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Serum gonadotrophins in rats after catration or heat treatment of the testes.

In rats spermatogenesis was disturbed by heat treatment of the testes. This resulted in increases of both LH and FSH. The increased gonadotrophin levels could be suppressed with testosterone. For suppression of FSH to levels of control animals more testosterone was needed than for LH. The increase of gonadotrophins after castration could be suppressed with testosterone released evenly from silastic capsules. For this suppression low serum levels of testosterone relative to testosterone levels in intact control animals were sufficient. This may indicate that testosterone episodically secreted has a lesser suppressive action on gonadotrophin secretion than a constant presence of this hormone. The suppressive action of testosterone on serum gonadotrophin levels after castration was potentiated by 1,4,6-androstatriene-3,17-dione, a steroid which inhibits strongly the enzymatic transformation of testosterone into oestradiol.

Animals↗

Effects of the dopamine agonist cabergoline on the pulsatile and TRH-induced secretion of prolactin, LH, and testosterone in male beagle dogs.

In the present study, the pulsatile serum profiles of prolactin, LH and testosterone were investigated in eight clinically healthy fertile male beagles of one to six years of age. Serum hormone concentrations were determined in blood samples collected at 15 min intervals over a period of 6 h before (control) and six days before the end of a four weeks treatment with the dopamine agonist cabergoline (5 microg kg(-1) bodyweight/day). In addition, the effect of cabergoline administration was investigated on thyrotropin-releasing hormone (TRH)-induced changes in the serum concentrations of these hormones. In all eight dogs, the serum prolactin concentrations (mean 3.0 +/- 0.3 ng ml(-1)) were on a relatively constant level not showing any pulsatility, while the secretion patterns of LH and testosterone were characterised by several hormone pulses. Cabergoline administration caused a minor but significant reduction of the mean prolactin concentration (2.9 +/- 0.2 ng ml(-1), p < 0.05) and did not affect the secretion of LH (mean 4.6 +/- 1.3 ng ml(-1) versus 4.4 +/- 1.7 ng ml(-1)) or testosterone (2.5 +/- 0.9 ng ml(-1) versus 2.4 +/- 1.2 ng ml(-1)). Under control conditions, a significant prolactin release was induced by intravenous TRH administration (before TRH: 3.8 +/- 0.9 ng ml(-1), 20 min after TRH: 9.1 +/- 5.9 ng ml(-1)) demonstrating the role of TRH as potent prolactin releasing factor. This prolactin increase was almost completely suppressed under cabergoline medication (before TRH: 3.0 +/- 0.2 ng ml(-1), 20 min after TRH: 3.3 +/- 0.5 ng ml(-1)). The concentrations of LH and testosterone were not affected by TRH administration. The results of these studies suggest that dopamine agonists mainly affect suprabasal secretion of prolactin in the dog.

Administration, Oral↗

Plasma testosterone and sleep: relationship to sleep stage variables.

A study was performed to determine whether the pattern of secretion of testosterone (T) during the night bears a systematic relationship to the cyclically recurring periods of rapid eye movement (REM) and non-REM (NREM) sleep. In four healthy male volunteers, 10-20 min sampling of plasma for T was carried out through a long indwelling catheter in conjunction with all-night polysmonography. Analysis of plasma T, comparing the samples drawn during the REM and NREM stages, did not reveal a significant difference in the mean concentration of T between the two sleep stages or among specified time segments of the NREM-REM cycles. A more exacting approach to exploring for a correlation of the secretory pattern with the sleep-stage cycle was then undertaken. This method used the NREM-REM cycle as the independent variable in the analysis. We were able to demonstrate that the positions of the peaks and troughs of T concentration in each REM-NREM cycle are discriminable when examined in relation to the time of REM sleep onset in each cycle. The tendency for peaks in T concentration to be associated with repetitive inaugurations of REM sleep is coordinate with a pattern of serial "upswing" in T concentrations that occurs in the period from 30 to 10 min before the transition from NREM to REM sleep. Accordingly, it proved possible to demonstrate certain signs of interaction between the activity of the pituitary-gonadal system and the mechanisms that regulate central nervous system state in sleep. The more traditional parameter of comparison (mean concentration of hormone in REM and NREM sleep) did not detect the association.

Adult↗

Postnatal exposure to androgens alters renal ornithine decarboxylase ontogeny and abolishes renal sexual dimorphism in mice.

