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PubMed1998

Endosulfan elevates testosterone biotransformation and clearance in CD-1 mice.

Toxicant-mediated induction of hepatic biotransformation enzymes is a mechanism by which endogenous steroid hormone metabolism and elimination may be altered. Endosulfan, an organochlorine insecticide that has been demonstrated to induce hepatic P450 biotransformation enzymes, was examined for its ability to alter the rate of steroid hormone metabolism in CD-1 mice. Our objective was to evaluate whether endosulfan-induced changes in the rate of testosterone metabolism were reflected in the rate of testosterone clearance and if those alterations were sufficient to disrupt steroid hormone homeostasis within the animal. Major pathways for testosterone metabolism in the liver, including hydroxylation, conjugation to glucuronic acid or sulfate, and reduction/dehydrogenation, were examined for changes due to endosulfan exposure. In female mice, endosulfan treatment elicited a dose-dependent increase in the rate of total testosterone hydroxyl metabolite formation by selectively increasing the rate of production of 16 beta-, 6 alpha, and 16 alpha-hydroxytestosterone metabolites. The hydroxylation of testosterone in the 16 beta position was most sensitive to endosulfan with a 3.3-fold increase in the rate of production of this metabolite observed following exposure to 7.5 mg/kg/day for 7 days. The rate of testosterone dehydrogenation to androstenedione was increased by 7.5 mg/kg/day of endosulfan, but the rate of direct glucuronic acid or sulfate conjugation to testosterone was not affected by any of the dosages investigated. Endosulfan was generally more toxic to male mice and did not significantly alter the rate of total hydroxytestosterone metabolite formation or glucuronic acid or sulfate conjugation. The ability of endosulfan to enhance the elimination of testosterone was, therefore, investigated in female mice. Exposure of mice to 7.5 mg/kg/day of endosulfan resulted in an approximately 3.6-fold increase in the rate of urinary elimination of [14C]androgen, but had no significant effect on the fecal elimination of [14C]androgen. The increase in androgen clearance was associated only with a small, nonsignificant decrease in serum testosterone levels. Results indicate that increases in testosterone biotransformation from endosulfan exposure can result in increases in the elimination of the steroid. However, homeostatic processes apparently compensate for the effect and minimize any consequences on serum hormone levels.

Animals↗

PubMed1992

Testosterone treatment of men with idiopathic hemochromatosis.

Patients with chronic liver disease usually exhibit low plasma levels of testosterone with loss of libido and potency; this is also valid in male patients suffering from idiopathic hemochromatosis (IHC), in whom nowadays the diagnosis is made at an earlier age. Therefore, the effect of testosterone treatment was studied in 10 patients with IHC. After the application of 250 mg testosterone enanthate i.m., the plasma testosterone (from 2.4 +/- 1.9 to 20.1 +/- 7.4 ng/ml) and estradiol (from 17.4 +/- 6.3 to 38.5 +/- 14.2 pg/ml) levels increased significantly. The rise of estradiol was in the range of controls and smaller than reported in other chronic liver diseases. In a long-term study, 250 mg testosterone enanthate was given 4-weekly for 33-96 months to 5 patients with IHC. General well-being, libido, and potency recovered almost immediately. Over a treatment period of 27.3 patient years, symptoms of hyperestrogenism (gynecomastia) or (portal vein) thrombosis were not seen, both of which had been described in patients with alcoholic liver cirrhosis. There was no deterioration of liver function. The effect of testosterone treatment on the patients' well-being and plasma hormone concentrations remained unchanged over the whole period of testosterone treatment. Thus, in male patients with IHC and lowered plasma testosterone, treatment with testosterone enanthate may be instituted. Because of the positive effects on general well-being, liver regeneration capacity, and potency, testosterone should especially be administered to younger subjects suffering from IHC.

Adult↗

PubMed1989

The relationship between total urinary testosterone and renal calculi.

