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PubMed1984

Metabolic effects of testosterone during prolonged physical exercise and fasting.

Previous studies have shown a decrease in plasma testosterone during prolonged physical exercise and 72 h fasting in rats. To determine whether this hormonal change has an influence upon energy metabolism, two experiments were carried out, in which the plasma levels of testosterone were elevated during prolonged physical exercise and fasting in male wistar rats. The effects of acute and chronic increases in the levels of circulating testosterone were studied, on the one hand after human chorionic gonadotropin (H.C.G.) injection, and on the other by prolonged testosterone perfusion with an osmotic minipump. Blood and tissue sampling were performed to evaluate blood glucose, alanine, and lactate, and tissue glycogen. The results in fed and rest control rats showed no changes in blood parameters under the effect of hypertestosteronemia but there was an increase in muscle glycogen after testosterone perfusion. In 72 h fasted rats both types of hypertestosteronemia were associated with a decrease in blood alanine and lactate ranging from 25% to 35%. Only testosterone perfusion was associated with higher concentrations of muscle glycogen. After 7 h of treadmill running, testosterone perfusion and H.C.G. injection induced a 35% decrease in blood alanine and a slight decrease in blood glucose, with no change in other parameters. Whereas an elevation in the level of testosterone can induce muscle glycogen compensation in the fed resting state, it cannot counteract the exhaustion of muscle glycogen during running.

Animals↗

PubMed1978

Serum testosterone and sexual activity and interest in men.

There is considerable interest in the relationship between testosterone and sexual behavior in men, but the few available data bearing on this issue are inconclusive. This study is an attempt to clarify the relationships among various components of sexuality and serum testosterone concentration through examination of these variables in a large homogenous group of men. Serum testosterone concentration was determined in two blood samples taken 1 week apart from 101 young adult men. Subjects reported their frequencies of various sexual activities and level of sexual interest. Testosterone concentrations in the two blood samples were highly correlated, indicating considerable intraindividual consistency. There was considerable variance among subjects in both mean testosterone and reported sexual activity. Testosterone concentration did not correlate with the sexual activity and interest variables. These results provide evidence that differences among men in circulating testosterone concentration within the normal range do not account for differences in sexual activity and interest. It is also unlikely that variations in sexual activity account for differences in testosterone concentration.

Adult↗

PubMed1999

Simulated weightlessness-induced attenuation of testosterone production may be responsible for bone loss.

This study examined the effects of simulated weightlessness on serum hormone levels and their relationship to bone mineral density (BMD). The tail-suspended (i.e., hindlimb suspended, HLS) rat model was used to simulate weightless conditions through hindlimb unloading to assess changes in hormonal profile and the associated bone loss. In the first study, 24 adult male rats were assigned to two groups with 12 rats being HLS for 12 d, and the remaining 12 rats serving as ground controls. On d 0, 6, and 12, blood samples were taken to estimate circulating hormone levels. HLS rats had significant reductions in testosterone, 1,25 (OH)2 vitamin D, and thyroxine levels by d 6 (p<0.01); their testosterone levels were almost undetectable by d 12 (p<0.001). Serum cortisol levels in these rats were elevated on d 6 (p<0.02), but returned to normal levels by d 12. No changes were observed with serum ionized calcium and other hormones examined, as well as the body weights, and weights of thymus, heart, and brain. In the second study, eight rats were ground controls, while an additional eight rats were HLS for 12 d before being removed from tail-suspension and maintained for a further 30 d. Blood samples were collected every 6th d for 42 d. This study showed that both serum thyroxine and 1,25(OH)2 vitamin D levels returned to normal levels soon after hind limb unweighting, while serum testosterone levels matched normal levels only after a further 3-4 wk. These studies showed a significant decrease of femur weights, but not weights of humeri in HLS rats suggesting that this is a specific effect on unloaded bones. On d 12 in both studies, a significant reduction in the lumbar spine (p<0.05) and the femoral neck (p<0.01) BMD appeared in HLS rats. This was confirmed in the second study, where HLS led to a significant decrease in BMD even extending to d 42. Previous studies have shown that space flight and tail-suspension lead to marked reductions in bone formation with little effect on bone resorption. Recently, we reported that androgen replacement can indeed prevent bone losses in this animal model. Therefore, it seems logical to propose that the significant decreases of serum testosterone observed in these tail-suspended animals are, at least in part, responsible for the losses of BMD seen in their affected weight-bearing bones (i.e., lumbar spine and the femur). Considering that 1. testosterone is anabolic to osteoblasts and also decreases the rate of bone turnover 2. serum testosterone levels are markedly suppressed in simulated weightlessness, and 3. testosterone replacement therapy prevented the bone loss in HLS rats, we propose that the testosterone deficiency in this animal model is related to their bone loss.

