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PubMed1992

The short-term effect of testosterone on growth in boys on hemodialysis.

In view of a possible resistance to hormones as a cause of growth failure in renal insufficient children, a short-term study was performed to assess the effect of low-dose testosterone administration in boys with end-stage renal failure. Eight boys with a mean age of 11.4 +/- 1.2 years and a mean height deviation of -3.9 SD according to French standards received 50 mg/m2/day of a testosterone or placebo gel in a double-blind crossover fashion, each for a period of four weeks. Growth velocity was assessed by knemometry. The mean plasma testosterone levels rose from 0.16 +/- 0.06 ng/ml to 1.98 +/- 0.35 ng/ml during the testosterone treatment (p less than 0.01), whereas it remained low during the placebo treatment: 0.23 +/- 0.09 ng/ml versus 0.19 +/- 0.06 ng/ml before. The mean growth velocity rose from 0.27 +/- 0.07 mm/week during the control period to 0.50 +/- 0.03 mm/week during the testosterone treatment (p less than 0.05). Two groups of boys could be distinguished: the four boys of the first group whose initial growth velocity was below the mean growth velocity of a healthy control group, showed a significant improvements during the testosterone treatment (p less than 0.01). The growth velocity of the four boys of the second group whose initial growth velocity was normal did not improve during the testosterone treatment. These facts suggest that low dose testosterone can stimulate short-term growth of boys on regular hemodialysis when the basal growth velocity is low.

Administration, Cutaneous↗

PubMed2005

Influence of maternal testosterone on the strategies in the open field behaviour of rats.

OBJECTIVES: The purpose of the present study was to characterize the influence of testosterone administered to pregnant females on offsprings postnatal behavioral strategies in the open field. METHODS: The influence of maternal testosterone on behaviour of 23 day old male and female offsprings was studied in a 20-minute open field test. A total of 9 behavioural events were compared between a control (male n=12, female n=8) and a testosterone group (male n=9, female n=9). Dynamics and patterns of association of these behavioural events were analyzed. The testosterone group was prenatally exposed to testosterone (a single intramuscular injection of 2.5 mg testosteroni isobutyras on gestation day 14). RESULTS: Male offsprings exposed prenatally to testosterone displayed significantly high levels of ambulation (P<0.05), sniffing (P<0.01), sniffing the air (P<0.05), urination (P<0.05) and significantly lower level of vocalization (P<0.05) than control. Female offsprings exposed prenatally to testosterone displayed significantly higher level of sniffing the air (P<0.05) than control. Significant differences in the dynamics of habituation process were registered only in the group of male. They were from 5 to 10 min in ambulation (P<0.05), from 10 to 15 min in sniffing (P<0.05) and vocalization (P<0.05), from 10 to 15 min and from 15 to 20 min in sniffing the air (P<0.05) and from 0 to 5 min in defecation (P<0.05) and urination (P<0.01). CONCLUSION: Our results suggest that maternal testosterone may influence especially male postnatal open field strategies.

Animals↗

PubMed1991

In vitro effects of estradiol, diethylstilbestrol and tamoxifen on testosterone production by purified pig Leydig cells.

The direct effects of estradiol-17 beta (E2), diethylstilbestrol (DES) and tamoxifen on testicular testosterone production by purified immature pig Leydig cells in vitro were studied. Leydig cells were obtained from 3-4 weeks old piglet testes by enzymatical dispersion followed by discontinuous Percoll gradient centrifugation. Leydig cells were treated with E2, DES, and tamoxifen in the absence or presence of LH after 12 h of incubation. Media were collected 48 h later for testosterone and cAMP measurement. E2 did not affect basal testosterone production. When Leydig cells were incubated with increasing concentrations (0.001-10.0 micrograms/ml) of E2, DES, or tamoxifen for 48 h, LH-stimulated testosterone production was reduced. The degree of this reduction was dependent on E2, DES, and tamoxifen, and a concentration of E2 and DES and tamoxifen higher than 100 ng/ml and 10 ng/ml was needed, respectively. DES and tamoxifen also reduced LH-stimulated cAMP formation. When equal concentrations of DES and tamoxifen were added concomitantly to Leydig cells, the inhibition was additive, indicating that tamoxifen does not prevent the inhibitory effects of DES. Forskolin, an activator of adenylate cyclase, stimulated testosterone production to an extent comparable to that attained with LH, and DES and tamoxifen reduced forskolin-stimulated testosterone production. DES and tamoxifen suppressed the conversion of exogenous pregnenolone and progesterone to testosterone, but did not affect the conversion of 17 alpha-hydroxyprogesterone to testosterone, suggesting a specific inhibition of 17 alpha-hydroxylase. These results suggest that E2, DES, and tamoxifen directly inhibit immature pig Leydig cell steroidogenesis, at least in part via an inhibition of cAMP formation and a decrease in the activity of 17 alpha-hydroxylase.

