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At least 55 records · Page 3Linked to original sources
PubMed1987

Relationship of testosterone, sex hormone binding globulin, and calculated free testosterone to subsequent clinical progress in patients with carcinoma of the prostate treated with bilateral orchidectomy or estrogens.

The concentration in serum of testosterone, sex hormone binding globulin (SHBG), and albumin has been measured, and from these measurements free testosterone has been calculated in 75 patients with carcinoma of the prostate treated with either bilateral orchidectomy, stilbestrol, or estramustine phosphate (Estracyt). After exclusion of 3 noncompliant patients, total testosterone did not differ significantly between treatments, but free testosterone was lower in estrogen-treated patients (5.9 +/- 0.9 (SEM) pmol/l, n = 28) compared with the orchidectomized patients (23 +/- 1.4 pmol/l, n = 44) (P less than 0.001); all of the estrogen-treated patients falling in the lower third of the range of the orchidectomized patients. Free testosterone did not change systematically during several years of treatment and there was no evidence of a rise with clinical deterioration. In the 33 patients with metastatic cancer treated with orchidectomy, the third with the lowest free testosterone or total testosterone showed a better survival over 2 years than the two-thirds with higher free or total testosterone; thereafter, the advantage was lost.

Aged↗
PubMed1976

Distinct testicular 17-ketosteroid reductases, one in interstitial tissue and one in seminiferous tubules. Differential modulation by testosterone and metabolites of testosterone.

The final step in the biosynthesis of testosterone is the reduction of androstenedione, which is catalyzed by the microsomal enzyme 17-ketosteroid reductase. Evidence is presented which suggests that there are two distinct 17-ketosteroid reductases in rat testes, one in interstitial tissue and one in seminiferous tubules. The two enzymes have different pH optima, 5.6 for the one from interstitial tissue and 6.5 for the one from seminiferous tubules. At the optimum pH, a 70-fold difference in Km values was observed, 17 muM for the interstitial tissue enzyme and 0.25 muM for the enzyme from seminiferous tubules. Testosterone and metabolites of testosterone have very different effects of each of these enzyme activities. The interstitial tissue enzyme activity is inhibited by testosterone and several 5alpha-reduced metabolites of testosterone and by estrogens. The most potent inhibitor of the steroids investigated was 5alpha-androstane-3alpha, 17beta-diol, followed by 17beta-estradiol approximately equal to dihydrotestosterone greater than testosterone greater than estrone greater than estriol. 5alpha-Androstane-3alpha, 17beta-diol and 17beta-estradiol were shown to act by competitive inhibition with apparent Ki values of 2.2 and 3.7 muM, respectively. In contrast, it was demonstrated that among the above steroids, only dihydrotestosterone inhibits the 17-ketosteroid reductase activity of seminiferous tubules and this inhibition was only observed at very high concentrations of inhibitor. Testosterone stimulated the 17-ketosteroid reductase activity of seminiferous tubules. 5alpha-Androstane-3alpha, 17beta-diol at low concentrations stimulated the enzyme activity from seminiferous tubules, while it had no effect at high concentrations. The remainder of the steroids tested had no effect on the 17-ketosteroid reductase activity of seminiferous tubules. The difference in response of the two enzyme activities suggests a mechanism for local regulation of testosterone synthesis in each testicular compartment that does not involve directly pituitary gonadotropins.

17-Ketosteroids↗
PubMed1988

Developmental changes in brain and serum binding of testosterone and in brain capillary uptake of testosterone-binding serum proteins in the rabbit.

Developmental changes in the brain uptake of circulating testosterone and of testosterone-binding proteins, such as testosterone-binding globulin (TeBG) or albumin, may play a role in the sexually dimorphic changes in brain structure that are mediated by circulating testosterone. The present studies examine developmental changes in binding of testosterone in both the serum and brain compartments in postnatal rabbits in vivo and developmental changes in the uptake of [3H]TeBG or [3H]albumin by capillaries isolated from developing rabbit brain. The results show that between 10 and 15 days postnatally both the brain sequestration of testosterone and rabbit serum binding of the hormone are markedly increased relative to the newborn period. In addition, both [3H]TeBG and [3H]albumin were taken up by microvessels isolated from 28-day-old rabbit brain, and this process for [3H]TeBG was more active in capillaries obtained from neonatal rats as opposed to adult rats. In summary, these studies show that the binding systems for testosterone are modulated in a parallel fashion in both the serum and brain compartments. In addition, uptake mechanisms for serum testosterone-binding proteins such as TeBG and, to a lesser extent, albumin exist in the capillaries of developing rabbits. These brain capillary plasma protein uptake systems may allow for the distribution into brain of circulating serum proteins such as TeBG and, to a lesser extent, albumin, in developing rabbits.

Aging↗
PubMed1985

Intratesticular regulation of testosterone secretion: comparison of the effects and interactions of hCG, an LHRH agonist and testicular interstitial fluid on Leydig cell testosterone secretion in vitro.