It is generally known that age and sex are risk factors of urolithiasis. Therefore the total urinary testosterone concentrations of persons with and without renal stones were investigated by means of radioimmunoassay. The total testosterone level of the first morning midstream urine was comparable with 24 urine samples of 16 healthy persons (rs = 0.9618). Investigation of the total urinary testosterone confirmed that the concentration is age dependent. A distinct decrease in total testosterone was observed in elderly persons. Therefore the total testosterone concentrations of the two groups, with and without stones, were studied within the same age interval (P = 0.8292). The the testosterone level differed significantly for these two groups (P = 0.0006). In general, the testosterone level of the kidney stone patients was lower than that of their healthy counterparts. In order to determine whether this variation in testosterone concentration would affect the urinary urokinase activity, a correlation study was undertaken. A positive correlation was found between the total urinary testosterone concentrations and the activity of urokinase (rs = 0.7305). It therefore seems that the total urinary testosterone concentrations may play a role in the pathogenesis of the multifactorial disease, urolithiasis.

Age Factors↗

PubMed1992

Divergent effects of different enzyme-inducing agents on endogenous and exogenous testosterone.

The effects of three different enzyme-inducing drugs (antipyrine 1200 mg, phenobarbital 100 mg, rifampicin 600 mg per day for 7 days) on plasma and urinary testosterone concentrations, plasma gonadotropin levels, antipyrine kinetics, and urinary 6 beta-hydroxycortisol excretion were studied in 18 healthy volunteers. Changes in plasma and urinary testosterone concentrations following exogenous testosterone undecanoate (TU) were also investigated. Although both antipyrine and rifampicin increased antipyrine clearance by about 60%, they produced contrary effects on testosterone: antipyrine lowered the total morning plasma testosterone and plasma testosterone AUC following TU, while rifampicin led to increases of about 20% and 78%, respectively. By contrast, phenobarbital did not significantly alter the endogenous and exogenous plasma testosterone concentrations, but it increased the urinary excretion of testosterone by more than 60%. The other two enzyme inducers did not alter this parameter. Gonadotropin levels remained unchanged. The results indicate that different enzyme-inducing agents exert divergent effects on endogenous and exogenous testosterone concentrations and suggest that the effect of enzyme induction on endogenous testosterone depends on the type of microsomal enzyme-inducing drug used rather than on the extent of the induction achieved.

Adult↗

PubMed1982

Effects of testosterone replacement on sexual behavior in hypogonadal men.

Fifteen patients with hypogonadism due to testicular, pituitary, or hypothalamic failure were studied. After a pretreatment period without substitution, patients received intramuscular injections of testosterone enanthate, equivalent to 25, 50, 100, and 250 mg testosterone, or placebo. Each dose was given for 4 weeks, with injections given every 2 weeks. All patients with plasma testosterone values below 2 ng/ml during the pretreatment period reported impaired sexual function. They responded to testosterone injections (50, 100, and 250 mg) with improvement of sexual behavior, as rated by sexual desire and frequency of erections and ejaculations. In the range between 2.0 and 4.5 ng testosterone per ml, four patients reported high frequencies of erections and ejaculations that did not change after testosterone treatment. Four other patients with testosterone values in the same range reported impaired sexual behavior and were successfully treated with testosterone enanthate. These data indicate that male sexual behavior is testosterone dependent and that the individual limit of plasma testosterone below which sexual behavior is impaired lies between 2.0 and 4.5 ng/ml.

Adolescent↗

PubMed2003

Testosterone replacement therapy in male hypogonadism.

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

Androgens↗

PubMed1998

The effects of cortisol and testosterone on renal function in male Antechinus stuartii (Marsupialia).

