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PubMed1994

Testes size and testosterone levels in a model for weightlessness.

The purpose of this study was to test whether the lack of testicular growth found in suspended rats would affect testosterone production in a way that might have consequences on muscle atrophy and function studies. Body and testes weight, food consumption, and testosterone levels in testes and plasma were measured at the beginning of the experiment and after 1, 3 or 8 weeks of suspension. Suspended animals ate more but gained less weight than their pair-fed controls. Testes testosterone concentration (microgram/g tissue) was increased at 3 and 8 weeks, but total tissue testosterone (microgram/testes) was not. Up to 3 weeks of suspension, tissue concentration was dependent on testes size and independent of treatment. Plasma testosterone was increased only after 8 weeks of suspension. At 8 weeks, plasma levels correlated with total testes testosterone. Our results show that use of the Morey-Holton rat tail-suspension model up to 3 weeks did not induce testosterone changes of consequence to a skeletal muscle study. For long term studies consideration should be given to possible hormonal effects as tissue and plasma testosterone levels increase after 8 weeks of suspension.

Animals↗

PubMed1982

Effect of testosterone on the rate of myofibrillar protein breakdown in castrated and adrenalectomized male rats measured by the urinary excretion of 3-methylhistidine.

Urinary output in N tau-methylhistidine (3-MeHis) was used to evaluate changes in myofibrillar protein breakdown rate in the skeletal muscles of castrated and adrenalectomized-castrated young male rats, and the response of breakdown to testosterone and corticosterone replacement. The castrated rats grew less well than intact control rats and excreted significantly less 3-MeHis. Administration of low and high doses of testosterone restored the weight of the levator ani of the castrated animals but failed to affect growth rate or 3-MeHis output. Although this might suggest that testosterone has an indirect effect on muscle turnover through changes in growth rate, this parallelism was not confirmed by studies on adrenalectomized-castrated rats. Adrenalectomy of castrated rats caused a further reduction in growth rate and in output of 3-MeHis, but administration of testosterone now reduced 3-MeHis output still further while stimulating growth. Treatment of the adrenalectomized-castrated rats with low doses of corticosterone increased growth modestly, while depressing 3-MeHis output, and again output of this metabolite was further reduced when testosterone was added to the treatment, although growth rate was unaffected. Finally, large doses of testosterone given to adrenalectomized-castrated rats receiving excessive amounts of corticosterone did not prevent the growth failure or the increased output of 3-MeHis due to the corticosteroid, though it appeared to reduce the magnitude of the response to corticosterone alone. It is concluded that the effects of testosterone on growth and on 3-MeHis output are not necessarily associated and that the functional status of the adrenal cortex modifies the response of myofibrillar breakdown rate to testosterone treatment.

Adrenalectomy↗

PubMed1989

Plasminogen activator inhibitor in plasma is related to testosterone in men.

Low plasma testosterone and high levels of the rapid inhibitor of plasminogen activator (PA-I) have been proposed as risk factors for myocardial infarction. In this study, the relationship between testosterone and PA-I activity levels in middle-aged men without thrombotic antecedent was investigated. In 54 normogonadic men (testosterone, 7.3 to 29.1 nmol/L), PA-I was related positively to body mass index (BMI) and triglycerides and negatively to testosterone. When these variables were controlled, the relation between PA-I and testosterone remained significant (P less than .01). In the 41 normogonadic men with BMI less than 25, testosterone was the only variable to influence PA-I. Fibrinolytic activity was evaluated by the euglobulin lysis plate method and the specific measurement of functional tissue plasminogen activator. The basal fibrinolytic activity and the response to venous occlusion were essentially controlled by PA-I but were not significantly related to testosterone. In 17 men with severe hypogonadotrophinic hypogonadism (testosterone less than 3 nmol/L), PA-I was significantly increased (18.5 +/- 1.8 AU/mL, mean +/- SE) compared with 9.5 +/- 0.8 AU/mL in 41 normogonadic men of normal weight (P less than .001). However, 14 hypogonadic men had a hypertriglyceridemia or a BMI greater than 25, which could explain high PA-I levels. This study shows that the level of the inhibitor of plasminogen activator is partly dependent on hormonal status in men and provides a link between independently established epidemiologic data.