Animals↗

PubMed1995

Effect of testosterone replacement therapy on the somatotrope responsiveness to GHRH alone or combined with pyridostigmine and on sympathoadrenal activity in patients with hypogonadism.

There is evidence suggesting that androgens influence GH secretion in man. Our aim was to verify whether the GH releasable pool is preserved and influenced by testosterone replacement in male hypogonadism. To this goal, in eight male hypogonadal patients (HP, age 32.2 +/- 5.0 yr; Body Mass Index 23.9 +/- 1.1 kg/m2) before and after 3 months testosterone therapy, we studied the GH response to GHRH (1 microgram/kg iv) alone and combined with pyridostigmine (PD, 120 mg po), a cholinesterase inhibitor which likely inhibits hypothalamic somatostatin release allowing exploration of the maximal somatotrope secretory pool. Sixteen normal subjects (NS, age 30.1 +/- 3.5 yr; Body Mass Index 22.5 +/- 1.8 kg/m2) were studied as controls. The GH response to GHRH in HP was similar to that in NS (AUC, mean +/- SE: 1238 +/- 362 vs 1018 +/- 182 micrograms/L/h). PD potentiated to the same extent the GH response to GHRH in both groups (2092 +/- 807 and 2840 +/- 356 micrograms/L/h). After three month testosterone therapy, in HP the GH responses to GHRH alone (1352 +/- 612 micrograms/L/h) and combined with PD (1948 +/- 616 microgram/L/h) were unchanged. Also IGF-I levels in HP were similar to those in NS (222 +/- 42 vs 210.6 +/- 55.8 micrograms/L) and were unchanged during testosterone replacement (280 +/- 31 micrograms/L). As androgens have been reported to modulate sympathoadrenal activity in the rat, both before and during testosterone replacement, we also measured plasma catecholamine levels. Basal NE (p < 0.05) but not E levels were lower in HP than in NS; testosterone restored basal NE levels to normal without affecting basal E. delta absolute increase of NE and E (p < 0.05 and 0.01 vs baseline, respectively) after PD in HP were similar to those in NS and were unchanged during testosterone replacement. In conclusion, these results demonstrate that the GH releasable pool is preserved in male hypogonadism. As in this condition a reduction of spontaneous GH secretion has been reported, it could be due to neurosecretory dysfunction but not to pituitary impairment. Subtle alterations of sympathoadrenal activity seem to be present in male hypogonadism and reversed by testosterone replacement.

Adrenal Glands↗

PubMed2000

Pilot study of the transdermal application of testosterone gel to the penile skin for the treatment of hypogonadotropic men with erectile dysfunction.