17-alpha-Hydroxyprogesterone↗

PubMed2006

Subcutaneous administration of testosterone. A pilot study report.

OBJECTIVE: To investigate the effect of low doses of subcutaneous testosterone in hypogonadal men since the intramuscular route, which is the most widely used form of testosterone replacement therapy, is inconvenient to many patients. METHODS: All men with primary and secondary hypogonadism attending the reproductive endocrine clinic at Royal Victoria Hospital, Monteral, Quebec, Canada, were invited to participate in the study. Subjects were enrolled from January 2002 till December 2002. Patients were asked to self-administer weekly low doses of testosterone enanthate using 0.5 ml insulin syringe. RESULTS: A total of 22 patients were enrolled in the study. The mean trough was 14.48 +/- 3.14 nmol/L and peak total testosterone was 21.65 +/- 7.32 nmol/L. For the free testosterone the average trough was 59.94 +/- 20.60 pmol/L and the peak was 85.17 +/- 32.88 pmol/L. All of the patients delivered testosterone with ease and no local reactions were reported. CONCLUSION: Therapy with weekly subcutaneous testosterone produced serum levels that were within the normal range in 100% of patients for both peak and trough levels. This is the first report, which demonstrated the efficacy of delivering weekly testosterone using this cheap, safe, and less painful subcutaneous route.

Adolescent↗

PubMed1991

In vivo regulation of apolipoprotein A-I gene expression by estradiol and testosterone occurs by different mechanisms in inbred strains of mice.

We tested the hypothesis that testosterone and estrogen modulate apoA-I gene expression and metabolism by different mechanisms that may be influenced by genetic factors. Male and female C3H/HeJ (atherosclerosis-resistant) and C57BL/6J (atherosclerosis-susceptible) mice (n = 5/group) were castrated (Placebo). Castrates were given 17 beta-estradiol (E2) at 0.16 microgram/g (E2L) or 5 micrograms/g (E2H) body weight per day, or testosterone (Testo) 1 microgram/g per day, 14 days after surgery, for 14 days. Plasma total cholesterol concentrations (TC) were higher in male Placebo mice than in females. Testosterone altered TC and high density lipoprotein (HDL) cholesterol by gender and strain; however (HDL-C)/TC ratios and apoA-I concentrations were unaltered. Testosterone did reduce HDL particle diameters in both genders of C3H mice only. Low density lipoprotein-cholesterol (LDL-C)/TC ratios remained constant and apoB increased in males only. E2L and E2H decreased TC, HDL-C/TC ratios, and apoA-I. Decrements varied by strain. HDL diameters decreased in both genders in C3H mice only; however, HDL size distributions were altered in both strains. LDL-C/TC ratios increased in all groups. E2L mice showed variable responses of apoB, but apoB rose uniformly in all E2H groups. Testosterone increased and E2H decreased hepatic apoA-I synthesis. ApoA-I mRNA concentrations remained stable in both Testo and E2 groups. ApoA-I gene transcription varied by strain and gender, but all changes were less than twofold. Testosterone did not affect hepatic apoB or LDL receptor mRNA, however, E2H increased both mRNAs in males but not in females. On Western blotting of liver membranes, E2H had little effect on mouse LDL receptor protein mass; by contrast, E2H increased LDL receptor approximately threefold in rats. In summary, responsiveness of mouse lipids to testosterone and E2 vary by strain and gender. Testosterone and E2 differ in their regulation of apoA-I production mainly at the level of translation. Hormones operate at several levels of gene regulation, suggesting that complex mechanisms are involved. Mice differ from rats and rabbits in their LDL receptor responsiveness to estradiol treatment.