Seasonal changes in the physiology of Antechinus stuartii result in complete male mortality after mating. The most important endocrine changes in males are large rises in plasma testosterone and cortisol concentrations. Glomerular filtration rate (GFR) in males declines coincident with high plasma testosterone and cortisol. In the present study GFRs were measured in males captured in May (when endogenous plasma testosterone and cortisol levels are low) and given depot injections of either saline, testosterone-only, cortisol-only or testosterone plus cortisol at doses designed to mimic plasma levels during the mating period. GFR decreased significantly with testosterone injection, independent of cortisol treatment. Urinary concentrations of sodium and chloride, and osmolality decreased significantly with cortisol treatment, although the addition of testosterone reversed the effect. Total urinary excretion of electrolytes was similar between groups. Plasma potassium levels significantly increased in testosterone plus cortisol treated males. Plasma sodium levels significantly increased and plasma chloride significantly decreased in all groups treated with cortisol. Water consumption significantly increased in all cortisol-treated males and food consumption significantly increased in all testosterone-treated males. The seasonal renal functional changes observed in A. stuartii were mimicked by testosterone administration.

Animals↗

PubMed1992

Post-transcriptional regulation of mouse renal cytochrome P450 2E1 by testosterone.

Our previous studies demonstrated that the sex-related difference in renal metabolism of N-nitrosodimethylamine in C3H/HeJ mouse was due to the sexual dichotomy of cytochrome P450 2E1 (P450 2E1) and that renal P450 2E1 in female mouse was inducible by testosterone. The present study demonstrates that the sex-related difference in renal P450 2E1 and the testosterone-mediated regulation also occurred in other mouse strains studied. The time- and dose-responses in the testosterone-mediated regulation of P450 2E1 were characterized. 19-Nortestosterone, an analog of testosterone, was shown to have an effect on the regulation of mouse renal P450 2E1 similar to that of testosterone. Testicular feminized mice (Tfm, a mouse strain devoid of functional androgen receptors) had about only one-tenth the renal P450 2E1 mRNA level as the wild-type male mice and testosterone treatment of the Tfm mice had no effect on the level of renal P450 2E1 mRNA. The result suggests that androgen receptor plays an important role in the sex- and testosterone-related regulation of mouse renal P450 2E1. To study the mechanism of the sex-related and testosterone-mediated regulation of P450 2E1 mRNA in mouse kidney, the transcription rate of the P450 2E1 gene was measured by a nuclear run-on transcription assay. Although the kidneys of male and testosterone-treated female mice had much higher steady-state levels of P450 2E1 mRNA, their transcription rates of the P450 2E1 gene were not higher than the kidneys of untreated female mice. This result suggests that the sex- and testosterone-related regulation of mouse renal P450 2E1 is predominantly at the post-transcriptional level.

Androgen-Insensitivity Syndrome↗

PubMed1992

The effect of budesonide and triamcinolone acetonide on hepatic microsomal testosterone metabolism in the rat.

The hepatic microsomal metabolism of testosterone was studied in male rats after treatment with either budesonide or triamcinolone acetonide for 13 weeks. The in vitro metabolism was determined using a testosterone concentration of 35 nM which is comparable to the levels found in plasma. It was shown that the total microsomal testosterone metabolism was decreased in budesonide-treated rats and increased in rats treated with triamcinolone acetonide. The testosterone metabolites produced were measured and thus it was revealed that budesonide treatment brought about its effect through a 50% decrease in the activity of steroid 5 alpha-reductase, but did not affect other reductive enzymes, or the oxidation of testosterone. Triamcinolone acetonide treatment decreased steroid 5 alpha-reductase activity by 95% and also decreased the activities of steroid 3 alpha- and 3 beta-reductases by more than 90%. In addition, treatment with triamcinolone acetonide caused a 50% increase in the oxidative metabolism of testosterone, which resulted in the observed increase in total testosterone metabolism. The presence of 0.1 microM budesonide in the microsomal incubations was without effect on testosterone metabolism. However, 0.1 microM triamcinolone acetonide inhibited testosterone oxidation by 65%, without affecting the reductive pathway of testosterone metabolism.