Androgens influence important central and peripheral mechanisms of the erectile system. The relevance of a moderate decrease of serum testosterone level for erectile dysfunction (ED) has not been clarified so far. The aim of our study was to offer an easy transcutaneous method of androgen application. A previous study on the pharmacokinetic profile of the testosterone gel applied, showed marked elevation of the serum levels of testosterone. In our study, 46 hypogonadal patients with ED and total lack of vaginal penetration applied testosterone gel (4 mg/day; supplied by Azupharma, Germany) to the penile skin twice a day over 6-8 weeks, after a run-in period with placebo gel of 2 weeks. All patients showed decreased testosterone serum levels (<3 ng/ml) in at least two morning samples over a period of 3 weeks before treatment. Psychogenic etiology was excluded by a sexual psychologist. Patient age was 37-69 years (mean 53.5). Three patients (6.5%) responded to placebo in the run-in phase and were withdrawn from further treatment. Fifteen patients (32.6%) showed improved erection, allowing penetration and sexual intercourse. Twenty-eight patients (60.9%) did not respond to therapy. Local genital skin irritation was not observed. Elevation of peripheral testosterone was not correlated to a positive therapy response. A success-rate of 32.6% in this group of patients after exclusion of psychogenic patients and placebo-responders seems to justify further investigations. A medication period of 6-8 weeks is most probably too short to induce imaginable regenerative effects of testosterone on the erectile system. We therefore suggest that future double-blind and placebo-controlled studies should be designed for a minimum of 3 months. Testosterone gel may be a cost effective form of androgen administration.

Administration, Cutaneous↗

PubMed1997

Supraphysiologic levels of testosterone affect cancellous and cortical bone in the young female cynomolgus monkey.

The goal of this study was to evaluate the effects of chronically-elevated male levels of the potent androgen testosterone on the quality and quantity of both cancellous and cortical bone in a young (mean age 8.0 years), nonhuman female primate model (M. fascicularis). Thirteen intact female monkeys received continuous testosterone supplementation via subcutaneous implants over a 24-month period. A group of 16 untreated, intact, age-matched female monkeys served as controls. At sacrifice, the lumbar vertebrae and femora were recovered in order to analyze the bone mineral quality and quantity of cancellous and cortical bone, respectively, and compared to the control group. Mineralization profiles of the vertebrae and femora were obtained using the density fractionation technique. Chemical analysis of the three largest fractions retrieved by density fractionation was performed to evaluate differences in %Ca, %P, Ca/P ratio, and mineral content (%Ca + %PO4) between the control and experimental groups. In addition, unfractionated bone powder was examined by X-ray diffraction to identify any changes in crystal size. Coronal sections of vertebrae were analyzed for structural parameters using histomorphometry and image analysis. Cross sections taken at the midshaft diaphyseal femora were analyzed for structural macroscopic and intracortical parameters. A nonsignificant shift in the mineralization profile of the vertebrae was observed whereas there was a significant shift in the mineralization profile towards more dense bone in the treated femora as compared with controls (P < 0.05). There was no difference in terms of size/strain of the cortical or cancellous bone crystal as detected by X-ray diffraction. There was a trend towards an increase in cancellous bone area (B.Ar.) in the testosterone-treated vertebrae (P = 0.08) as compared with controls. The architecture of the cancellous bone remained nonsignificantly different between the treatment and control groups as evaluated by image analysis. There was a decrease in osteoid perimeter (P = 0.05) in the experimental group as compared with controls. There was a significant decrease in eroded perimeter measurements in the experimental group as compared with controls (P < 0.03). Although there was a trend towards an increase in cancellous bone area, mineralization was not significantly different in the vertebrae of testosterone-treated female monkeys, indicating that the newly-formed bone tissue became relatively normally mineralized over the two-year period. An increase in bone area, with indices of an overall decreased remodelling pattern as compared with controls, suggests that cancellous bone in the young, nonhuman female primate had been receptive to supraphysiologic levels of testosterone supplementation over the two-year period. There was a trend for an increase in cortical bone area and width with an increased periosteal perimeter in the testosterone-treated group as compare with controls. There was an increase in intracortical remodelling activity with a significant increase in percent porosity (P < 0.05), osteonal bone (P < 0.05), and mean wall width (P < 0.05) in the testosterone-treated group. In conclusion, the cancellous bone from female monkeys appeared to respond to the antiresorptive stimulus of male levels of testosterone with significantly diminished turnover parameters in this compartment. In contrast, the cortical bone compartment responded by displaying significant intracortical remodelling over a two-year period.