Animals↗

PubMed1991

[Inhibition of testosterone metabolism by 17-alpha-estradiol in rat liver slices].

Inhibition of the Testosterone Metabolism in Rat Liver Slices by 17 alpha-Estradiol. The influence of 17 alpha-estradiol (CAS 57-91-0), a hormonally almost inactive isomer of physiological 17 beta-estradiol, on the metabolism of [14C]-labeled testosterone in rat liver slices was investigated. The analysis of extracts from incubates (3.0 ml medium, 100 mg liver slices, 416 nmol [14C]-testosterone, 0.1-30 micrograms 17 alpha-estradiol, 37 degrees C, 30 min) by thin layer chromatography showed, that 30 micrograms of 17 alpha-estradiol inhibited the testosterone turnover in liver slices of female animals. The failure of a significant inhibitory effect in liver slices of male animals is attributed to the known, much smaller total turnover of testosterone in male liver cells. The amount of unchanged 4-en-3-oxo-steroid (testosterone and 4-androstene-3,17-dione) was increased by a factor of 2.65 and 2.25, respectively. With high probability, the inhibition was the result of a decreased hydrogenation of testosterone to dihydrotestosterone (DHT, 17 beta-hydroxy-5 alpha-androstan-3-one), catalyzed by 5 alpha-reductase, since the production rates of DHT and the DHT-transformation metabolites (5 alpha-androstane-3 alpha,17 beta-diol and 5 alpha-androstane-3,17-dione) were significantly lowered (factors: 0.16, 0.61, 0.61, respectively). In further experiments 17 beta-estradiol and 17 alpha-ethinylestradiol could be shown to inhibit the testosterone turnover in liver slices of female rats, too, but to a lower extent that 17 alpha-estradiol (relative inhibitory effects: 17 alpha-estradiol:17 beta-estradiol:17 alpha-ethinylestradiol = 100 : 73 : 58).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1978

[Variation of the serum testosterone level in boars during 24 hours and during a period of several days].

Seven sexually mature boars were studied in two-hour intervals for 8 to 32 hours, as to the variation of testosterone levels in the blood plasma. Blood samples were obtained by means of a cannula inserted in the v. cava cranialis. The hormone level under study showed marked fluctuation. The coefficient of variation of testosterone concentration ranged from 12.7% to 35.2% in the individual animals and for the whole part of the study it was 33.0%. It appeared impossible to derive seriously any regular periodicity of testosterone concentration in boar blood in the 24-hour period from the analysis of the variation of the levels of the hormone in individual animals during the period under study. Further, the study revealed a marked fluctuation of testosterone levels in the blood plasma of twelve sexually mature boars in the course of several days' study. The coefficient of variation of testosterone concentration in individual animals ranged from 18.1% to 106.5%, reaching 77.0% for the whole part of study. The analysis of variance showed statistically significant differences of hormonal levels in individual boars in which the fluctuation of testosterone was studied in the 8- to 32-hour period as well as in several days' period. This proved the role of the animals' individuality in determining the concentration of testosterone in their blood. The discussion concerns the importance of these findings for the evaluation of the role of basal testosterone levels in the blood in classifying the incretion function of the gonads and in the diagnosis of incretion hypogonadism of boars.

Age Factors↗

PubMed1983

Effects of testosterone on the zona fasciculata of the male rat adrenal cortex. A correlated stereological and biochemical study.