Adult↗

PubMed1979

Effects of sustained-release testosterone on marking behavior in the Mongolian gerbil.

Utilizing subcutaneous silastic implants containing testosterone the effect of sustained low-level release of testosterone on marking behavior in castrated Mongolian gerbils was determined. Castration resulted in a decrease in marking frequency from 38 +/- 4 to 4 +/- 1. Sustained release of 6 micrograms testosterone per day from implants did not stimulate marking behavior. Daily release of 11 micrograms increased marking 550% after one week. Release of 17 micrograms per day was required to restore marking to intact levels. Similar release rates of cholesterol did not increase marking. Release rates which increased marking in males did not increase marking in females. The minimum effective sustained-release dose of testosterone necessary to stimulate marking in females was five times greater than that in males. This difference is not due to a sex difference in plasma testosterone removal rates, since the circulating half-life of 3H-testosterone measured by testosterone-specific radioassay was not different in castrated males (72 +/- 5 min) and females (66 +/- 4 min). The present data are consistent with the hypothesis that there is a sexual dimorphism in the testosterone responsiveness of the neural substrate regulating territorial marking behavior.

Animals↗

PubMed1985

Individual marking activities not reflected by respective testosterone levels in male gerbils.

The hormonal regulation of scent marking behavior in the male Mongolian gerbil was studied. Experiment 1 investigated the developmental patterns of testosterone concentration and scent marking. Concurrent serum samples were repeatedly obtained, by venipuncture, from the same individuals that were used for behavior testing. Experiment 2 studied the relationship between testosterone and marking behavior in individual males before and during castration and after testosterone replacement. Repeated blood sampling did not influence body weight and marking activity as compared to the controls. Despite a high correlation between weekly mean measures of testosterone and marking activity during development no such correlation was observed on the individual level. That means that individual testosterone concentrations did not reflect individual differences in marking activity. After castration scent marking activities decreased. Testosterone treatment restored marking activities to the individual maximum levels observed during puberty; however, even high doses of testosterone did not equalize individually different marking activities. It is suggested that the individual levels of behavioral activity are fixed during perinatal development, possibly through the action of testosterone or its metabolites.

Animals↗

PubMed1986

Testosterone removal in rats results in a decrease in social aggression and a loss of social dominance.

Alpha male rats from mixed sex colony groups were tested for aggressiveness toward nonaggressive male intruders. Afterward, they were castrated and implanted with testosterone filled Silastic tubes, castrated and implanted with empty tubes, or sham castrated and implanted with empty tubes. There were significant declines in the aggressiveness (lateral attacks, bites, and piloerection but not on-top) of castrated rats without testosterone replacement but not in castrated rats with testosterone replacement. At a second operation, castrated animals had their testosterone capsules removed or had their empty capsules replaced with testosterone filled capsules. When tested for aggression toward nonaggressive intruders, those alpha males which had testosterone removed declined in aggressiveness while those which had it implanted returned to a level of aggressiveness close to that emitted by sham castrated control animals. Subordinate males became dominant when alpha males were castrated and not given testosterone replacement. In a final series of observations, sham castrated males were found to be more aggressive than castrated males when pitted against one another. It is argued that testosterone plays a primary role in intermale social aggression and that the decline in aggressiveness following castration is typically accompanied by a loss of social dominance.

Aggression↗

PubMed1992

Interaction of estradiol, testosterone, and progesterone in the modulation of hormone-dependent aggression in the female rat.