Animals↗

PubMed2006

Vehicle effects on the in vitro penetration of testosterone through equine skin.

The effects of three vehicles, phosphate-buffered saline (PBS), ethanol (50% in PBS w/w) and propylene glycol (50% in PBS w/w) on in vitro transdermal penetration of testosterone was investigated in the horse. Skin was harvested from the thorax of five Thoroughbred horses after euthanasia and stored at -20 degrees C until required. The skin was then defrosted and placed into Franz-type diffusion cells, which were maintained at approximately 32 degrees C by a water bath. Saturated solutions of testosterone, containing trace amounts of radiolabelled [14C]testosterone, in each vehicle were applied to the outer (stratum corneum) surface of each skin sample and aliquots of receptor fluid were collected at 0, 2, 4, 8, 16, 20, 22 and 24 h and analysed for testosterone by scintillation counting. The maximum flux (Jmax) of testosterone was significantly higher for all sites when testosterone was dissolved in a vehicle containing 50% ethanol or 50% propylene glycol, compared to PBS. In contrast, higher residues of testosterone were found remaining within the skin when PBS was used as a vehicle. This study shows that variability in clinical response to testosterone could be expected with formulation design.

Administration, Cutaneous↗

PubMed2006

Testosterone therapy for men at risk for or with history of prostate cancer.

Since the early 1940s when Huggins showed that severe reductions in serum testosterone by castration or estrogen therapy caused regression of prostate cancer (PCa), it has been assumed that higher testosterone levels cause enhanced growth of PCa. For this reason, it has been considered taboo to offer testosterone replacement therapy (TRT) to any man with a prior history of PCa, even if all objective evidence suggests he has been cured. The fear has been that higher testosterone levels would "awaken" dormant cells and cause a recurrence. Thus, US Food and Drug Administration-mandated language in all testosterone package inserts states that testosterone is contraindicated in men with a history of, or suspected of having, PCa. Although there is little modern experience with administration of testosterone in men with known history of PCa, there is a varied and extensive literature indicating that TRT does not pose any increased risk of PCa growth in men with or without prior treatment. For instance, the cancer rate in TRT trials is only approximately 1%, similar to detection rates in screening programs, yet biopsy-detectable PCa is found in one of seven hypogonadal men. Moreover, PCa is almost never seen in the peak testosterone years of the early 20s, despite autopsy evidence that men in this age group already harbor microfoci of PCa in substantial numbers. The growing number of PCa survivors who happen to be hypogonadal and request treatment has spurred a change in attitude toward this topic, with increasing numbers of physicians now offering TRT to men who appear cured of their disease. Publications have now reported no prostate-specific antigen (PSA) recurrence with TRT in small numbers of men who had undetectable PSA values after radical prostatectomy. Although still controversial, there appears to be little reason to withhold TRT from men with favorable outcomes after definitive treatment for PCa. Monitoring with PSA and digital rectal examination at regular intervals is recommended.

Androgens↗

PubMed1980

Total and free testosterone during pregnancy.

Total and free testosterone levels were measured throughout pregnancy and were compared with values found in nonpregnant women to determine whether the increase in plasma testosterone levels during pregnancy can be accounted for entirely by an increase in sex hormone-binding globulin or by an increase in testosterone production that would be reflected by an elevation in plasma free testosterone. The study employed a practical and precise method of determining free testosterone by means of equilibrium dialysis. Even though the testosterone level increased significantly throughout pregnancy, the free testosterone level remained within the range for nonpregnant women until week 28, after which time it was significantly elevated. This indicates that the increase in the total testosterone level before week 28 is due to a decrease in metabolic clearance rate, but after week 28 the production rate is increased. The source of this increase is unknown, but it might be fetal.

