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PubMed1999

Regulation of prostatic glutathione-peroxidase (GSH-PO) in rats treated with a combination of testosterone and 17 beta-estradiol.

In order to confirm the relationship between sex hormone administration and glutathione-peroxidase (GSH-PO) in the rat ventral prostate, the levels of GSH-PO mRNA, GSH-PO activity, and lipid peroxide (TBA) value in the ventral prostate were investigated. Male Crj:CD(SD)IGS rats were divided into six experimental groups. Group 1 consisted of intact controls. In group 2, rats were sacrificed two days after castration. In groups 3 and 4, rats were subcutaneously administered 1 mg/animal of testosterone daily for three or seven days after two days of castration, respectively. In groups 5 and 6, rats were subcutaneously administered 1 mg/animal of testosterone plus 0.01 mg/animal of 17 beta-estradiol (E2) daily for three or seven days after two days of castration, respectively. GSH-PO activity of the ventral prostate homogenate for testosterone or testosterone plus E2 administration to the castrated rat was increased and the TBA value was remarkably decreased. The prostatic GSH-PO mRNA level was diminished in the castrated rat ventral prostate, but was increased by testosterone or testosterone plus E2 administration. In particular, the GSH-PO mRNA level of testosterone plus E2-treated animals was higher than that of testosterone-treated animals. These findings strongly suggest that expression of GSH-PO in the rat ventral prostate is considered to be testosterone- or E2-dependent. Furthermore, it is suggested that the transcription of prostatic GSH-PO mRNA was regulated by testosterone or E2 and de novo synthesis of GSH-PO would thus be regulated at transcription level by testosterone or E2.

Animals↗

PubMed2005

Sildenafil improves sleep-related erections in hypogonadal men: evidence from a randomized, placebo-controlled, crossover study of a synergic role for both testosterone and sildenafil on penile erections.

To study the effects of sildenafil on human sleep-related erections according to the state of androgenization, we evaluated the effects of sildenafil on sleep-related erections in hypogonadal men before and during testosterone replacement treatment and in control subjects. We enrolled 24 hypogonadal men and 24 healthy men as a control group. All hypogonadal subjects had very low testosterone levels (<200 ng/dL [6.9 nmol/L]) [corrected] All subjects underwent nocturnal penile tumescence and rigidity monitoring (NPTRM) for 3 consecutive nights and were randomly assigned to consume either 50 mg of sildenafil or placebo 1 hour before bedtime on the second or third night of nocturnal penile monitoring. The hypogonadal subjects were tested twice, first without replacement treatment (H-T) and then after at least 6 months of testosterone replacement therapy (H+T). The subjects of the control group (C) were tested once. The following parameters of sleep-related erections were analyzed: total number of valid erections, total duration of both rigidity greater than or equal 70% and increase in penile circumference greater than or equal 30 mm, maximum rigidity, and maximum increase in penile circumference. NPTRM parameters were reduced in hypogonadal men before testosterone treatment (H-T+P) when compared with control subjects taking placebo (C+P). NPTRM parameters after testosterone (H+T+P) and sildenafil (H-T+S) administration were similar to that of control subjects taking placebo (C+P). When the statistical analysis was restricted to the hypogonadal men before testosterone treatment, sildenafil alone significantly increased NPTRM parameters when compared with placebo (H-T+S vs H-T+P). Testosterone restored normal erections when administered to hypogonadal subjects (H+T+P vs H-T+P); in hypogonadal men, however, the combined treatment (sildenafil plus testosterone) resulted in the maximum positive effect on NPTRM parameters. When the increase from baseline was analyzed, the effects of testosterone plus sildenafil were greater than the sum of the effects of each drug used alone. In conclusion, sildenafil administered at bedtime improves sleep-related erections in hypogonadal men, suggesting that the nitric oxide pathway may be pharmacologically enrolled and enhanced despite low serum testosterone. Furthermore, these data strongly support the idea of a synergic effect on sleep-related erections of sildenafil and testosterone.