The mouse kidney presents marked sexual dimorphism, manifested not only in renal size but also in the subcellular structure and enzyme activity. Ornithine decarboxylase (ODC), a key enzyme in the biosynthetic pathway of polyamines, is induced in the kidney by androgens, and its activity is higher in the kidney of male mice. The renal differences between male and female mice are not manifested during the first weeks of life and start to be expressed after weaning, simultaneously with the increase in plasma testosterone concentration. Treatment of newborn mice before postnatal day 21 with a single dose of testosterone propionate (TP, 200 microg/animal) did not increase renal ODC activity or renal size. From day 21 the same treatment elicited significant increases in renal ODC, especially in females where the basal activity of control animals was much lower than in males. The repeated injection of TP during the first 10 days of life (200 microg/animal, days 1, 4, 7 and 10) promoted an early increase in renal ODC activity but abolished the physiological rise observed in male mice at puberty and adulthood. This treatment dramatically reduced the secretion of the sexual hormones, testosterone, estradiol and progesterone, by the gonads, and diminished renal size as well as ODC and beta-glucuronidase activities in male mice. Stanozolol produced effects similar to those of TP, while the nonsteroidal antiandrogen, flutamide, did not apparently affect the normal development of the male or female kidney. The results indicate that: (a) kidney sexual dimorphism is not congenital; (b) neonatal androgens are not required to induce the sexual dimorphism of the mouse kidney; (c) the neonatal kidney is unresponsive to testosterone; (d) the premature and repeated exposure to supraphysiological levels of testosterone may accelerate the ontogeny of renal ODC but can abolish later testosterone secretion and hence alter the sexual characteristics of the male kidney, and (e) the postnatal treatment with androgens does not affect the response of the adult kidney to exogenous androgens. One can conclude that the postnatal manipulation of androgens may accelerate the development of the mechanisms of androgen responsiveness in some tissues but it may alter neural structures, probably the GnRH pulse generator, that control testosterone secretion.

Aging↗

Effects of acutely increased plasma testosterone concentrations on pulsatile luteinizing hormone secretion in the male rat.

To assess the role of testosterone (T) in regulating the minute-to-minute release of pulsatile luteinizing hormone (LH) secretion in the adult male rat, we investigated the negative feedback of acute increases in plasma T concentrations on pulsatile LH secretion in acutely castrated male rats. At the time of castration, we implanted T-filled Silastic capsules, s.c., which maintained plasma T concentrations at approximately 1.8 ng/ml and suppressed LH pulses. On the next day, the capsules were removed; blood sampling (every 6 min) was started 8 h after implant removal, thereby allowing LH pulses to be reinitiated. Immediately following a control bleeding interval of 2 h, either T or vehicle alone was infused s.c., and blood sampling continued for another 4 h. In animals receiving vehicle alone, LH pulse frequency and mean LH levels increased over the 6 h bleeding period. The administration of 200 ng T/min caused a rapid rise in plasma T concentrations of about 4 ng/ml ("physiological") and prevented the increase in pulse frequency that occurred in the control group; it did not, however, reduce pulse frequency over the 4 h infusion period. When T was infused at the rate of 400 ng/ml, plasma T concentrations rose to approximately 18 ng/ml ("supraphysiological") and LH pulse frequency was significantly reduced, but not completely inhibited, during the last 2 h of the infusion. The pulse amplitude of luteinizing hormone did not change significantly in any of the groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Testosterone replacement therapy in male hypogonadism.

In human males 6-7 mg of testosterone are secreted by the testes in a circadian rhythm with a nocturnal rise in testosterone followed by a decline during the day. Testosterone is necessary to induce and maintain secondary sexual characteristics, lean muscle mass, bone density and for normal sexual behaviour and cognitive function in men. Replacement therapy has been shown to be beneficial in men with overt hypogonadism. Natural testosterone should be used and not modified molecules. Testosterone is currently available in oral, intramuscular, subcutaneous and transdermal preparations. Recent advances in testosterone replacement therapy include testosterone gels which provide flexibility in dosing and minimal skin irritation resulting in good compliance, and the development of longer acting intramuscular preparations which result in more stable testosterone levels with longer injection intervals. All patients receiving testosterone should be carefully monitored for changes in hematocrit, liver function, lipid parameters and prostate specific antigen (PSA).This article reviews the current experience with the use of various forms of testosterone for the treatment of male hypogonadism.

Androgens↗

Testosterone regulation of luteinizing hormone and follicle stimulating hormone secretion in young male lambs.