Female↗

PubMed1986

Acute modulation of the hypothalamic-pituitary axis by intravenous testosterone in normal women.

Intravenous testosterone was infused for 6 hours in 23 ovulatory women, divided into five groups according to dose, to assess the effects of testosterone on gonadotropin secretion. Serum testosterone increased from 0.24 +/- 0.08 to steady-state levels of 1.63 +/- 0.18 ng/ml in the lowest-dose group (1) and to 42.1 +/- 3.3 ng/ml in the highest-dose group (4). In another group (5), patients were pretreated with testolactone, which prevented the estradiol rise associated with testosterone infusion. All groups except group 1 exhibited significant reductions in the delta maximum responses of luteinizing hormone to gonadotropin-releasing hormone during testosterone infusion compared with pretreatment levels (p less than 0.01). This was also evident for the testolactone group (5). There were no observed changes in serum follicle-stimulating hormone. Luteinizing hormone pulse frequency was decreased (p less than 0.05) with testosterone concentrations of 27.2 +/- 0.77 and 42.1 +/- 3.3 ng/ml (groups 3 and 4), but only in the highest group (4) was there a decrease in pulse amplitude (p less than 0.05). No luteinizing hormone pulse changes were observed with lower concentrations of testosterone. Plasma immunoreactive gonadotropin-releasing hormone levels remained undetectable or low in some of the groups sampled. These data suggest that short-term infusions of testosterone inhibit hypothalamic-pituitary function of normal women when high doses are used, and this effect may be independent of aromatization to estrogen.

Adult↗

PubMed1988

Inhibition of steroid 5 alpha-reductase and its effects on testosterone hydroxylation by rat liver microsomal cytochrome P-450.

It has been shown previously that liver microsomal steroid 5 alpha-reductase activity increases with age in female but not male rats, which coincides with a female-specific, age-dependent decline in the cytochrome P-450-dependent oxidation of testosterone to 1 beta-, 2 alpha-, 2 beta-, 6 alpha-, 6 beta-, 7 alpha-, 15 beta-, 16 alpha-, 16 beta-, and 18-hydroxytestosterone and androstenedione. To determine whether the increase in steroid 5 alpha-reductase activity is responsible for the decrease in testosterone oxidation, we have examined the effects of the steroid 5 alpha-reductase inhibitor, 4-MA (17 beta-N,N-diethylcarbamoyl-4-methyl-4-aza-5 alpha-androstan-3-one), on the pathways of testosterone oxidation catalyzed by rat liver microsomes. We have also determined which hydroxytestosterone metabolites are substrates for steroid 5 alpha-reductase. At concentrations of 0.1 to 10 microM, 4-MA completely inhibited steroid 5 alpha-reductase activity without inhibiting the pathways of testosterone oxidation catalyzed by liver microsomes from rats of different age and sex, and from rats induced with phenobarbital or pregnenolone-16 alpha-carbonitrile. 4-MA (10 microM) had little or no effect on the oxidation of testosterone catalyzed by liver microsomes from mature male rats (which have low steroid 5 alpha-reductase activity). In contrast, the hydroxylated testosterone metabolites formed by liver microsomes from mature female rats (which have high steroid 5 alpha-reductase activity) accumulated to a much greater extent in the presence of 4-MA. Evidence is presented that 4-MA increases the accumulation of hydroxytestosterones by two mechanisms. First, 4-MA inhibited the 5 alpha-reduction of those metabolites (such as 6 beta-hydroxytestosterone) that were found to be excellent substrates for steroid 5 alpha-reductase. In the absence of 4-MA, these metabolites eventually disappeared from incubations containing liver microsomes from mature female rats. Second, 4-MA inhibited the formation of 5 alpha-dihydrotestosterone, which otherwise competed with testosterone for oxidation by cytochrome P-450. This second mechanism explains why 4-MA increased the accumulation of metabolites (such as 7 alpha-hydroxytestosterone) that were found to be poor substrates for steroid 5 alpha-reductase. Despite its marked effect on the accumulation of hydroxylated testosterone metabolites, 4-MA had no effect on their initial rate of formation by liver microsomes from either male or female rats.(ABSTRACT TRUNCATED AT 400 WORDS)

Androstanes↗

PubMed1990

Reconstitution of testosterone oxidation by purified rat cytochrome P450p (IIIA1).