Adult↗

PubMed2005

Testosterone and atherosclerosis in aging men: purported association and clinical implications.

Two of the strongest independent risk factors for coronary heart disease (CHD) are increasing age and male sex. Despite a wide variance in CHD mortality between countries, men are consistently twice as likely to die from CHD than their female counterparts. This sex difference has been attributed to a protective effect of female sex hormones, and a deleterious effect of male sex hormones, upon the cardiovascular system. However, little evidence suggests that testosterone exerts cardiovascular harm. In fact, serum levels of testosterone decline with age, and low testosterone is positively associated with other cardiovascular risk factors. Furthermore, testosterone exhibits a number of potential cardioprotective actions. For example, testosterone treatment is reported to reduce serum levels of the pro-inflammatory cytokines interleukin (IL)-1beta and tumor necrosis factor (TNF)-alpha, and to increase levels of the anti-inflammatory cytokine IL-10; to reduce vascular cell adhesion molecule (VCAM)-1 expression in aortic endothelial cells; to promote vascular smooth muscle and endothelial cell proliferation; to induce vasodilatation and to improve vascular reactivity, to reduce serum levels of the pro-thrombotic factors plasminogen activator inhibitor (PAI)-1 and fibrinogen; to reduce low-density lipoprotein-cholesterol (LDL-C); to improve insulin sensitivity; and to reduce body mass index and visceral fat mass. These actions of testosterone may confer cardiovascular benefit since testosterone therapy reduces atheroma formation in cholesterol-fed animal models, and reduces myocardial ischemia in men with CHD. Consequently, an alternative hypothesis is that an age-related decline in testosterone contributes to the atherosclerotic process. This is supported by recent findings, which suggest that as many as one in four men with CHD have serum levels of testosterone within the clinically hypogonadal range. Consequently, restoration of serum levels of testosterone via testosterone replacement therapy could offer cardiovascular, as well as other, clinical advantages to these individuals.

Aging↗

PubMed1981

Short-term parenteral and peroral testosterone administration in men with alcoholic cirrhosis.

Serum concentrations of testosterone were measured in 24 male patients with alcoholic cirrhosis during testosterone administration. The purpose was to compare serum concentrations of testosterone during peroral with those during parenteral testosterone administration in these patients. Patients who were injected intramuscularly with a combination of short- and long-acting testosterone (Triolandren, 348 mg testosterone) had median peak values of serum testosterone of about 40 ng/ml, which fell to basal levels after a fortnight. During testosterone propionate injections (84 mg testosterone) every other day, rather constant serum concentrations with median values of about 30 ng/ml were reached after 4 days. Peroral testosterone administration (800 mg micronized free testosterone) each day also resulted in fairly constant serum concentrations after 4 days, and the median values were about 50 ng/ml. No side effects were observed.

Administration, Oral↗

PubMed1991

Neonatal exposure to Aroclor 1254: effects on adult hepatic testosterone hydroxylase activities.

1. The effects of neonatal exposure to Aroclor 1254 (100 mumol/kg) on the metabolism of testosterone by adult male and female rats were determined by comparing their hepatic microsomal testosterone hydroxylase activities at 60, 90 and 120 days after the initial exposure. 2. The most pronounced effects in male rats were observed 90 days after treatment with Aroclor 1254, whereas in female rats the major changes in testosterone hydroxylase activities were observed after 60 days. 3. Ninety-day-old male rats neonatally treated with Aroclor 1254 exhibited decreased basal testosterone 7 alpha-hydroxylase and increased basal testosterone 16 alpha-, 2 alpha- and 15 beta-hydroxylase activities and androstenedione formation. In addition, the Aroclor 1254-mediated induction of testosterone 7 alpha- and 6 alpha-hydroxylase activities and androstenedione formation was decreased, and that of testosterone 2 beta- and 15 beta-hydroxylase activities was increased. 4. Sixty-day-old female rats exposed neonatally to Aroclor 1254 exhibited increased basal testosterone 16 alpha-, 2 beta-, 6 alpha- and 15 beta-hydroxylase activities and androstenedione formation, and increased Aroclor 1254-induced metabolism of testosterone at all positions except 16 alpha and 2 alpha. 5. Changes in testosterone hydroxylase activities indicative of permanent damage (or imprinting) in androgen metabolism, i.e. altered activities in 120-day-old animals, were observed only in male rats. These activities included basal testosterone 6 beta-, 16 alpha- and 2 alpha-hydroxylase activities and androstenedione formation.