The effects of long-term testosterone administration on the adrenal cortex of male rats were investigated by coupled morphometric and biochemical methods. Morphometry showed that testosterone treatment provoked a time-dependent atrophy of the zona fasciculata cells, which was mainly due to the decrease in the volume of the mitochondrial compartment and smooth endoplasmic reticulum (SER). Biochemical assays demonstrated that the decrease in the surface area per cell of SER membranes and mitochondrial cristae was tightly paralleled by the decrease in the activity per cell of two key enzymes of steroid synthesis contained in them (delta 5-3 beta-hydroxysteroid dehydrogenase and 11 beta-hydroxylase). The testosterone-induced inhibition of the growth maintenance and steroidogenic capacity of adrenocortical cells provoked a significant fall in the plasma concentration of corticosterone and a consequential increase in the level of circulating ACTH. Chronic administration of testosterone caused a notable suppression of the activity of the adrenal 5 alpha-reductase and this in turn provoked a rise in the intracellular concentration of corticosterone. Moreover, testosterone inhibited the incorporation of 3H-uridine into the nuclear and mitochondrial fractions of male rat adrenocortical cells. These findings exclude the possibility that the testosterone-provoked atrophy of the male rat adrenal glands is mediated by the suppression of the hypothalamo-hypophyseal axis, and suggest that the mechanism underlying this action of testosterone involves inhibition of nuclear and mitochondrial RNA synthesis. Whether this effect of testosterone is directly or indirectly mediated by the rise in the intracellular content of corticosterone due to the inhibition of 5 alpha-reductase activity, remains to be elucidated.

3-Hydroxysteroid Dehydrogenases↗

PubMed1982

[Concentration of plasma testosterone in adult roosters of a low-weight strain].

The levels of blood-plasma testosterone were studied in the adult light bodied strain cocks. Blood was sampled (1 ml) from the wing vein by means of a heparinized syringe six times within a 24-hour interval. The plasma obtained by centrifugation was kept in a refrigerator at a temperature of --18 degrees C. Testosterone was determined by the radioimmunological method. The testosterone levels were significantly higher (P less than 0.001), 18.8 nmol/l on the average, in the blood samples taken during the dark period of the day (10 o'clock p.m., 2 and 6 o'clock a.m.) than in the samples taken in the light part of the day (8 and 10 o'clock a.m., 2 o'clock p.m.) when the average concentration of the studied hormone was 10.7 nmol/l of plasma. the lowest levels of testosterone were recorded in the morning and the highest values were recorded late in the evening (10 o'clock p.m.). The differences in the levels of the hormone between sampling terms indicate that the testosterone level in adult animals shows diurnal variances. It was found by the study of the concentration of testosterone in the blood plasma of the same individuals within short intervals of time (30-60 min) that testosterone secretion in adult cocks had a pulsatory manner. The evaluation of hormone levels should include not only the diurnal variances but also the pulsatory manner of testosterone secretion.

Animals↗

PubMed1982

An improved ultrafiltration method for determining free testosterone in serum.

In this method, we use the Amicon MPS-1 centrifugal ultrafiltration device and the YMB membrane in measuring free testosterone in serum. Two independent assays are combined: total testosterone and the ultrafiltrable fraction of added [3H]testosterone. The unbound fraction is determined in 0.15-0.5 mL ultrafiltrates of 0.6 to 1 mL of variably diluted serum that has been equilibrated with [3H]testosterone at 37 degrees C. The assay is rapid (less than 1 h), practicable (requires 0.6 mL of serum), and reproducible (CV 3.2% within assay, 3.9% between assays). Accuracy was evaluated as the fraction of free testosterone in the ultrafiltrate of dialyzed serum vs that in a prior dialysate; they were the same confirming the validity of the free testosterone measurement. Samples from ostensibly healthy men and women and from hirsute and pregnant women gave results that agreed with those obtained by equilibrium dialysis. Total testosterone concentrations for normal and hirsute women showed considerable overlap, but data on free testosterone concentrations in these populations were better resolved.

Adult↗

PubMed1980

Morphine exerts testosterone-like effects in the hypothalamus of the castrated male rat.