Polydimethylsiloxane (Silastic) capsules containing crystalline testosterone were implanted subcutaneously in castrate lambs and evaluated for their ability to (1) provide stable, physiological concentrations of serum testosterone and (2) regulate secretion of LH and FSH. Testosterone was nondectable (< .2 ng/ml) between 12 and 24 weeks of age in the serum of castrate lambs implanted with empty capsules but was increased at those ages in lambs implanted with 20 cm (1.2 +/- .1 and .5 +/- .1 ng/ml), 60 cm (2.8 +/- .1 and .9 +/- .1 ng/ml) and 180 cm (6.6 +/- .3 and 1.9 +/- .2 ng/ml) of testosterone-filed Silastic tubing. Serum concentrations of LH and FSH were suppressed by exogenous testosterone and did not exceed concentrations in intact control rams as long as serum testosterone concentrations were greater than 1 ng/ml. In conclusion, simultaneous suppression of serum LH and FSH by concentrations of testosterone that cause a dose-dependent stimulatory effect on accessory sex gland weights indicates that testosterone is a physiological regulator of gonadotropin secretion in ram lambs. Although testosterone per se may not be directly responsible for negative feedback on LH and FSH secretion, the results presented herein question the need for a nonsteroidal "inhibin-like" testicular hormone to regulate FSH in lambs.

Animals↗

Endocrine changes in male stumptailed macaques (Macaca arctoides) as a response to odor stimulation with vaginal secretions.

In mammalian species, social chemosignals are important in modulating endocrine reproductive functions. In nonhuman primates, previous studies have described a high frequency of mounting behavior by females in the follicular and periovulatory phases of the menstrual cycle. Stumptailed macaque females do not signal receptivity by means of sexual swellings, as do others macaques, therefore providing a good model in which to study chemical signaling of reproductive status. We exposed anesthetized stumptailed males to vaginal secretions of either late follicular or menses phase or to saline solution to determine the endocrine changes promoting male sexual behavior. In males exposed to follicular secretions, plasma testosterone concentrations were sustained up to 120 min after exposure. Such an effect was not observed in animals exposed to menses or saline odor sources. A luteinizing hormone surge, occurring 30 minutes after exposure to late follicular phase secretion swabs, preceded this sustained testosterone effect. The fact that late follicular scents induce sustained testosterone concentrations provides support to the idea that stumptailed males draw information concerning female reproductive status from the female's vaginal odor.

Animals↗

Arachidonic acid metabolites as intratesticular factors controlling androgen production.

The effect of inhibitors and products of arachidonic acid metabolism on rat testicular steroidogenesis has been investigated. In the presence of indomethacin (inhibitor of cyclooxygenase) and nordihydroguaiaretic acid (NDGA) (inhibitor of lipoxygenase), the activity of 3 beta-hydroxysteroid dehydrogenase (3 beta-HSD) and 17 beta-hydroxysteroid dehydrogenase (17 beta-HSD) were both inhibited. The LH-stimulated increase in secretion of testosterone and progesterone was also inhibited by indomethacin and NDGA. On the other hand, vitamin E (antioxidant and inhibitor of lipoxygenase), stimulated the activity of both 3 beta-HSD and 17 beta-HSD and enhanced LH-stimulated androgen production. The metabolites of lipoxygenase (15-HPETE, 15-HETE, 5-HPETE and 5-HETE) and cyclooxygenase (PGF2 alpha) pathways stimulated 3 beta-HSD and 17 beta-HSD activity and enhanced the secretion of progesterone and testosterone. It is concluded that arachidonic acid metabolites are intratesticular factors which can regulate LH-stimulated testicular steroidogenesis.

17-Hydroxysteroid Dehydrogenases↗

Effect of 2-bromo-alpha-ergocryptine (CB-154) on estrogen induced growth of the rat prostate.

Castrate male Sprague-Dawley rats were treated with either testosterone; testosterone and estradiol; testosterone, estradiol and 2-Bromo-alpha-Ergocryptine (CB-154), an inhibitor of prolactin secretion; or testosterone and CB-154. Estradiol potentiated testosterone-induced growth of the dorsal, lateral, and ventral prostate and this effect was not counteracted by CB-154. Estradiol only induced hypertrophy of the dorsal and ventral prostate, however, hyperplastic changes occurred in the lateral prostate.

Animals↗

Temperature regulation of ovarian steroid production in the common carp, Cyprinus carpio L., in vivo and in vitro.