Animals↗

PubMed1988

Hepatic testosterone metabolism in male rats with portal bypass.

This study was performed to ascertain whether testosterone metabolism is altered in male rats with portal bypass, and whether such changes could contribute to the reduction in serum testosterone concentration and raised serum estrogen levels that are observed in this situation. The metabolic clearance rate of testosterone was determined by a prime-dose constant-infusion technique in male rats subjected to complete portal vein ligation and in sham-operated controls. Testosterone clearance was similar in rats with portal vein ligation and control rats (9.01 +/- 2.29 and 8.26 +/- 2.83 ml/min, respectively) but the clearance per gram of liver was greater in rats with portal vein ligation than in controls (1.18 +/- 0.18 versus 0.68 +/- 0.24 ml/min.g liver, p less than 0.0001). After 180 min of [3H]testosterone infusion, [3H]estradiol comprised 1.2% of plasma total radioactivity in male controls but was increased to 11% in rats with portal vein ligation (p less than 0.005). Similarly, biliary excretion of [3H]estradiol was eightfold greater in male rats with portal vein ligation compared with controls (p less than 0.001). In control male rats, the major metabolites of testosterone present in bile were 2 alpha-hydroxytestosterone, 16 alpha-hydroxytestosterone, and 7 alpha-hydroxytestosterone. Portal bypass was associated with reduced biliary excretion of 2 alpha-hydroxytestosterone and 16 alpha-hydroxytestosterone to approximately 50% of control, but there was no change in the excretion of 7 alpha-hydroxytestosterone. Conversely, portal bypass was associated with increased formation of dihydrotestosterone, indicating stimulated activity of testosterone 5 alpha-reductase. It is concluded that portal bypass in male rats is associated with altered pathways of testosterone metabolism and, in particular, with increased aromatization of testosterone to estradiol. The site of such estradiol formation has not been determined by this in vivo study. However, selective changes occurred in the regiospecific and stereospecific hydroxylation pathways of testosterone and in 5 alpha-reductase activity after portal bypass in male rats. It is concluded that portal bypass, in the absence of parenchymal liver damage, results in demasculinization and feminization of C19 steroid metabolism in the male rat liver. These metabolic changes could be revelant to the pathogenesis of changes in sexual characteristics in cirrhosis.

Animals↗

PubMed1993

Effect of testosterone on atherogenesis in cholesterol-fed rabbits with similar plasma cholesterol levels.

The aim was to examine the effect of testosterone on atherogenesis in cholesterol-fed, castrated male rabbits not mediated via different plasma cholesterol levels. The rabbits in the testosterone group (n = 19) and in the placebo group (n = 17) were injected intramuscularly twice weekly for 17 weeks with 25 mg testosterone enantate and placebo, respectively, reaching plasma testosterone levels of 50-150 nmol/l in the testosterone group. No effect of testosterone on liver function or body weight was detected, but at week 15 mean blood pressure was 75 +/- 2 mmHg (mean +/- S.E.) in the testosterone group compared with 69 +/- 2 mmHg in the placebo group (P < 0.05). To reduce variation in plasma cholesterol between the two groups, the amount of cholesterol fed to each rabbit was adjusted on the basis of weekly determinations of plasma cholesterol; the mean plasma cholesterol levels during the 17 weeks were 20.9 +/- 1.0 and 20.4 +/- 0.9 mmol/l for the placebo and testosterone groups. In the intima-inner medias of the aortic arch, the thoracic and the abdominal aorta there were no consistent significant differences in aortic cholesterol content, expressed either as nmol/cm2 or nmol/mg protein, between the two groups. However, the aortic cholesterol content tended to be lower in the testosterone group than in the placebo group. These findings suggest that in cholesterol-fed, castrated male rabbits, testosterone does not promote atherogenesis by an effect directly on the arterial wall.

Animals↗

PubMed1996

Effect of testosterone replacement therapy on lipids and lipoproteins in hypogonadal and elderly men.