The stimulatory effects on Leydig cell testosterone secretion of a polypeptide(s) factor present in testicular interstitial fluid (IF) were compared with those of hCG and an LHRH agonist (LHRH-A). The actions of IF and LHRH-A were similar in showing (1) a delayed onset of action, (2) enhancement of testosterone production in response to a maximally stimulating concentration (5 nM) of hCG, and (3) near cessation of stimulation following their removal from the incubation medium. However, addition of an LHRH antagonist blocked only the actions of LHRH-A. Moreover, IF continued to stimulate testosterone production up to at least 20 h either on its own or in the presence of 5 nM hCG, whereas the stimulatory effects of LHRH-A disappeared beyond 6 h. IF was also able to enhance testosterone production in response to LHRH-A or in response to hCG + LHRH-A. IF enhanced testosterone production over 4-20 h in response to all doses of hCG and increasing concentrations of IF caused dose-dependent increments in the rate of hCG (5 nM) stimulated testosterone production. With submaximally stimulating doses of hCG or with LHRH-A alone, the stimulatory effect of IF was more or less additive, whereas with maximally stimulating doses of hCG the effect of IF was clearly synergistic. Thus, whereas the rate of testosterone production by Leydig cells in response to 5 nM hCG declined progressively from 4 to 20 h, addition of IF attenuated or prevented this decline. These findings have implications with respect to the physiological control of intratesticular testosterone levels and with respect to the regulation of steroidogenesis.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1971

Testosterone action in the rat ventral prostate. The effects of diethylstilboestrol and cyproterone acetate on the metabolism of ( 3 H)testosterone and the retention of labelled metabolites by rat ventral prostate in vivo and in vitro.

Recent reports have indicated that the prior metabolism of testosterone by the secondary sexual tissues may be necessary for its androgenic effect. The effects of two anti-androgens, diethylstilboestrol and cyproterone acetate (17alpha-acetoxy-6-chloro-1,2alpha-methylenepregna-4,6-diene-3,20-dione) used in the chemotherapy of human prostatic carcinoma, have been examined on both the metabolism of testosterone and the retention of its metabolites by the rat ventral prostate gland. Cyproterone acetate was found to inhibit the retention of labelled metabolites of [(3)H]-testosterone by prostatic nuclei, both in vivo and in vitro. This inhibition appeared to be competitive. In contrast with its effect on nuclear retention of metabolites of testosterone, cyproterone acetate had no significant effect on the metabolism of [(3)H]testosterone by rat ventral prostate tissue. Diethylstilboestrol similarly had little effect on the metabolism of [(3)H]testosterone by prostatic tissue, although it did appear partially to inhibit its initial metabolism in all the incubation systems used. Diethylstilboestrol inhibited the nuclear retention of dihydrotestosterone when both [(3)H]testosterone and diethylstilboestrol were injected intraperitoneally in vivo, but had no effect on dihydrotestosterone retention when both testosterone and diethylstilboestrol were supplied directly to the prostate either in vivo or in vitro. It was concluded that if diethylstilboestrol has an anti-androgenic effect at the level of the target organ as distinct from its effect on androgen production by the testes, then it is probably due to a mechanism differing from that of cyproterone acetate.

Androgen Antagonists↗
PubMed1982

Salivary testosterone: relationship to unbound plasma testosterone in normal and hyperandrogenic women.

A sensitive radioimmunoassay (RIA) was used to measure salivary testosterone levels in normal women, in patients with polycystic ovaries (PCO), and in women with hirsutism. There was a highly significant correlation (r = 0.79, P less than 0.001) between the concentration of testosterone in saliva [12.3 +/- 7.8 (SD) pg/ml] and the concentration of unbound testosterone in plasma (5.2 +/- 3.1 pg/ml) in matched samples collected from 56 women including normals, patients with clinical signs of hyperandrogenism, and women treated with a combination of cyproterone acetate (CA) and ethinyl oestradiol (EE). The unbound plasma testosterone was measured in the dialysate directly using a sensitive RIA. Salivary and plasma testosterone levels in patients with PCO (20.6 +/- 8.5 and 626 +/- 187 pg/ml respectively, n = 14) and in those with hirsutism (13.9 +/- 5.6 and 421 +/- 170 pg/ml, n = 30) were significantly higher (P less than 0.001) than levels in normal women (7.7 +/- 2.6 and 196 +/- 68 pg/ml, n = 36). Treatment for 3 months with CA and EE resulted in a decrease (mean 68%) in salivary testosterone levels in all patients studied (n = 15), but the suppression of plasma testosterone (mean 34%) was not observed in all cases. It is concluded that measurement of salivary testosterone gives a useful indication of levels of biologically available androgen in hyperandrogenic women, before and during CA/EE therapy.

Adolescent↗
PubMed1975

Radioimmunoassay of serum LH and testosterone in male rabbits actively immunized against testosterone.

Five male rabbits were actively immunized against testosterone to determine if this procedure could permanently inactivate circulating testosterone. To assess the response to immunization, serum LH, serum testosterone and antitestosterone titer (titer) were measured by radioimmunoassay at various times after immunization. All rabbits produced antisera to testosterone and developed serum LH levels similar to those measured in castrated males. The rise in serum LH was particularly pronounced after a booster immunization but these elevated levels were not maintained which suggests that biological neutralization was only transient. Serum testosterone rose dramatically after immunization and was directly correlated with titer. High serum testosterone concentrations were associated with both high and low serum LH. No correlation existed between titer ans serum LH. It is concluded that active immunization against testosterone does not necessarily result in a permanent neutralization of circulating testosterone and that titer alone is an inadequate criterion of neutralization.

Animals↗