Female rats that had become aggressive as a result of cohabiting with a sterile male were ovariectomized and implanted with Silastic tubes of estradiol, testosterone, and progesterone, estradiol and testosterone alone, or with empty tubes. The implants were designed to model serum concentrations present during the last week of pregnancy (estradiol, 0.06 ng/ml; testosterone, 2.6 ng/ml; progesterone, 70 ng/ml). Following a test of aggression 1 week postoperatively, estradiol and testosterone implants were replaced with ones designed to maintain the lower hormone levels present following parturition (0.02 ng/ml; 0.6 ng/ml, respectively). Progesterone was not replaced. At the first aggression test, females with estradiol and testosterone alone displayed significantly more aggression than females with these hormones plus progesterone. Both groups were more aggressive than females without hormone replacement. Following the exchange of large implants for small ones, females that previously had progesterone increased in aggression while females that previously had only estradiol and testosterone decreased in aggression. Both groups continued to be more aggressive than the group without hormone replacement. High serum progesterone present near the end of pregnancy appears to moderate the expression of aggression supported by estradiol and testosterone. Conversely, progesterone's decline at parturition appears to produce a rebound facilitation of aggression even though serum estradiol and testosterone simultaneously decline.

Aggression↗

PubMed1996

Testosterone facilitates aggression by modulating vasopressin receptors in the hypothalamus.

In many species, testosterone treatment facilitates offensive aggression tested in resident-intruder models. As the mechanisms of action of testosterone remain unclear, we hypothesized that testosterone interacts with neurotransmitter systems involved in the regulation of offensive aggression. We tested this hypothesis with the vasopressinergic system in golden hamsters in three separate experiments. First, we compared the density of V1 vasopressin (VAP) receptor binding between castrated animals treated with testosterone and their untreated controls. The most noticeable difference was found within the ventrolateral hypothalamus (VLH), a site involved in the control of aggression in several species of mammals. Within this area, V1 AVP receptor binding disappeared after castration, while being maintained by testosterone-treatment. Second, we tested behavioral effects of AVP within the VLH. Microinjections of AVP (100 nl, 1 or 100 microM) within the VLH accelerated the onset of offensive aggression in testosterone-treated animals. However, AVP-injected animals did not bite more than their vehicle-injected controls. Third, microinjections of AVP failed to activate offensive aggression in animals deprived of testosterone. As AVP receptors appeared to overlay previously described distributions of androgen and estrogen receptors in golden hamsters, we propose that testosterone facilitates the onset of offensive aggression, at least partly, through an activation of AVP receptors within the VLH.

Aggression↗

PubMed1977

Diurnal variations of serum testosterone levels in intact and gonadectomized male and female rhesus monkeys.

A radioimmunoassay for serum testosterone which does not require chromatographic separation was used to measure the diurnal variations in intact and orchidecomized males and intact and ovariectomized females. The intact male rhesus monkey shows a distinctive diurnal variation in serum levels of testosterone characterized by lower values during the day and a marked increase in the early evening (1900-2200 hr). The testosterone levels remain high throughout most of the lights-off period in the intact male. In contrast to the intact male, the markedly lowered serum levels of testosterone in the orchidectomized male were higher during the day and consistently showed a nadir during the early evening (2000-2200 hr). The evening nadir of testosterone levels was 51.0% lower than the 24-hr mean whereas the maximum serum level was 46.4% higher. A similar circadian pattern of testosterone was seen in both the intact and ovariectomized females. The testosterone values were higher during the day and consistently showed a nadir during the early evening. These results suggest that the adrenal secretion of testosterone varies in a diurnal pattern characterized by an early evening nadir. This adrenal pattern is overshadowed by a much larger gonadal rhythm in the intact male.

Animals↗

PubMed1977

Testosterone synthesis in vitro by the fetal testis of the guinea pig.

Synthesis and secretion of testosterone by testes of guinea pig fetuses were studied in organ culture. The amount of testosterone secreted into the culture medium was estimated by radio-immunoassay. It was demonstrated that testosterone was already secreted by testes explanted at 25 days. The amount of testosterone secreted during the first day in culture by testes from fetuses of different ages (25-30 days) increased with fetal age. The amount of testosterone extracted from fetal guinea pig testes at ages used for explantation (25-30 days) were much lower than the amount secreted during the first 24 hours in culture. During subsequent days in culture, an increase in the amount of testosterone secreted was observed only for testes explanted at 25 days. The amount secreted by testes from older fetuses (26-30 days) stayed constant or decreased. Aminogluthetimide phosphate (100 micron) decreased significantly testosterone secretion by testes explanted at 25 days. These findings indicate that the capacity for biosynthesis of testosterone is present in fetal guinea pig testes at 25 days and increases during the subsequent days.