We investigated the effects of long-term testosterone replacement in hypogonadal and elderly men on lipids and lipoproteins. Twenty-two men with initial serum testosterone concentrations below 3.5 ng/ml took part in the study: 11 with hypopituitarism (1st group) and 11 otherwise healthy elderly men with low testosterone levels (2nd group). Testosterone deficiency was replaced by intramuscular injections of testosterone enanthate 200 mg every second week. Plasma levels of sex hormones, gonadotropins, SHBG, lipids and lipoproteins were determined before the treatment and after 3, 6 and 12 months of treatment. During the treatment serum testosterone and estradiol increased significantly, reaching normal levels. This was associated with a decrease in total cholesterol (from 225 +/- 16.9 mg/dl to 202 +/- 13.6 mg/dl after 6 months and 198 +/- 12.8 mg/dl after 1 year of testosterone administration, P < 0.0001 in men with hypoandrogenism associated with aging and from 255 +/- 12.1 mg/dl to 214 +/- 10.6 mg/dl after 6 months and 206 +/- 9 mg/dl after 1 year of treatment, P < 0.0001 in men with hypopituitarism) and LDL-cholesterol concentrations (from 139 +/- 12.5 mg/dl to 126 +/- 10.7 mg/dl after 6 months and 118 +/- 9.8 mg/dl after 1 year of testosterone administration, P < 0.0001 in men with hypoandrogenism associated with aging and from 178 +/- 10.3 mg/dl to 149 +/- 10.2 mg/dl after 6 months and 140 +/- 7.3 mg/dl after 1 year of treatment, P < 0.001 in men with hypopituitarism). However, no significant decrease in HDL-cholesterol levels or HDL2- and HDL3-cholesterol subfractions was observed. The effects of testosterone replacement therapy on lipids and lipoproteins were similar in both groups with different aetiology of hypogonadism. No side effects on the prostate were observed. The results of this study indicate that testosterone replacement therapy in hypogonadal and elderly men may have a beneficial effect on lipid metabolism through decreasing total cholesterol and atherogenic fraction of LDL-cholesterol without significant alterations in HDL-cholesterol levels or its subfractions HDL2-C and HDL3-C.

Adolescent↗

PubMed1987

Serum testosterone concentrations in men with alcoholic cirrhosis: background for variation.

Median serum testosterone concentration of men with alcoholic cirrhosis (n = 216) did not differ significantly from normal controls (n = 51), but serum testosterone concentrations varied by a factor 43.9 in patients compared to 3.2 in controls (P less than .001). Nineteen percent of the patients had serum testosterone concentrations above 30 nmol/L. Serum concentrations of sex-hormone-binding globulin (SHBG) were significantly (P less than .001) raised, and serum concentrations of calculated nonprotein-bound and non-SHBG-bound testosterone were significantly (P less than .001) decreased in patients compared to normal control values. A number of background variables were analyzed with reference to serum testosterone concentrations by means of multiple regression techniques after having divided the patients into groups (A, B, C) with decreasing liver function by a modification of the Child-Turcotte's criteria. The only significant (P less than .01) background variables associated with log serum testosterone concentrations were: group C (beta = -0.828), group B (beta = -0.222), age (years) (beta = -0.012), duration of hospitalization (days) (beta = -0.0077), and concentration of SHBG (nmol/L) (beta = 0.0044). Neither previous nor recent (within last six months) alcohol consumption influenced serum testosterone concentrations significantly, but about 50% of the patients had abstained from ethanol for two months or more. The same background variables as above were included as significantly (P less than .01) associated with log serum concentrations of calculated nonprotein-bound testosterone and calculated non SHBG-bound testosterone, except that SHBG was insignificantly associated to any of the two proportions and that testicular volume was significantly (P less than .05) associated with log non-SHBG bound testosterone.(ABSTRACT TRUNCATED AT 250 WORDS)

Humans↗

PubMed1989

Competitive experience activates testosterone-dependent social aggression toward unfamiliar males.