Previous research has indicated that endogenous opioids participate in the regulation of activity in the hypothalamic-pituitary-luteinizing hormone (LH) axis and mediate the negative feedback control exerted by testosterone. If this assumption is correct, then two predictions can be made. First, the effects of testosterone should be competitively inhibited by narcotic antagonists; and, second, opiates should mimic the acute and chronic effects of testosterone in the castrated male rat. The results of the present investigations support both of these predictions. We found that naloxone competitively antagonized the depressive effects of testosterone on serum LH in the castrated rat and, conversely, that testosterone competitively antagonized the LH-releasing properties of naloxone. In addition, morphine and testosterone both depressed serum LH levels in a dose-dependent fashion in the acutely castrated animal. Moreover, morphine was just as effective as testosterone in reversing the castration-induced fall in hypothalamic-LH-releasing hormone (LH-RH), which occurs in the chronically castrated male rat. On the other hand, morphine failed to reverse the long-term changes in pituitary LH content and increase in serum LH, which is consistent with prior observations that morphine affects only the hypothalamic aspect of the hypothalamic-pituitary-LH axis in the male rat. These results, thus, support the concept that an as yet unidentified opioid-containing neuronal system regulates activity in the hypothalamic-pituitary-LH axis and mediates the effects of testosterone on this axis.

Animals↗

PubMed1995

The effect of varicocelectomy on serum testosterone levels in infertile men with varicoceles.

PURPOSE: We evaluated the effect of varicocelectomy on serum testosterone. MATERIALS AND METHODS: We retrospectively reviewed the effect of varicocelectomy on serum testosterone levels in 53 infertile men with varicoceles. RESULTS: Mean serum testosterone increased from a preoperative level of 319 +/- 12 to 409 +/- 23 ng./dl. postoperatively (p < 0.0004). Men with at least 1 firm testis preoperatively had a greater increase in serum testosterone (p < 0.005). An inverse correlation was noted between preoperative testosterone levels and change in testosterone after varicocelectomy (r = -0.34, p < 0.013). CONCLUSIONS: Varicocelectomy can increase serum testosterone for infertile men with varicoceles. Although improvement in serum testosterone does not necessarily cause a direct improvement in semen quality, varicocelectomy may improve hormonal and spermatogenic function.

Adult↗

PubMed1994

Decreased testosterone levels in men with rheumatoid arthritis: effect of low dose prednisone therapy.

OBJECTIVE: To determine whether men with rheumatoid arthritis (RA) have abnormal hypothalamic-pituitary-gonadal axis function and to measure the effects of low dose prednisone therapy in these patients. METHODS: We measured testosterone, follicle stimulating hormone (FSH), and luteinizing hormone (LH) in 36 men aged 38-75 (mean age +/- 1 sd = 62 +/- 10 years) who had longstanding active RA (mean disease duration = 17 +/- 12 years) and in 70 healthy elderly male controls, aged 53-83 (mean age 68 = +/- 6 years). We divided the group with RA into those taking no prednisone (n = 12) and those taking 5 to 10 mg/day of prednisone (n = 24) and analyzed these groups separately to determine whether low doses of prednisone affected testosterone levels. RESULTS: Compared to the healthy controls, patients with RA not taking prednisone had normal testosterone levels but significantly elevated levels of FSH and LH (p < 0.01 for both comparisons). In contrast, patients with RA taking prednisone had significantly lower testosterone levels (p < 0.05), but levels of FSH and LH were only slightly elevated compared to controls. Compared to patients not taking prednisone, patients taking prednisone had lower levels of testosterone, FSH, and LH. CONCLUSION: Male patients with RA who are not taking prednisone have significantly elevated levels of FSH and LH with normal testosterone levels, suggesting a state of compensated partial gonadal failure. Male patients with RA taking low doses of prednisone have lower testosterone and gonadotropin levels, suggesting that prednisone may suppress the hypothalmic-pituitary-testicular axis. Since testosterone affects immune function as well as bone and muscle metabolism, androgen deficiency in some men with RA may predispose these patients to more severe disease and to increased complications of steroid therapy such as myopathy and osteoporosis.