Aminoglutethimide↗

PubMed1989

Non-polar extracts of serum from males contain covert radioimmunoassayable testosterone.

Non-polar extracts of sera from human males contain immunoreactive testosterone in a form that is released by mild alkaline hydrolysis. The non-polar derivative shows no immunoreactivity with testosterone antibody prior to hydrolysis. Hydrolyzed non-polar serum extracts from ten adult male volunteers contained 2.0 +/- 0.8 (SD) ng/mL of testosterone. Neither non-polar serum extracts of normal females nor a water blank substituted for non-polar extract of serum yields any immunoreactive testosterone after alkaline hydrolysis. Testosterone palmitate hydrolyzed alone or after addition to non-polar extract of serum yields the expected quantities of radioimmunoassayable testosterone. Previously described conjugates of testosterone are polar and are neither extractable by petroleum ether nor hydrolyzable by alkali. These observations suggest that fatty acid esters of testosterone may be present in serum of human males.

Adult↗

PubMed1979

Testosterone metabolism by the prostate of the aging canine.

Examination of testosterone metabolism in the dorsal, lateral, and ventral regions of the beagle prostate showed an absence of regional heterogeneity for testosterone metabolite production and metabolic capacity. Testosterone metabolism by the hyperplastic prostate of aged beagles (11.1 years old) was distinguished from that of young mature (2.5-year-old) and mature adult (4.5-year-old) beagle prostate by increased reductive metabolism. The change was principally the consequence of increased production of 5 alpha-dihydrotestosterone and decreased production of 4-androstenedione. These alterations in testosterone metabolism occurred progressively and may be weakly linked to other changes in canine prostate which occur during aging. 5 alpha-Androstane-3 alpha, 17 beta-diol production was maximal for prostate from 4.5-year-old beagles and the amount of this metabolite produced appeared to be unrelated to prostate size. Co-incubation of prostate from any of the beagles with testosterone and estradiol showed that estradiol had no in vitro effect upon testosterone metabolism. Mean plasma testosterone content of aged beagles (11.1 years old) was not significantly different from that of younger individuals; however, the heterogeneity of the values for the subject groups was notable. The data demonstrate that the consequences of aging upon testosterone metabolism by canine prostate, which principally develops benign prostatic hyperplasia, are opposite to those characteristic of senescent rat prostate, which does not develop bening prostatic hyperplasia and has a high incidence of spontaneous adenocarcinoma.

Aging↗

PubMed1994

Relationship between diurnal rhythm of serum testosterone and two prostatic markers (PSA and PAP) in untreated prostate cancer.

OBJECTIVE: To clarify the relation between diurnal rhythm of serum levels of testosterone and two prostatic markers, prostate-specific antigen (PSA) and prostatic acid phosphatase (PAP). METHODS: Blood was obtained every four hours during a thirty-two-hour period from fourteen men with untreated prostate cancer. RESULTS: Serum levels of PSA and PAP showed circadian rhythm in 4 and 5 patients, respectively. About half of the remaining patients, the highest or nearly highest peaks of serum levels of PSA or PAP were observed in the afternoon rather than the morning. In 3 patients, circadian rhythms were not observed in serum levels of PAP, but the fluctuation patterns were the same as those of testosterone and showed synchronous movement. In 7 patients, serum testosterone levels were followed by the same fluctuation pattern for either PSA or PAP after some time delay. Little change in serum levels of PSA was seen throughout the thirty-two-hour period despite large fluctuations of testosterone and PAP levels in 5 patients. CONCLUSIONS: Close relation between the fluctuation in serum levels of PSA and PAP, and that in serum levels of testosterone during diurnal periods could be considered. However, the relationship between serum testosterone levels and those of PSA and PAP was ambiguous because of both the difference in the time delay of PSA and PAP in relation to testosterone and the small fluctuation in PSA despite obvious fluctuations in testosterone and PAP in some cases.