Male hooded rats (350 to 450 g) were castrated and given subcutaneous implants of testosterone-filled or empty Silastic tubes. Four weeks later, half of the animals with testosterone implants were housed with an animal with an empty implant and left for 6 weeks. The other animals were adapted to a food-deprivation schedule, housed in testosterone-implant/sham-implant pairs and given a series of food-competition tests. Following the competition tests, all animals were observed individually in their living cage for aggression toward an unfamiliar intruder. Within the competitive situation, animals with testosterone implants were more aggressive and more successful at maintaining access to food than their cagemates with sham implants. In the unfamiliar intruder test, animals with testosterone implants that had been subjected to food competition were more aggressive toward an unfamiliar intruder than were animals with testosterone implants that had not been given competitive experience. Animals with testosterone implants given competitive experience were more aggressive than their castrated cagemates, but animals with testosterone implants not given competitive experience were not more aggressive than their cagemates. These results demonstrate that testosterone-dependent social aggression fostered by a competitive situation is elicited by an unfamiliar male intruder. They also confirm other evidence that activation of social aggression does not appear to require increased testicular testosterone secretion.

Aggression↗

PubMed1990

Aggression by ovariectomized female rats with testosterone implants: competitive experience activates aggression toward unfamiliar females.

Female hooded rats (250 to 325 g) were ovariectomized and bilaterally implanted with testosterone-filled or empty Silastic tubes. The testosterone-filled space in each tube was 10 mm long and this should produce a serum testosterone concentration 4 to 5 times that of an intact female, but well below that of a male. Three weeks following surgery, half of the animals with testosterone implants were housed with an animal with an empty implant and left for 6 weeks. The remaining animals were placed on a 23-hr food deprivation schedule, housed in testosterone implant/empty implant pairs, and then subjected to a series of food competition tests. Following the competition tests, all animals were individually tested in their living cage for aggression toward an unfamiliar female. In food competition, females with testosterone implants were more successful and more aggressive than their cagemates with empty implants. When tested for aggression toward an unfamiliar intruder, females with testosterone implants given competitive experience were more aggressive toward an intruder than were their cagemates with empty implants or females with testosterone implants not given the competitive experience. Females with testosterone implants but without competitive experience were not more aggressive toward an unfamiliar female than were their cagemates with empty implants. These results suggest that, in ovariectomized females with testosterone implants, hormone-dependent aggression fostered by a competitive situation is displayed toward unfamiliar females.

Aggression↗

PubMed1978

Prostaglandin inhibition of testosterone production induced by luteinizing hormone, dibutyryl cyclic AMP or 3-isobutyl-1-methyl xanthine in dispersed rat testicular interstitial cells.

Testicular interstitial cells were utilized to study the effects of prostaglandins (PG) on in vitro testosterone production and to examine the role of cyclic adenosine-3',5'-monophosphate (cAMP) in this process. Testosterone production was assessed after 3 hour incubations while cAMP accumulation was examined after a 0.5 hour incubation period. Testosterone and cAMP were measured by radioimmunoassay. None of the PGs tested (PGA, PGA2, PGB1, PGE1, PGE2, PGF1alpha PGF2alpha) altered basal testosterone production when present in incubates at concentrations of 1.3 X 10(-8) M to 1.3 X 10(-4). However, at concentrations of 1.3 X 10(-4) M all of these PGs were capable of decreasing Luteinizing Hormone (LH; 100ng)-induced testosterone production. The inhibition of LH-induced testosterone production by the B, E and F series PGs was less pronounced than that for the A series. PGA1 and PGA2 exhibited 80% and 95% inhibition, respectively, at 1.3 X 10(4) M. The inhibitory action of 4 X 10(5) M PGA1 or PGA2 was evident within 30 minutes. Preincubation of interstitial cells with indomethacin (10(-5) or 10(-6) M) for 30 minutes did not alter subsequent basal or LH (100ng)-induced testosterone production. Accumulation of cAMP was stimulated by LH (10 microgram) or by PGs (1.3 X 10(-4) M PGA1, PGA2, PGB1, PGE1 or PGF2alpha). The PG-induced cAMP accumulation thus occurred at concentrations where LH-stimulated testosterone production was inhibited. Furthermore, PGA1 and PGA2 (1.3 X 10(-4) M) inhibited testosterone production induced by either 3-isobutyl-1-methyl xanthine (MIX; 10(-4) M or 10(-3) M) or dibutyryl cAMP (dbcAMP; 10(-4) M or 10(-3) M). These results indicate that PGs can block testosterone production by a direct effect on testicular interstitial cells and suggest that PGs exert their inhibitory action distal to stimulation of cAMP formation. PGs do not appear to play a role in the mechanism of LH action.