The effect of temperature on ovarian steroid production in the common carp, Cyprinus carpio L., has been studied in vitro with exogenous and endogenous precursors, and in fish held at three different temperatures in vivo. With radioactive testosterone as substrate, the major metabolite was testosterone glucuronide, but androstenedione and 5 alpha-androstane-3 beta,17 beta-diol were also identified. 5 alpha-Androstane-3 beta,7 alpha,17 beta-triol was tentatively identified and two other polar metabolites were isolated, one of which was convertible to this triol. A significant increase in production of most metabolites occurred between 20 and 24 degrees. Production of estradiol and testosterone from endogenous substrate under gonadotrophin stimulation in vitro showed a marked temperature dependence, but the response was closely related to ovarian maturity. Stage 4-5 ovaries produced testosterone, while late Stage 3 tissue produced only estradiol. Neither steroid was produced in significant quantities by less mature ovaries. The results indicate that the "switch off" of ovarian aromatase activity at the end of vitellogenesis is actuated by an ovarian rather than by a pituitary factor. Secretion of testosterone and estradiol showed a very significant change with temperature with the optimum at 24-29 degrees. Profiles for individual fish show that this optimal range is extremely narrow, particularly for estradiol, where secretion may increase as much as twentyfold over 5 degrees. The results in general correlate well with 24 degrees as the most favourable temperature for reproduction in carp. Plasma concentrations of testosterone and estradiol closely paralleled the in vitro secretion rates of these hormones. Plasma testosterone levels were greatest in the most mature fish, whereas plasma estradiol was significantly higher in late Stage 3 fish than in those of greater or lesser ovarian maturity. More Stage 4 and 5 fish were found in the group held at 24 degrees than at 20 or 29 degrees for 4 weeks, but all groups contained a high proportion of early Stage 3 fish.

Androstane-3,17-diol↗

Polychlorinated biphenyls (PCB 153 and PCB 126) action on conversion of 20-hydroxylated cholesterol to progesterone, androstenedione to testosterone, and testosterone to estradiol 17beta.

To look for one of the possible mechanisms of action we investigated the effect of two congeners of polychlorinated biphenyls (PCB153 as one of the most prominent environmental contaminants and PCB 126 as one of the most toxic contaminants similar to dioxin) on the cellular conversion of steroid precursors as an indicator for enzyme activity (20-hydroxylated cholesterol to progesterone for P450 (scc,) androstendione to testosterone for 17-beta-HSD, and testosterone to estradiol for P450 (arom)). The net synthesis and secretion of particular steroids was used as the indicator of enzyme activity. Co-culture of pig granulosa and theca cells isolated from small (SF) and large (LF) follicles, was carried out in medium M199 supplemented with 100 ng/ml of PCB 153 or 100 pg/ml of PCB 126. The inhibitory action of both PCB 126 and PCB 153 on progesterone secretion by cells isolated from SF and LF follicles was reversed in the presence of 20-hydroxylated cholesterol. The addition of PCB 126 into the culture medium caused a decrease in testosterone secretion by cells isolated from both SF and LF and this effect was reversed in the presence of androstendione. The inhibitory action of PCB 153 on testosterone secretion was reversed by the addition of androstendione to the culture medium in SF, while it caused even additional stimulatory action on cells collected from LF. No effect of PCB 126 and statistically significant decrease in estradiol secretion by cells collected from SF under the influence of PCB153 was observed. The inhibitory effect of PCB 153 was reversed when the culture was supplemented with testosterone. The opposite effect of both tested congeners on estradiol secretion in both basal and testosterone supplemented culture was seen in LF. PCB 126 increased it while PCB 153 decreased both, the basal and testosterone-stimulated estradiol secretion. In conclusion, the presented results suggest that the effect of both PCBs on steroid secretion observed in an early stage of the follicular phase of the estrus cycle is due to the inhibition of cholesterol mobilisation and thus insufficient substrate availability for hormone synthesis. On the contrary, in large preovulatory follicles inhibition of testosterone secretion is due to their action on 17-beta-HSD while stimulatory or inhibitory action on estradiol secretion is the result of their action on P450 aromatase activity.

Animals↗

Circadian rhythm of plasma testosterone in men with idiopathic hypogonadotrophic hypogonadism before and during pulsatile administration of gonadotrophin-releasing hormone.