Adult↗

PubMedDate not supplied

Testosterone feedback on gonadotropin secretion and gene expression in transgenic mice expressing human growth hormone gene.

To determine the effects of testosterone on the regulation of gonadotropins in metallothionein-1/human growth hormone (MT/hGH) transgenic mice, basal and gonadotropin-releasing hormone (GnRH)-stimulated luteinizing hormone (LH) and follicle-stimulating hormone (FSH) release from incubated pituitaries, as well as pituitary content of LH, FSH, and mRNA for their respective beta subunits, were measured in normal and transgenic males that were injected with testosterone propionate (5 micrograms/g body weight; 24 hours before autopsy), injected with oil vehicle, castrated for 10 days, or sham operated. In normal (non-transgenic) males, exogenous testosterone induced the expected suppression, and castration induced the expected stimulation of various parameters of gonadotropin synthesis and release. In contrast, in testosterone-treated and in castrated MT/hGH transgenic mice the release of LH and the pituitary levels of LH-beta mRNA did not differ from the corresponding values measured in vehicle-injected and sham-operated transgenic controls. Pituitary LH content was elevated in testosterone-treated MT/hGH transgenic mice but was not changed in castrated transgenic males. The changes in pituitary levels of FSH and FSH-beta mRNA and in FSH release in MT/hGH transgenic mice in response to testosterone and castration were different from the changes in LH and LH-beta mRNA in the same mice, but similar to the changes of FSH and FSH-beta message produced in normal mice by identical treatments. We suggest that hGH expression attenuates the effects of testosterone on the mechanisms controlling LH release, with less influence on testosterone regulation of LH synthesis. These effects of hGH expression appear to be selective for LH, without influencing the FSH control system.

Animals↗

PubMed1993

Endogenous testosterone, fibrinolysis, and coronary heart disease risk in hyperlipidemic men.

To assess relationships of endogenous testosterone with fibrinolysis and coronary heart disease risk factors in 55 newly referred hyperlipidemic men, we studied the relationships of testosterone to basal fibrinolytic activity, lipids, lipoproteins, and apolipoproteins. Testosterone correlated positively with the major stimulator of fibrinolysis, tissue plasminogen activator activity (r = 0.30; p = 0.02) and correlated inversely with two independent coronary heart disease risk factors, plasminogen activator inhibitor activity, the major fibrinolysis inhibitor (r = -0.33; p = 0.01), and fibrinogen (r = -0.39; p = 0.004). Testosterone correlated inversely with plasma triglycerides (r = -0.33; p = 0.01). Stepwise multiple regression was done with fibrinolytic activities as the dependent variables, and age, Quetelet Index (relative ponderosity), apolipoprotein A-I, apolipoprotein B, triglyceride, testosterone, time of blood sampling, and lipoprotein (a) as explanatory variables. Testosterone was an inverse, independent predictor of fibrinogen (p = 0.002); 53% of the variance of fibrinogen could be accounted for by age and triglyceride level (positive; p = 0.001, p = 0.01), and by apolipoprotein A-I and testosterone (negative; p = 0.02, p = 0.002). Testosterone was an independent inverse predictor of tissue plasminogen activator antigen (p = 0.0008), with tissue plasminogen activator antigen correlating inversely with tissue plasminogen activator activity. Quetelet index and apolipoprotein B were independent negative predictors of tissue plasminogen activator activity (p = 0.02, p = 0.03); Quetelet index and triglycerides were independent positive predictors of plasminogen activator inhibitor activity (p = .0001, p = .0001) and alpha 2-antiplasmin (p = 0.0003, p = 0.009).(ABSTRACT TRUNCATED AT 250 WORDS)

Apolipoprotein A-I↗

PubMed1993

Response to gonadotrophin-releasing hormone by the intact male dog: serum testosterone, luteinizing hormone and follicle-stimulating hormone.