Cytochrome P450p (IIIA1) has been purified from rat liver microsomes by several investigators, but in all cases the purified protein, in contrast to other P450 enzymes, has not been catalytically active when reconstituted with NADPH-cytochrome P450 reductase and dilauroylphosphatidylcholine. We now report the successful reconstitution of testosterone oxidation by cytochrome P450p, which was purified from liver microsomes from troleandomycin-treated rats. The rate of testosterone oxidation was greatest when purified cytochrome P450p (50 pmol/ml) was reconstituted with a fivefold molar excess of NADPH-cytochrome P450 reductase, an equimolar amount of cytochrome b5, 200 micrograms/ml of a chloroform/methanol extract of microsomal lipid (which could not be substituted with dilauroylphosphatidylcholine), and the nonionic detergent, Emulgen 911 (50 micrograms/ml). Testosterone oxidation by cytochrome P450p was optimal at 200 mM potassium phosphate, pH 7.25. In addition to their final concentration, the order of addition of these components was found to influence the catalytic activity of cytochrome P450p. Under these experimental conditions, purified cytochrome P450p converted testosterone to four major and four minor metabolites at an overall rate of 18 nmol/nmol P450p/min (which is comparable to the rate of testosterone oxidation catalyzed by other purified forms of rat liver cytochrome P450). The four major metabolites were 6 beta-hydroxytestosterone (51%), 2 beta-hydroxytestosterone (18%), 15 beta-hydroxytestosterone (11%) and 6-dehydrotestosterone (10%). The four minor metabolites were 18-hydroxytestosterone (3%), 1 beta-hydroxytestosterone (3%), 16 beta-hydroxytestosterone (2%), and androstenedione (2%). With the exception of 16 beta-hydroxytestosterone and androstenedione, the conversion of testosterone to each of these metabolites was inhibited greater than 85% when liver microsomes from various sources were incubated with rabbit polyclonal antibody against cytochrome P450p. This antibody, which recognized two electrophoretically distinct proteins in liver microsomes from troleandomycin-treated rats, did not inhibit testosterone oxidation by cytochromes P450a, P450b, P450h, or P450m. The catalytic turnover of microsomal cytochrome P450p was estimated from the increase in testosterone oxidation and the apparent increase in cytochrome P450 concentration following treatment of liver microsomes from troleandomycin- or erythromycin-induced rats with potassium ferricyanide (which dissociates the cytochrome P450p-inducer complex). Based on this estimate, the catalytic turnover values for purified, reconstituted cytochrome P450p were 4.2 to 4.6 times greater than the rate catalyzed by microsomal cytochrome P450p.

Animals↗

PubMed1987

Testosterone-induced responsiveness to androgen in Shionogi mouse carcinoma cells.

Primary cell cultures from an androgen-dependent mouse mammary carcinoma, the Shionogi-SC 115 tumor, were cultured in the presence or absence of testosterone (50 nM). Characteristic changes in cellular morphology and cell growth were observed according to the presence or absence of the androgen. In testosterone-containing medium, cells formed individual clones, piling up one over another and showed no contact inhibition, whereas in the absence of the androgen, cells had a flattened morphology, they grew in a monolayer and cell multiplication was reduced. The testosterone-dependent changes were observed in culture as long as cells were maintained in androgen-containing medium. Only a few (3-5) days of culture in the absence of testosterone rendered cells irreversibly unresponsive to the androgen, and they could no longer produce tumours after inoculation in the host animal. Cellular proteins were analysed after culture in the presence or absence of testosterone. After [35S]methionine labelling of cells and SDS-PAGE of the cytosol, several proteins were specifically synthesized in the presence of testosterone, predominantly a 45 kD protein, which was not seen in the absence of the androgen. Conversely, a protein of 35 kD present in absence of the hormone disappeared in the presence of testosterone. The anti-androgen cyproterone acetate inhibited the characteristic cellular morphology, cell proliferation and protein synthesis observed in the presence of the the androgen. The antiprogestin and anti-glucocorticosteroid RU 486 also showed limited anti-androgen activity. The concentration of specific androgen receptor-binding sites did not change significantly after 3 months of culture with or without testosterone, i.e., in responsive and unresponsive cells.