1-Methyl-3-isobutylxanthine↗

PubMed1979

Testosterone metabolism by the prostate of the aging AXC rat.

Testosterone metabolism by the ventral prostate of inbred, senescent (36-month-old) AXC rats showed a shift to increased oxidative and diminished reductive metabolism when compared to young mature (3-month-old) or mature adult (6-month-old) AXC rats. The change was principally attributable to diminished production of 5 alpha-dihydrotestosterone and increased production of 4-androstenedione. By contrast, dorsolateral prostate testosterone metabolism in these same rats was always more reductive than that of ventral prostate and failed to show the post-maturation shift to oxidative testosterone metabolism which characterized ventral prostate. Co-incubation of either ventral or dorsolateral prostate from any of these rats with testosterone and estradiol showed that estradiol did not significantly affect prostate testosterone metabolism. Plasma testosterone content of senescent AXC rats was only 28% of that of mature adult rats. Chronic exogenous testosterone treatment enhanced reductive testosterone metabolism by ventral prostate and eliminated those changes in metabolite distribution which had differentiated testosterone metabolism by young and senescent AXC rats. The data support the interpretation that the aging-related diminution in AXC rat ventral prostate reductive metabolic capacity is primarily the consequence of diminished 5 alpha-dihydrotestosterone production secondary to diminished plasma testosterone content.

Aging↗

PubMed1994

Interactions between 5-hydroxytryptamine (5-HT) and testosterone in the control of sexual and nonsexual behaviour in male and female rats.

Two 5-hydroxytryptamine2 (5-HT2) agents, ritanserin and 1-(2,5-dimethoxy-4-iodophenyl)-2-aminopropane HCl (DOI) (both at 0.25 mg/kg IP), were administered to castrated males bearing graded testosterone implants (empty, 2.5-, 5-, and 10-mm length) and to normal and neonatally androgenized ovariectomized females bearing 10-mm testosterone implants. The results indicate that testosterone stimulates male sexual behaviour and appears to have a dose-related anxiolytic effect, but no effect on other nonsexual activities. 5-HT and testosterone had opposite effects on male sexual behavior, with ritanserin (5-HT antagonist) enhancing activity in both sexes and DOI (5-HT agonist) inhibiting behaviour in males, the latter being testosterone-dependent. Independent of testosterone, ritanserin reduced locomotion and exploration and increased anxiety in males, while DOI increased locomotion and exploration in both sexes. Ritanserin had a gender-specific effect on anxiety which was independent of testosterone, since in castrated males it was anxiogenic whether they bore testosterone implants or not, while in females it was anxiolytic whether the female were neonatally androgenized (250 micrograms/pup testosterone proprionate [TP] on day 1) or not. These results show that 5-HT and testosterone have opposite effects on male sexual behaviour and these may be interrelated. In adulthood, their effects on nonsexual activities are not inversely related and are independent of each other in contrast to the relationship seen in the neonatal period.

Amphetamines↗