of the hypothalamo-pituitary-testis axis, nine healthy subjects were subjected to LH-RH tests before and after treatment with 5\g=a\-DHT. A double antibody radio-immunoassay technique was used to measure the concentration of LH and FSH in the plasma. Our results clearly show that the pituitary LH release by LH-RH after pre-treatment with 5\g=a\-DHTis more pronounced. In the light of actual findings from several laboratories it is not possible to interpret clearly the results of our own experiments, and hence we advance only some hypotheses.Recent research has shown that in target organs, testosterone is converted into 5a-androstan-17/?-ol-3-one (dihydrotestosterone, DHT) its biological active form (Robel 1971). This change apparently takes place in the feed-back mechanism of the brain, the hypothalamus and the pituitary (Jaffe 1969;Tveter 1970;Massa et al. 1972; Zanisi et al. 1912b); consequently this steroid, together with testosterone, progesterone and oestradiol, could be involved in the mechanism controlling gonadotrophin release.Recent studies have shown that oestradiol, progesterone and testosterone (Fang et al. 1969; Sholiton 8c Werk 1969; Arimura 8c Schally 1971; Reeves et al 1971; Debeljuk et al. I972a,b; Davidson 1969; Guai et al. 1972; Zanisi et al. 1972a; Blake et al. 1972; D'Agata et al. 1974) influence the gonado¬ trophin response to synthetic LH-RH.These findings were the bases for our studies on the behaviour of plasma
Steroidogenic responsiveness to long term hCG administration (1500 U three times a week for 23 months) was characterized in 8 males with hypogonadotropic hypogonadism (HH). During hCG treatment, testosterone (T), which was in the prepuberal range under basal conditions, rose considerably to the upper end of the normal range and remained at that level during the 23 months of observation. A 2.5-fold increase was observed in serum levels of 17 beta-estradiol (E2) an increment less than seen with T. The increment in 17 alpha-hydroxyprogesterone was also lower than that in T throughout the study; thus, the 17 alpha-hydroxyprogesterone to T ratio, despite continuous hCG administration, remained low. Serum androstenedione was slightly increased during hCG therapy. No significant changes were observed in serum levels of dehydroepiandrosterone. These data indicate that continuous long term hCG administration stimulated T levels in HH, with a relatively small change in E2. The kinetics of the T and E2 responses to 2000 U hCG, evaluated after 23 months of therapy, indicated that the testicular response was markedly reduced. No increment in T levels was observed at 24 h; the maximal response occurred at 48 h. This pattern of T response supports the idea that partial testicular desensitization occurs in HH patients receiving chronic treatment with hCG.
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