OBJECTIVE: The aim was to investigate whether a pulsatile discharge of LH from the pituitary is necessary to achieve the circadian secretion of testosterone. DESIGN: The daily rhythm of the androgen has been studied in patients with idiopathic hypogonadotrophic hypogonadism (IHH) both in the absence of therapy and during pulsatile administration of gonadotrophin releasing hormone (GnRH). PATIENTS: Six patients with IHH and ten normal subjects were analysed. Blood sampling was performed at 2-hourly intervals, for 24 hours. The IHH patients then received synthetic GnRH i.v. at the rate of one pulse every 2 hours (10 micrograms/pulse). On day 11 of treatment, blood samples were taken for the rhythm analysis every 2 hours, for 24 hours. MEASUREMENTS: Plasma testosterone and LH were measured in the individual samples by radioimmunoassay. Evaluation of the rhythm was performed by cosinor analysis. RESULTS: A significant circadian rhythm of plasma testosterone was statistically validated in the normal subjects, whereas no rhythm was detected in the IHH patients in the absence of therapy. On day 11 of GnRH pulsatile administration the IHH patients showed normal testosterone levels and a statistically significant circadian rhythm of the androgen was evident, with acrophase between 0700 and 0800 h. Moreover, the amplitude, acrophase and mesor of testosterone rhythm in IHH patients in the course of treatment were statistically indistinguishable from the corresponding values in the normal subjects. Plasma LH did not show statistically significant circadian variations, either in the control group or in the IHH patients before or during therapy. CONCLUSIONS: We conclude that a physiological circadian rhythm of plasma testosterone can be obtained, in IHH men, by treatment with GnRH. Since the pulsatile administration of exogenous GnRH at constant doses induced a circadian rhythm in testosterone and no daily variations in LH were evident, we suggest that, although a pulsatile secretion of LH is probably necessary for the synchronization of the circadian rhythm with acrophase in the morning, the testosterone variations might be the results of a local testicular modulation of LH action.

Adult↗

The effect of oxytocin and vasotocin upon progesterone, testosterone and estradiol 17 beta-secretion by the luteal cells from cyclic pigs.

Porcine luteal cells were obtained from the corpora lutea on the 13th day of the estrous cycle. The cells were digested with 0.25% trypsin and suspended in the Medium 199 with an addition of 10% calf serum, at a concentration of 5 X 10(4) cells/ml. The cells were incubated with or without 4 and 40 mi.u./ml of oxytocin, 10 and 100 ng/ml of arginine-vasotocin, 1 microgram LH and 50 U/ml hCG. Levels of progesterone, testosterone and estradiol 17 beta were determined with the radioimmunological method, following 6 h incubation. It was found that progesterone secretion under the influence of oxytocine (4 mi.u./ml) was less than in the control group and in the group with LH. Similarly, arginine-vasotocin at a dose of 10 ng/ml inhibited progesterone secretion (P less than 0.05). Higher doses of these peptides had no suppressive effect on the luteal cells. Oxytocin and arginine-vasotocin had no influence on testosterone secretion by luteal cells. However, these cells produced less (P less than 0.05) estradiol 17 beta under the influence of oxytocine than of hCG. The results point to a direct effect of oxytocin and arginine-vasotocin on steroidogenesis in the corpora lutea of cyclic pigs.

Animals↗

In vitro exposure of porcine ovarian follicular cells to PCB 153 alters steroid secretion but not their viability--preliminary study.

In our previous paper, we demonstrated that porcine follicles collected during the early stage of development are the most sensitive to the toxic action of polychlorinated biphenyl 153 (PCB 153). Follicles of this type were collected to test the effect of PCB 153 on cell steroidogenesis and viability. Cocultures of granulosa and theca cells were grown in M199 medium at 37 degrees C. Control cultures were maintained in that medium alone, while experimental ones were supplemented with PCB 153 at doses of 5, 10, 50, and 100 ng/ml. After 48, 96, and 144 h, media were collected for steroid analysis and cell viability was measured using an LDH (lactate dehydrogenase activity) cytotoxicity test. A 2-day exposure of follicular cells to all the investigated doses of PCB 153 caused a statistically significant decrease in progesterone (P4) secretion, while in doses of 50 and 100 ng/ml there was also a decrease in testosterone (T) secretion. No effect on estradiol (E2) secretion was observed. The observed decrease in P4 and T secretion, and lack of any statistically significant effect on E2 secretion by cells from small follicles exposed for 48 h to PCB, suggests that PCB 153 acts before P4 formation. Longer exposures caused an increase in P4 secretion, with a concomitant drastic decrease in T secretion and a tendency to decrease the E2 secretion, suggesting inhibition of P450 17 alpha hydroxysteroid dehydrogenase, an enzyme that converts P4 to T. The observed PCB 153-induced increase in P4 secretion by cells collected from small antral follicles, with a concomitant decrease in E2 secretion, accounts for the induction of luteinization and, in this case, inhibition of aromatization process in the follicles. However, in all doses tested and at all times of exposure, PCB 153 had no effect on cell viability. These findings suggest different time of exposure-dependent action of PCB 153 on particular steps of steroidogenesis but not action on cell viability. These results should be considered preliminary, pending confirmation by other studies.