Acid Phosphatase↗

PubMed1982

Catecholamine stimulation of testosterone production via cyclic AMP in mouse Leydig cells in monolayer culture.

The effects of the beta-adrenergic hormone agonist, isoproterenol, on testosterone and cyclic AMP production in mouse Leydig cells in culture have been investigated. It was found that isoproterenol increased testosterone production on days 1, 2 and 3 of culture but not in freshly cultured cells. Cyclic AMP production was however increased on all days of culture. In subsequent studies carried out on day 2 of culture the amounts of testosterone formed during incubation with isoproterenol were 20-90% of those obtained with maximum stimulating levels of luteinizing hormone. The amounts of cyclic AMP formed were extremely low compared with those obtained with luteinizing hormone (22 +/- 5.3 and 2320 +/- 100 pmoles/10(6) cells/2 h respectively). Isoproterenol (10(-8) -10(-7) M) gave a significant increase in testosterone production and reached a maximum with 10(-6) M. Similar dose-response curves for cyclic AMP production were obtained. The stimulation of cyclic AMP and testosterone by isoproterenol was highly dependent on the presence of the phosphodiesterase inhibitor, methylisobutylxanthine. Propranolol blocked, in a dose-dependent manner, both isoproterenol-stimulated cyclic AMP and testosterone production. In the presence of excess luteinizing hormone no additional effects of isoproterenol were detected. Epinephrine also stimulated testosterone production. It is concluded that catecholamines stimulate testosterone production in mouse Leydig cells in monolayer culture and that this effect if mediated by cyclic AMP.

1-Methyl-3-isobutylxanthine↗

PubMed1983

Effect of prolactin, testosterone and estrogen on prolactin binding in the rat testis, prostate, seminal vesicle and liver.

We have studied the hormonal control of prolactin (PRL) binding in the male rat sex glands and liver, subsequent to the recent demonstration and characterization of specific PRL binding sites in rat testis, prostate and seminal vesicle. Ovine PRL (200 micrograms/rat/day, 7 days) caused a time-dependent reduction in testicular binding of 125I-labelled PRL (measured 2 days after last injection) to 58% of control. Testosterone alone (1 mg/rat/day, 7 days) or PRL caused similar reductions in binding, while their coadministration further lowered PRL binding to 10% of control. The synergism of PRL and testosterone suggests that either these doses are submaximal, or that they are acting on different systems. Estradiol was administered as a single dose of 2 mg/rat and the PRL binding determined on day 10 and day 19 was reduced to 37% of control, as after testosterone. Addition of PRL whether from day 1 to day 7 or from day 11 to day 17 of estradiol injection had no effect, suggesting that the EB site of action is closer to the PRL receptor than that for PRL or testosterone. Estradiol resulted in a 72% reduction of PRL binding in the prostate, after 10 days, which subsequent PRL completely restored. PRL also partially restored the estradiol-induced time-dependent weight reduction of the prostate, but PRL coadministered from day 1 of estradiol did not inhibit the estradiol effects, suggesting a competitive mechanism for the two. While testosterone more than doubled PRL binding in the seminal vesicle, estradiol reduced it by 32% and organ weight by 21%. PRL given after estradiol restored the weight loss, but not the binding, suggesting that two different mechanisms of action are involved. In the liver, coadministration of testosterone with PRL could not inhibit the induction by PRL of its own hepatic sites, in keeping with a more direct site of action for PRL than for testosterone. These results demonstrate the profound effects of PRL, and of the sex steroids testosterone and estrogen, on PRL binding in the male sex glands and liver. The physiological implication of these findings on the role of PRL in male sexual function is currently being investigated.

Animals↗

PubMed1983

Absence of gonadotropin-induced desensitization of testosterone production in the neonatal rat testis.