Animals↗

PubMed2003

Anemia, testosterone, and pituitary adenoma in men.

OBJECT: Older men with clinically nonfunctioning pituitary tumors have been noted to be anemic, to have hypopituitarism, and to have low serum levels of testosterone. The authors hypothesized that men with pituitary adenomas and hypogonadism have a physiologically related decrease in hematocrit. METHODS: A retrospective analysis was conducted of 216 patients older than 50 years of age who harbored pituitary adenomas. In 100 men serum testosterone levels and a complete blood (cell) count (CBC) were obtained before treatment; a CBC was also acquired in a series of women with pituitary adenomas. Using clinical laboratory standards, anemia was defined as a hematocrit less than 40% in men and less than 35% in women. Thirty-one (46.3%) of 67 men with low serum concentrations of testosterone were anemic. In men with low levels of testosterone, the average hematocrit was 39.9%, compared with 45.6% for men with normal testosterone levels (p < 0.001). Men with macroadenomas were most likely to have both anemia and a low serum concentration of testosterone. Anemia was associated with a low level of testosterone, adjusting for tumor size (odds ratio 19, 95% confidence interval 4.86-77.03). Of patients with anemia, 84% were men and 16% were women (p < 0.001). The prevalence of anemia in women was low and was not correlated with tumor size. Men receiving testosterone replacement therapy had a significantly higher hematocrit value than men with low or normal testosterone levels. CONCLUSIONS: These findings support a direct relationship between serum testosterone levels and hematopoiesis in men, and demonstrate that hematopoiesis is compromised in men who have low concentrations of testosterone due to a pituitary adenoma.

Adenoma↗

PubMed2005

Low testosterone levels predict incident depressive illness in older men: effects of age and medical morbidity.

OBJECTIVE: Prior studies found that chronic low testosterone levels are associated with an increased risk of depression. We investigated whether low testosterone levels in older men predict depressive illness over 2 years, while controlling for age and medical morbidity. METHOD: Participants were 748 men, aged 50 years or older, without prior ICD-9-diagnosed depressive illness, with a testosterone level obtained between 1995 and 1997. Measures were age, mean total testosterone levels (low: < or = 2.5 ng/mL), medical morbidity, and incidence and time to depressive illness. RESULTS: Men with low testosterone levels had a greater 2-year incidence of depressive illness (18.5% vs. 10.4%, df = 1, p = .006) and a shorter time to onset of depressive illness (log-rank chi(2) = 8.1, df = 1, p = .004). The unadjusted hazard ratio (HR) for depressive illness in men with low testosterone levels was 1.9 (95% confidence interval [CI] = 1.2 to 3.0, p = .005). After adjustment for age and medical morbidity, men with low testosterone levels continued to have a shorter time to depressive illness (adjusted HR = 2.1; 95% CI = 1.3 to 3.2, p = .002). Due to a significant interaction between age and medical morbidity, we conducted stratified Cox regression analyses and found that low testosterone levels and high medical morbidity or an age of 50 to 65 years were associated with increased depressive illness (p = .002). CONCLUSION: Low testosterone levels are associated with an earlier onset and greater incidence of depressive illness. Men with low testosterone levels who had high medical morbidity or were aged 50 to 65 years had an increased risk for depressive illness. Further prospective studies are needed to examine the role of testosterone in depressive illness in older men.