Animals↗

Quantitative maintenance of spermatogenesis in cyclosporine-treated rats by exogenous administration of testosterone propionate.

The authors had previously shown that the subcutaneous administration of cyclosporine (CsA) resulted in an impairment of spermatogenesis. Testosterone levels declined and gonadotropin levels increased, suggesting that CsA primarily affects the synthesis and secretion of testosterone. In this study, the authors attempted to determine whether the exogenous administration of testosterone would maintain spermatogenesis in animals treated with a very high dose of CsA. Sexually mature, male Sprague-Dawley rats were treated subcutaneously with CsA (40 mg/kg per day) alone, or in combination with testosterone propionate (TP; 2 and 5 mg/d per rat), for 14 days. As expected, CsA reduced the body and reproductive organ weights and the levels of serum testosterone, while elevating the levels of follicles-stimulating hormone (FSH) and luteinizing hormone (LH). Quantitative analysis of spermatogenesis revealed a decline in all the different types of germ cells in tubules at stage VII of the cycle of the seminiferous epithelium. Administration of TP in 2 and 5 mg/d per rat doses restored the body and reproductive organ weights and the circulating levels of FSH. The serum levels of LH were below the assay's minimum level of detectability. Analysis of spermatogenesis revealed a dose-dependent increase in the germ cell counts after the administration of 2 and 5 mg of TP. The circulating levels of CsA were also significantly reduced after TP administration. These results revealed that CsA-induced alteration in spermatogenesis can be prevented by the exogenous administration of testosterone.

Animals↗

Estradiol augments while tamoxifen inhibits rat mast cell secretion.

Mast cells have been studied extensively for their involvement in allergic reactions, where they secrete numerous powerful mediators in response to immunoglobulin E and specific antigens. However, they are also triggered by neuropeptides, they have been found in close contact with neurons, and they are activated in diseases such as angioedema, interstitial cystitis and irritable bowel disease, the prevalence of which is much higher in women. When tested on purified rat peritoneal mast cells, 17 beta-estradiol augmented secretion of histamine and serotonin, starting at 1 microM and in a dose-dependent manner, whether stimulated by the mast cell secretagogue compound 48/80 or the neuropeptide substance P. However, 17 beta-estradiol did not augment mast cell secretion stimulated by immunoglobulin E and specific antiserum indicating that immunologic stimulation is under different regulation. Testosterone inhibited secretion induced by compound 48/80. Tamoxifen, an estrogen receptor antagonist used in the treatment of breast cancer, inhibited serotonin and histamine release from purified rat peritoneal mast cells triggered by compound 48/80 or substance P. Tamoxifen also inhibited the increase in intracellular free Ca2+ originating from an influx of extracellular Ca2+ in response to compound 48/80. Moreover, tamoxifen antagonized the synergistic effect of phorbol myristate and the cation ionophore A23187 on mast cell secretion, suggesting that tamoxifen's inhibition may be due to regulation of protein kinase C activity. Tamoxifen may, therefore, have a beneficial effect in other neuroimmunoendocrine disorders both through estrogen receptor blockade and inhibition of mast cell secretion.

Animals↗

Effects of chronic bromocriptine-induced hypoprolactinemia on plasma testosterone responses to human chorionic gonadotropin stimulation in normal men.

To study the role played by normal levels of plasma prolactin (PRL) in the secretion of testosterone (T) in the testes, we induced hypoprolactinemia with a daily dose of 5 mg bromocriptine administered orally in five normal men 20 to 35 years of age for 8 weeks. The basal PRL, T, luteinizing hormone, follicle-stimulating hormone, and maximum responses of plasma T to human chorionic gonadotropin (hCG) stimulation were measured every 2 weeks. Basal levels of plasma T were reduced in the 1st 2-week-long period of hypoprolactinemia. In the 4-week-long period of hypoprolactinemia, the maximal response of plasma T to hCG stimulation was significantly reduced. The findings suggest that normal levels of plasma PRL may play an important role in the secretion of T in the human testes in vivo.

Adult↗