Androgen Antagonists↗

PubMed1985

Taenia taeniaeformis: inhibition of rat testosterone production by excretory-secretory product of the cultured metacestode.

In 3- to 5-month-old male Sprague-Dawley rats infected with the hepatic metacestode, Taenia taeniaeformis, the serum testosterone level was significantly lower than in comparable uninfected controls. By transmission electron microscopy, testicular Leydig cells of infected rats had less smooth endoplasmic reticulum than control Leydig cells. Cultured metacestodes isolated from the hepatic cysts secreted or excreted substances into the incubation medium. The effect of the excretory-secretory product on testosterone concentration in the sera and testes of 15-day-old rats was examined. Subcutaneous injection of 50-200 micrograms of excretory-secretory product/0.1 ml saline/rat for 2 days significantly reduced human chorionic gonadotropin-stimulated serum and testicular testosterone concentrations. Furthermore, the effect of the excretory-secretory product on isolated rat Leydig cell testosterone production was examined. Rat Leydig cells produced testosterone in vitro and, in the presence of 50 IU human chorionic gonadotropin/ml incubation medium, they responded with approximately 100% increase in testosterone production. Addition of 2-10 micrograms excretory-secretory product protein/ml of culture medium significantly reduced the testosterone production by rat Leydig cells in vitro. These results indicate that excretory-secretory product of cultured T. taeniaeformis metacestodes has a direct inhibitory effect on Leydig cell testosterone production under stimulation with human chorionic gonadotropin.

Animals↗

PubMed1989

Testosterone, and winning and losing in human competition.

Testosterone and cortisol were measured in six university tennis players across six matches during their varsity season. Testosterone rose just before most matches, and players with the highest prematch testosterone had the most positive improvement in mood before their matches. After matches, mean testosterone rose for winners relative to losers, especially for winners with very positive moods after their victories and who evaluated their own performance highly. Winners with rising testosterone had higher testosterone before their next match, in contrast to losers with falling testosterone, who had lower testosterone before their next match. Cortisol was not related to winning or losing, but it was related to seed (top players having low cortisol), and cortisol generally declined as the season progressed. These results are consistent with a biosocial theory of status.

Achievement↗

PubMed1991

Testosterone stimulates reproductive behavior during autumn in mockingbirds (Mimus polyglottos).

Mockingbirds normally secrete little or no testosterone during the period of autumnal territoriality. To determine the behavioral effects of exogenously administered testosterone, 20-mm lengths of Silastic tubing filled with crystalline testosterone were implanted into free-living resident mockingbirds during the autumn. Control residents were given sealed empty implants. Focal animal sampling showed that T-implanted males sang significantly more than controls. Perhaps as a consequence, a significantly greater percentage of the T-implanted males acquired mates. Though nest building does not naturally occur in autumn, T-implanted males also showed significantly more nest building than control males. However, T-implanted males only built if there was a female in the territory, suggesting a synergy between the presence of testosterone and social cues provided by the female. Examination of the effects of testosterone on territorial aggression showed that despite the high levels of territorial activity common in this species in autumn, territorial fights were unaffected by the presence of testosterone. One aggressive call, known to function in fall territorial defense, was significantly decreased in T-implanted versus control males. The presence of fall testosterone appears to stimulate a number of reproductive activities in mockingbirds, leaving autumnal aggressive interactions either unchanged or decreased. We discuss the application of these data to the effects of testosterone on the mockingbird's reproductive behavior during the breeding season.