Age Factors↗

PubMed1993

[Effects of testosterone on smooth muscle in the isolated rabbit corpus cavernosum penis].

It has been reported that there is no relationship between serum testosterone level and erectile function and that testosterone mainly acts on the brain and not on the penis. However, we have found that erectile dysfunction in some patients with low serum testosterone improved after androgen replacement therapy. We therefore studied the effects of testosterone on the contraction and relaxation of the corpus cavernosum penis. Four groups of rabbits were studied over a similar time span. The testosterone group were non-operated and received testosterone propionate 10 mg/day for 14 days before sacrifice. Two groups (castration+testosterone group and castration group) were castrated 28 days before sacrifice. The castration group received sesame oil for 14 days, and the castration+testosterone group received testosterone 10 mg/day for 14 days. Entire penis were removed immediately after death by desanguination and dissected to obtain corpus cavernosum strips. These strips were suspended under 1 g tension in a 20 ml organ bath containing Tyrode's solution. After equilibration for 2 hours, the addition of drugs was started. Changes in tension were monitored with an isometric transducer and recorded. The vasoactive drugs used were norepinephrine bitartrate, 1-phenylephrine hydrochloride, clonidine hydrochloride, acetylcholine chloride and vasoactive intestinal polypeptide. The contractility of the corpus cavernosum strips increased significantly in the testosterone group and the castration + testosterone group, but decreased significantly in the castration group as compared with the control after adding norepinephrine, phenylephrine and clonidine.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed2002

The circalunar cycle of salivary testosterone and the visual-spatial performance.

BACKGROUND: A circalunar cycle is thought to be female sex specific. Results of studies observing the relationship of testosterone and spatial abilities are controversial. OBJECTIVE: To describe the infradian variations of testosterone and the correlations between salivary testosterone levels and spatial abilities in young healthy volunteers of both sexes. SUBJECTS AND METHODS: Testosterone levels in saliva were determined in 53 young adult male and female subjects (mean age--20.89 +/- 0.91 years). The samples of saliva were collected either once (22 subjects) or daily during a period of 30 days (31 subjects). Salivary testosterone was analyzed by RIA. Both groups of subjects were tested on their visual-spatial performance (mental rotation and spatial visualization). All important data about the menstrual cycle of female subjects were also collected. This data and the results of the visual-spatial tests as well as the circalunar cycle in their relationship to the testosterone levels were analyzed. RESULTS: In this study a circalunar rhythm of testosterone related to the menstrual cycle with a maximum peak in the periovulatory phase was confirmed in women and an analogical circalunar cycle in men was described. A positive correlation of the salivary testosterone levels and the performance in visual-spatial tests in women and a negative dependence in men was found. The outcomes showed a significant statistical difference between the results of the test during the high-testosterone and the low-testosterone phase in both sexes. CONCLUSIONS: The levels of testosterone between the high female and low male range seem to be associated with the best spatial ability performance in adults. A male circalunar rhythm similar to the female one is very likely. Recognizing of the infradian fluctuations in women as in men should have many various clinical implications. (Tab. 2, Fig. 7, Ref. 143.)

Adult↗

PubMed2003

Expression of prostatic glutathione-peroxidase (GSH-PO) in the rat treated with a combination of testosterone and 17beta-estradiol.