The formation of testosterone and some of its precursors (pregnenolone, progesterone, 17-hydroxyprogesterone and androstenedione) was studied in response to hCG stimulation in neonatal (5-day-old) and adult (60-day-old) male rats. Evidence for a biphasic testosterone response was observed at both ages, with a sharp increase within the first hours, and a secondary peak at 2-3 days after the hormone injection, when monitored by intratesticular and serum steroid measurements. The decreased testosterone production between the two peaks coincided in the adult animals with a marked increase of progesterone and 17-hydroxyprogesterone production, in keeping with the known gonadotropin-induced lesions of testicular androgen production. In contrast, no increase in C21-form testosterone precursors could be observed in the neonatal rat. When in vitro testicular production of cAMP, testosterone and progesterone was studied at the two ages 24 h after the hCG injection, a decrease in extracellular cAMP and testosterone but an increase in progesterone was observed in the adult testis. In the neonate, cAMP production was decreased, but testosterone production stayed high, and progesterone production increased only marginally. The present results indicate that the adult-type steroidogenic lesions following in vivo hCG stimulation, resulting in decreased testosterone production and accumulation of C21 steroid precursors, are not operative during the fetal-neonatal growth phase of rat testis Leydig cells.

17-alpha-Hydroxyprogesterone↗

PubMed1992

Adult rat Leydig cell cultures: minimum requirements for maintenance of luteinizing hormone responsiveness and testosterone production.

The aim of this study was to establish the minimum conditions required to maintain adult rat Leydig cell testosterone production and luteinizing hormone (LH) responsiveness in short term culture, at a level similar to that observed in vivo, which could be used to study factors which may have a delayed or chronic effect on Leydig cell function. Percoll gradient-purified adult rat Leydig cells (5.0 x 10(4)/250 microliters) were cultured in Dulbecco's modified Eagle's medium/Ham's F12 (DMEM/F12) with 0.1% bovine serum albumin at 32 degrees C for up to 3 days, with daily medium changes. A combination of submaximal rat LH (0.1 ng/ml) and a maximal concentration of rat serum lipoproteins (0.5 mg/ml) maintained testosterone production at between 5 and 15 ng/10(6) cells/h; subsequent stimulation of the Leydig cells with a maximum dose of rat LH (8 ng/ml) over 24 h resulted in testosterone production of 75-240 ng/10(6) cells/h on all 3 days of culture. However, the addition of 0.1% fetal calf serum instead of rat lipoproteins could not maintain LH-stimulated testosterone production in the same culture period. In cultures containing submaximal LH and lipoproteins, levels of testosterone production and responses to maximal LH stimulation were constant over the culture period when expressed as either testosterone production per 10(6) cells plated, or testosterone production per microgram DNA recovered at end of incubation. Reduction of the oxygen tension from 19% to 5%, or to 1% did not significantly alter testosterone production by Leydig cells under these established conditions.(ABSTRACT TRUNCATED AT 250 WORDS)

Analysis of Variance↗

PubMed1996

Testosterone effects on the neuronal ultrastructure in the medial preoptic nucleus of male Japanese quail.

Dorsolateral neurons of the medial preoptic nucleus (POM) of male Japanese quail are sensitive to the plasma levels of testosterone: their volume and optical density in Nissl-stained sections increase in castrated birds treated with testosterone. The present study was performed on castrated male quail treated or not with Silastic implants filled with testosterone to describe the ultrastructural variations induced by testosterone in these neurons. Gonadally intact male birds were included as controls. The ultrastructure of neurons, taken from the dorsolateral portion of the POM, was dramatically affected by the endocrine manipulations. Quantitative evaluations demonstrated a significant decrease in castrated birds of the rough endoplasmic reticulum (RER), of free polyribosomes, of Golgi complexes, and of dense bodies; these changes paralleled the decrease in cell size. The cell size and the percentage of volume occupied by the intracellular organelles in castrated birds treated with testosterone were comparable to values observed in controls. These ultrastructural changes are similar to those observed in neuronal targets for other gonadal hormones, supporting the idea that testosterone stimulates the development of cytoplasmic structures involved in protein synthesis and secretion. In addition, exposure to testosterone affects the synaptic inputs to POM. These ultrastructural changes are presumably related to the physiological effects (e.g., activation of male sexual behavior) exerted by testosterone on this preoptic region.

Analysis of Variance↗