Animals↗

PubMed1987

Androgen metabolism in the male hamster--1. Metabolism of testosterone in the pituitary gland and in the brain of animals exposed to different photoperiods.

It is known that the metabolism of testosterone in the brain and in the anterior pituitary is different in mammalian and in photoperiodic avian species. In many mammalian species, testosterone is mainly metabolized to 5-alpha-reduced compounds (e.g. 17-beta-hydroxy-5-alpha-androstan- 3-one, 5 alpha-DHT and 3-alpha,17-beta-dihydroxy-5-alpha-androstane, 5-alpha,3-alpha-diol) and, to a smaller extent, to 4-androstene-3,17-dione (androstenedione), while in birds, androstenedione is the main testosterone metabolite and the conversion to the 5-alpha-reduced compounds is quantitatively negligible. In avian species, testosterone is also converted to 5-beta-reduced steroids (mainly 17-beta-hydroxy-5-beta-androstan-3-one, 5-beta-DHT and 3-alpha,17-beta-dihydroxy-5-beta-androstane, 5-beta,3-alpha-diol), and there is also evidence that in these species testosterone metabolism in the central structures may be influenced by the photoperiod. Since the hamster is a mammal whose reproductive cycle is controlled by day length, it has been analyzed whether: (a) the central structures of the hamster (cerebral cortex, hypothalamus and anterior pituitary) metabolize testosterone in vitro following a mammalian (5-alpha-reduced derivatives) or an avian (androstenedione and 5-beta-reduced compounds) pattern; and (b) the metabolism of testosterone in the same structures may be modified by the exposure to different photoperiods (LD 14:10 or LD 8:16). The present data indicate that no one of the hamster structures examined produces the 5-beta-reduced derivatives. Moreover, the formation of the 5 alpha-DHT is quantitatively low, and is not affected by the photoperiod. In contrast, androstenedione is formed in quite high yields and the exposure of the animals to 60 days of short photostimulation increases the formation of this steroid in the pituitary gland, but not in the brain structures. From these data, it appears that the central structures of the hamster metabolize testosterone with a pattern which is intermediate between that of birds and mammals.

Androstenedione↗

PubMed1987

Testosterone stimulation of mitochondrial aspartate aminotransferase levels and biosynthesis in rat ventral prostate.

The effects of testosterone on mitochondrial aspartate aminotransferase (mAAT) synthesis in rat ventral prostate was investigated. Procedures for the isolation, purification and characterization of AAT isozymes were developed and described. Purified mAAT preparations contained no demonstrable contaminating proteins. Prostatic mAAT was characterized as a cationic protein with an estimated mol. wt of 120,000. Cytoplasmic AAT (cAAT) isozyme was identified as an anionic protein with an estimated mol. wt of 132,000. A cytosolic cationic isozyme, similar to mAAT, was also identified as pre-mAAT. Testosterone administration to castrated rats resulted in significant increases in leucine incorporation into mAAT, in the level of mAAT, and in mAAT activity. These effects of testosterone were observed within 2 h of administration. Conversely, testosterone administration had none of these effects on cAAT or on non-AAT protein pool. Testosterone treatment did appear to increase leucine incorporation into pre-mAAT. Testosterone treatment in organ cultures and in prostate epithelial cell cultures resulted in the same stimulatory effects on mAAT as observed in the in vivo studies. The hormone was effective at the physiological concentration of 2 X 10(-9) M. These results indicated that testosterone has a rapid and specific effect on the biosynthesis of mAAT. This continues to support our proposal that testosterone regulates prostate citrate production via a stimulatory effect on mAAT which results in increased mitochondrial synthesis of citrate from aspartate.

Animals↗