In order to confirm the relationship between sex hormone administration and glutathione-peroxidase (GSH-PO) in the rat ventral prostate, the levels of GSH-PO mRNA, GSH-PO activity, and lipid peroxide (Thiobarbituric acid: TBA) value in the ventral prostate were investigated. Male Crj: CD (SD) IGS rats were divided into six experimental groups. Group 1 consisted of intact controls. In group 2, rats were sacrificed two days after castration. In groups 3 and 4, rats were subcutaneously administered 1 mg/animal of testosterone daily for three- or seven-day administration two days after castration, respectively. In groups 5 and 6, rats were subcutaneously administered 1 mg/animal of testosterone plus 0.01 mg/animal of 17beta-estradiol (E2) daily for three- or seven-day administration two days after castration, respectively. GSH-PO activity of the ventral prostate homogenate for testosterone or testosterone plus E2 administration to the castrated rat was increased and the TBA value was remarkably decreased. The prostatic GSH-PO mRNA level was diminished in the castrated rat ventral prostate, but was increased by testosterone or testosterone plus E2 administration. In particular, the GSH-PO mRNA level of testosterone plus E2-treated animals was higher than that of testosterone-treated animals. These findings strongly suggest that expression of GSH-PO in the rat ventral prostate is testosterone- or E2-dependent. We speculate that the transcription of prostatic GSH-PO mRNA was regulated by testosterone or E2 and de novo synthesis of GSH-PO would thus be regulated at transcription level by testosterone or E2.

Animals↗

PubMed1992

Imprinting of hepatic microsomal cytochrome P-450 enzyme activities and cytochrome P-450IIC11 by peripubertal administration of testosterone in female rats.

The influence of peripubertal exposure to physiological doses of testosterone on the adult androgen responsiveness of hepatic microsomal cytochrome P-450 was investigated. Male and female Sprague-Dawley rats were sham-operated or gonadectomized before puberty, at 25 days of age. They were injected subcutaneously with testosterone enanthate (5 mumol/kg/day) during the pubertal time period, on days 35-49. Responsiveness to this same dose of testosterone was tested by administering the compound during adulthood, on days 81-89. The females provided a model that had not been exposed to neonatal androgen imprinting, in contrast to the males. Testosterone 2 alpha-hydroxylase activity and cytochrome P-450IIC11, which are normally expressed only in adult males, were expressed in the gonadectomized females administered testosterone during puberty with no further exposure to the hormone for the next 40 days. The levels found were similar to those in the gonadectomized male group. When the combined pubertal and adult testosterone regimen was used, a synergistic effect was produced; the 2 alpha-hydroxylase activity reached control male levels in both gonadectomized and sham-operated females and, in addition, cytochrome P-450IIC11 attained control male levels in the gonadectomized females. Testosterone 6 beta-hydroxylase and erythromycin N-demethylase activities were used as indicators of the cytochrome P-450IIIA subfamily. These activities were significantly increased only in the females treated with testosterone during both the pubertal and adult periods, reaching control male levels of 6 beta-hydroxylation. A similar effect, but in the opposite direction, was found with testosterone 7 alpha-hydroxylase, an enzyme activity indicative of cytochrome P-450IIA1. A decrease in this enzyme was produced in the females administered testosterone during both time periods, resulting in levels equivalent to those found in control males. In general, a highly significant interaction was found between the pubertal and adult treatment periods for the females, indicating a chronic effect of the pubertal exposure. The experiments with castrated males did not result in synergistic interactions, although there was some evidence of an additive effect. The results of this study support the hypothesis that the peripubertal period is a time during which testosterone imprinting of both increased basal levels and adult androgen responsiveness of some hepatic cytochrome P-450 enzymes can occur in the female rat.

Animals↗

PubMed2006

Testosterone induces neuroprotection from oxidative stress. Effects on catalase activity and 3-nitro-L-tyrosine incorporation into alpha-tubulin in a mouse neuroblastoma cell line.