In Expt 1, gonadotropin-releasing hormone (GnRH) (Cystorelin, CEVA) was administered intramuscularly to two intact male dogs; one dog received one injection of 50 micrograms GnRH and one dog received four daily injections of 50 micrograms GnRH. Both dogs exhibited a significant and immediate rise in luteinizing hormone (LH) following GnRH administration, with a peak observed at 15 min following injection. Testosterone was increased over baseline concentrations for 5 and 7 days, respectively, after the injection. In Expt 2, eight intact male dogs were injected intramuscularly with 0.7 microgram GnRH (Factrel, Fort Dodge) kg-1. Baseline testosterone concentrations were established by daily sampling for 14 days before treatment. All dogs exhibited an LH peak 15 min and a testosterone peak 60 min after the GnRH injection. Testosterone concentrations had returned to baseline concentrations by 4 h after the injection. Testosterone tended to fall below baseline concentrations for several days following the injection of GnRH. No peak was noted for follicle-stimulating hormone. In Expt 3, five additional dogs were injected with 0.7 microgram GnRH (Factrel, Fort Dodge) kg-1. Testosterone concentrations rose in all dogs 1 h after the injection and returned to baseline concentrations by 24 h after injection. In the male dog, GnRH stimulated an LH peak 15 min and a testosterone peak 1 h after injection. Further investigations are needed to elucidate the different effects on testosterone concentration observed with two different GnRH preparations.

Animals↗

PubMed1996

[Relationship between cortisol and testosterone during resting conditions, after acute stress and hormone stimulation in steers].

In this study the relationship between peripheral concentrations of cortisol and testosterone was investigated in 7 adult bulls under resting conditions as well as after sexual and hormonal stimulation. The animals were kept under natural photoperiods of 16L:8D and for hormone determinations blood was withdrawn from an indwelling jugular vein catheter every 30 minutes for 24 and 48 h, respectively. Evaluation of the hormonal profiles revealed that both steroids are secreted episodically characterized by irregular, short term fluctuations with high individual variability. A clear circadian rhythm with high levels in the morning and during the day and low concentrations in the evening and during night was observed for cortisol only. Concentrations of both steroidal hormones were not significantly correlated with each other. Intense sexual stimulation (mounting several times with ejaculation) during 30 minutes caused a rapid increase of cortisol without affecting testosterone secretion. After intravenous application of 1500 IU hCG and 0.5 mg GnRH a sharp rise of testosterone concentrations occurred with high values remaining for several hours but leaving the circadian cortisol pattern unchanged. The intravenous injection of 5 mg PGF2 alpha stimulated both the cortisol and testosterone secretion. Results from this investigation show that cortisol and testosterone are secreted episodically without any interrelationship under resting conditions. Sexual stress induced an increase of cortisol which did not inhibit testosterone secretion and high testosterone levels did neither influence the cortisol pattern. The concomitant increase of cortisol and testosterone after PGF2 alpha suggests a central (hypothalamus/hypophysis) action for prostaglandin.

Animals↗

PubMedDate not supplied

[Blood levels of testosterone and its urinary excretion in women of reproductive age both neurosis-free during the climacteric period and with climacteric neuroses].

Blood testosterone content was studied by the radioimmunological method in 12 healthy women (5 of reproductive age, and 7 with climacteric age changes) and in 4 patients at the postmenopause suffering from climateric neurosis. Urinary excretion of testosterone glucuronide was studied by means of fluorometry in 11 healthy women (4 of reproductive age, and 7 at the climacteric) and in 6 patients at the postmenopause with climacteric neurosis. Healthy women of reproductive age displayed marked individual variations in the blood testosterone content both during the folliculin and the lutein cycle phases. The indices of urinary testosterone excretion varied in this group lees. As to healthy women with age climacteric changes and a regular cycle and those during the postmenopause--they showed marked variations both in blood testosterone content and in urinary testosterone excretion. There were no significant differences in the indices studied in healthy women of reproductive age and in healthy women with age climacteric changes. But in 8 of 11 women with climacteric neurosis blood testosterone content and urinary testosterone excretion were much greater than the upper borders of its variations in healthy women.

Adult↗