3-nitro-L-tyrosine is formed by nitric oxide following different pathways such as NADPH oxidase, xanthine oxidase or glutamate NMDA receptor activation and is involved in the pathology of different neurological disorders. Unlike estradiol, a neuroprotective role of androgens against oxidative cell injury has not been fully investigated. This work targets the possible effects of testosterone on neuroblastoma cells exposed to 3-nitro-L-tyrosine. C1300 mouse undifferentiated neuroblastoma cells exposed to 3-nitro-L-tyrosine were cultured in the presence of testosterone. Morphological examination, proliferation and nuclear viability assays were performed. The expression of tyrosinated alpha-tubulin and incorporation of 3-nitro-L-tyrosine into protein were also estimated. Cells exposed to 3-nitro-L-tyrosine showed globular shape, reduced cytoplasmic processes and growth inhibition in comparison with controls. When testosterone was added to the medium, these changes were not evident. In addition, testosterone induced an upregulation of tyrosinated alpha-tubulin, a marker of neuronal plasticity, and a decrease in 3-nitro-L-tyrosine incorporation into tubulin. Our results suggest that testosterone exposure can diminish 3-nitro-L-tyrosine toxic effects on the morphology and growth rate of neuroblastoma cells. The upregulation of tyrosinated alpha-tubulin in testosterone-exposed cells would be consistent with concurrent plasticity events. Failure in alpha-tubulin nitration detected in cells exposed to both 3-nitro-L-tyrosine and testosterone, may support the idea that testosterone interferes with 3-nitro-L-tyrosine protein incorporation. Moreover, testosterone-induced neuroprotection likely entails a linkage with the androgen receptor as is suggested by the flutamide-induced inhibition of the hormone activity. Finally, the neuroprotective effects of testosterone in neuroblastoma cells could deal with the cellular antioxidant defence system, as shown by testosterone-induced increase in catalase activity.

Androgen Antagonists↗

PubMed2006

The influence of testosterone on blood pressure and risk factors for cardiovascular disease in a black South African population.

OBJECTIVES: Traditionally high testosterone levels have been thought to have a detrimental effect on lipid profiles. Recently, reports have shown that testosterone has a beneficial effect on lipid profiles. On the other hand, androgens may increase blood pressure via the renin-angiotensin system. The aim of this study was to determine whether the level of testosterone is increased in hypertensive subjects or if other cardiovascular risk factors are altered with increased levels of testosterone in the Black population of South Africa. METHODS: For this study, 536 male and 666 female Black subjects were included. The subjects were divided into hypertensive and normotensive groups and high and low testosterone groups. Resting blood pressure was recorded with a finger arterial pressure device. Blood sampling and biochemical analyses were done by using standardized methods. RESULTS: The levels of testosterone in the hypertensive males and females were significantly higher compared to the normotensives. In the male high testosterone group, the level of triglyceride was significantly lower, while the high-density lipoprotein cholesterol level was significantly higher. In the female high testosterone group, systolic blood pressure, cortisol level, and renin activity were significantly higher. CONCLUSION: In the males, we found beneficial effects of testosterone, which may explain the reported lower incidence of atheroma. However, the testosterone level is also higher with hypertension. The elevated levels of systolic blood pressure and renin activity that were found in the female group with high testosterone levels may be an indication of the role of the renin-angiotensin system in this regard.

Adult↗

PubMed1991

Alcohol affects rat testicular interstitial fluid volume and testicular secretion of testosterone and beta-endorphin.

The effects of alcohol on testicular interstitial fluid (TIF) volume and the secretion of testosterone and beta-endorphin (beta E) into this important testicular compartment were assessed in the rat. Alcohol time- and dose-response curves were constructed for changes in TIF volume and the bioactive concentrations of testosterone and immunoreactive beta E (i-beta E). Alcohol (3 g/kg) decreased TIF volumes and increased TIF i-beta E secretion 0.5 to 6 hr after injection and decreased TIF testosterone 1 to 6 hr after injection. These effects were dose-related at 2 hr postinjection. The possible role of alcohol-induced reductions in serum luteinizing hormone and testosterone levels in mediating the effects of alcohol on TIF volume was also examined. We found that pretreating rats with human chorionic gonadotropin, which reversed alcohol-induced suppression in levels of serum gonadotropins and testosterone, failed to reverse the effects of alcohol on TIF volume and the secretion of testosterone and i-beta E. These results indicate that alcohol decreases TIF volume, inhibits TIF testosterone secretion and stimulates TIF i-beta E secretion and, furthermore, suggest that these effects are not indirectly mediated by decreased levels of gonadotropins or testosterone, but by direct effects of alcohol on gonadal function. The strong inverse correlation between TIF i-beta E and testosterone secretion after alcohol administration and previous evidence that testicular opioids inhibit the biosynthesis of testosterone suggest that alcohol may act through testicular beta E to suppress the synthesis and release of testosterone in the testes.

Animals↗

PubMed1988

Effect of the absence of neonatal testosterone imprinting on the activity of the microsomal enzyme system and on the dexamethasone binding of the thymus in adulthood.

Healthy and neonatally castrated male rats were treated with testosterone twice perinatally, while other groups were treated with testosterone also in adulthood or received testosterone only in adulthood. Castration resulted in a moderate (but in some instances significant) decrease of PSMO (polysubstrate monooxygenase) level measured in adulthood. The decrease could partially be compensated by perinatal testosterone treatment. Further testosterone treatment administered in adulthood did not result in further alteration when compared either with the controls or with the neonatally treated animals. However, since in the controls the second testosterone treatment (following the neonatal one), had a decreasing effect, therefore the testosterone treatment administered in adulthood was responsible for the disappearance of the difference between the castrated animals and the controls treated both perinatally and in adulthood. On the basis of these findings it seems likely that the perinatal presence of testosterone plays a major role in the development of enzymatic imprinting and thus, in securing the capability of the liver to split testosterone in adulthood. Since testosterone influences the glycocorticoid receptors of the thymus (presumably by its overlapping effect), so the amount of free glycocorticoid receptors is always higher in the animals castrated neonatally than in the controls. Conversely, neonatal testosterone treatment somewhat increases the number of receptors detectable in adulthood.

Animals↗

PubMed1985

Alcohol effects on luteinizing hormone and testosterone in male macaque monkeys.

The effects of alcohol (2.5 and 3.5 g/kg) on luteinizing hormone (LH) and testosterone were studied in adult male macaque monkeys under both basal and naloxone-stimulated conditions. Integrated plasma samples were collected at 30-min intervals for 90 min before nasogastric intubation of alcohol (2.5 and 3.5 g/kg) or a sucrose control solution, isocalorically equivalent to 2.5 g/kg of alcohol. Under basal (non-naloxone-stimulated) conditions, alcohol (2.5 or 3.5 g/kg) did not change LH levels significantly from prealcohol control levels. When basal testosterone levels were normal (600-1300 ng/dl), alcohol significantly suppressed testosterone levels in a dose-dependent manner. Testosterone levels decreased by 52% (P less than .05) within 30 min after a 3.5 g/kg dose of alcohol. As average blood alcohol levels increased to 400 mg/dl and above, testosterone levels fell monotonically and remained over 70% below base-line levels (P less than .01). After administration of 2.5 g/kg alcohol, testosterone levels were significantly suppressed within 90 min (P less than .05) and remained 52 to 63% below control levels (P less than .02-.05) as average blood alcohol levels increased to 300 mg/dl. However, when basal testosterone levels were abnormally low (100-200 ng/dl), alcohol had no effect on testosterone or LH. Naloxone stimulation was used to circumvent the high incidence of abnormally low testosterone levels observed. Naloxone (0.5 mg/kg i.v.) administration 90 min after alcohol (2.5 and 3.5 g/kg) or sucrose control administration significantly increased LH levels in comparison to base line (P less than .02-.001). LH reached peak values within 60 min after naloxone administration. A significant increase in testosterone (P less than .001) was observed 90 min after naloxone administration as LH levels began to decline. Alcohol (2.5 and 3.5 g/kg) did not attenuate or delay naloxone-stimulated increases in LH and testosterone in comparison to sucrose control conditions.

Animals↗

PubMed1983

Paradoxical effects associated with supranormal urinary testosterone excretion in premenopausal women with breast cancer: increased risk of postmastectomy recurrence and higher remission rate after ovariectomy.

Urinary testosterone excretion was measured in 18 normal premenopausal women, 80 women studied shortly after mastectomy for primary operable breast cancer, and 93 women with either metastatic breast cancer (77) or primary inoperable breast cancer (16) who were to be ovariectomized. Forty-two of the 93 were restudied after the ovariectomy. The control women showed a normal distribution of testosterone excretion, up to 12 micrograms daily; the postmastectomy patients showed a bimodal distribution, with 14 patients (17.5%) having values above 12 micrograms (up to 39 micrograms) daily. In the metastatic group, 24 of 77 patients (31.1%) had urinary testosterone excretion greater than 12 micrograms daily (up to 77 micrograms). The difference in percentage of high excretors was significant (p less than 0.02). Of the patients treated by ovariectomy, 27 had supranormal testosterone excretion preoperatively, and 16 of these (59.2%) had remissions; 66 had normal excretion preoperatively, and 21 of these (31.8%) had remissions. The difference was significant (p less than 0.02). Urinary testosterone excretion was restudied postoperatively in 42 of the 93 ovariectomized patients. Values were normal preoperatively in 31, and these were unchanged postoperatively. Values were supranormal preoperatively in 11; all of these fell significantly after ovariectomy, to normal in 8 cases. These findings appear to confirm the ovarian source of the excessive urinary testosterone. The following conclusions were drawn. There is a subgroup of premenopausal women with primary operable breast cancer who have supranormal urinary testosterone excretion; the incidence of this abnormality in women with recurrent metastatic disease after mastectomy is nearly twice as high. It can be calculated that the finding of supranormal urinary testosterone shortly after mastectomy represents virtually a 100% risk of recurrence, in contrast to a recurrence rate of about 38% in women with normal testosterone excretion. Patients with supranormal testosterone excretion prior to therapeutic ovariectomy have nearly twice as high a remission rate as do those with normal testosterone excretion.

Adult↗

PubMedDate not supplied

Pharmacokinetics and pharmacodynamics of a parenteral testosterone microsphere formulation in the male rat. Demonstration of dose dependence and controlled release.

This study examined the pharmacokinetics (the time course and pattern of testosterone release) and pharmacodynamics (effects on accessory sex organ weights, and serum LH and FSH levels) of a biodegradable testosterone microsphere formulation in the male rat. Two hundred seventy-five 55-day-old, sexually mature male rats underwent surgical orchiectomy or sham surgery and were divided into five groups as follows, to receive placebo or testosterone microsphere systems designed to release 25, 75, or 225 micrograms/day testosterone: group I: intact age-matched controls, sham operated, placebo microspheres; group II: surgically orchiectomized, placebo microspheres; group III: surgically orchiectomized, 25 micrograms/day testosterone microspheres; group IV: surgically orchiectomized, 75 micrograms/day testosterone microspheres; and group V: surgically orchiectomized, 225 micrograms/day testosterone microspheres. Serum testosterone levels were fairly uniform from day 2 to 85 without any significant trend. After day 100, serum testosterone levels gradually fell into the castrate range by day 196. There was a dose-dependent increase in serum testosterone levels in groups III, IV, and V over those seen in group II (castrated rats, placebo treated). Prostate and seminal vesicle weights were significantly lower in castrated animals treated with placebo or the 25-micrograms/day testosterone microsphere system (group III). Mean prostate and seminal vesicle weights in groups IV and V were not significantly different from those in intact controls (group I) in the first 85 days. After day 85-100, seminal vesicle and prostate weights declined gradually in groups III, IV, and V, approaching castrate range by day 196.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