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PubMed1977

Electrophysiological and contractile properties of the levator ani muscle after castration and testosterone administration.

Electrical and contractile properties of the levator ani muscle were studied in normal rats, in castrated rats and in castrated rats treated with testosterone. 2. No significant changes in the frequency of miniature end-plate potentials were found 6 months after castration. The frequency increased already 6 h after testosterone treatment; an increase of about 100% was observed after 7 days of testosterone treatment. 3. Castration led to a 2-fold increase of the input resistance of the muscle fibres. After 7 days of testosterone treatment the input resistance was only slightly higher than normal. 4. The weight of the muscle was decreased to 18% of the control value after 6 months castration. It increased to 46% after 7 days of testosterone treatment. 5. The muscles of castrated animals revealed a prolongation of contraction time and marked changes in maximal rate of tension development and half relaxation time. Partial recovery of these parameters was found after 7 days of testosterone treatment. 6. Long-term castration did not induce any denervation-like changes of action potential parameters, and no tetrodotoxin resistance was found in spite of marked muscle atrophy.

Anal Canal↗

PubMed1975

The effect of castration and testosterone replacement on specific proteins and androgen levels of the rat epididymis.

The normal weight increase of the epididymis during sexual maturation and its maintenance through adulthood were found to be dependent on the provision of androgens. Binding of [3H]dihydrotestosterone (DHT) to the epididymal 8S cytoplasmic receptor gradually decreased after castration to become undetectable after 25 days. Binding to the androgen binding protein (ABP) was absent 4 days after castration and was not reinduced by 3 weeks of testosterone (T) administration. Unilateral castration for periods of up to 27 days showed the disappearance of ABP with preservation of the 8S receptor on the castrated side, indicating a testicular source for ABP and the epididymal origin of the 8S receptor. The tissue concentrations of T and DHT in the epididymis became undetectable 30 days after castration and were restored to normal values by administration of testosterone in large doses (1.5 mg/100 g BW). Similar results were obtained in rats castrated at 10 days of age and injected with testosterone until 60 days old. The ratio DHT/T was depressed in the castrate and increased with testosterone treatment. The protein content of the epididymis (mg of protein/g wet weight) was also found to be influenced by androgens. Our results show evidence of some mechanisms involved in the trophic effect of androgens upon the epididymis and suggest the possible androgenic control of epididymal 5alpha-reductase activity. They also indicate that a testicular factor is required for the maintenance of the 8S cytoplasmic androgen receptor. It is not known whether this factor is testosterone or some other testicular secretion.

Androgens↗

PubMed1975

Relation between circulating levels of testosterone lh and fsh in intact and castrated, adult, male rats after testosterone administration.

Serum levels of LH, FSH and testosterone were measured by radioimmunoassay in intact and castrated, adult, male rats after testosterone was administered subcutaneously for seven days in doses ranging from 25 to 200 mug per 100 g body weight per day. Such treatment increased circulating testosterone both in intact and castrated rats, but its effects on serum gonadotrophins were different in these animal groups. All doses of testosterone suppressed serum LH and FSH in the normal rat. In the castrates, treatment with the lowest dose of testosterone resulted in serum LH levels significantly above the high castrate levels, while serum FSH tended to drop. Administration of the highest doses of testosterone did not depress serum LH and FSH in the castrates to those of intact, normal animals, though serum testosterone in these castrates was much higher than in normal, male rats. It is concluded, that the sensitivity of the hypothalamic-pituitary system for daily, subcutaneous testosterone administration during seven days is not the same in the intact and castrated, adult, male rat and that testicular factors different from testosterone may play a role in regulating production and/or secretion of gonadotrophins by the hypophysis in male animals.

Animals↗

PubMed1979

Interaction of luteinizing hormone-releasing hormone, cyproterone acetate and arginine vasotocin on plasma levels of luteinizing hormone in intact and castrated adult male rats.

Treatment of unanesthetized castrated adult male rats every 3 h for 48 h with either 5 microgram of arginine vasotocin (AVT) and/or 1 microgram luteinizing hormone-releasing hormone (LRH) caused a significant inhibition of plasma levels of luteinizing hormone (LH) and compared to castrated control rats receiving diluent only. However, the intravenous (iv) injection of 1 microgram of AVT into urethane-anesthetized male rats which had been castrated for 0, 24 or 48 h did not affect plasma levels of LH at 10, 20 or 60 min following injection compared to their respective diluent-treated castrated control rats. Similarly, the iv injection of either 100 ng, 1 microgram or 10 microgram AVT was unable to acutely affect plasma levels of LH in intact male rats. Following the iv injection of 2 doses of 50 ng LRH spaced 1 h apart in anesthetized castrated male rats, 2 peaks of equal magnitude in plasma LH were noted. Castrated rats treated with 2 injections spaced 1 h apart of LRH + AVT had significantly higher plasma levels of LH than did rats treated with LRH alone. In subsequent studies, both AVT and arginine vasopressin were observed to augment the plasma response of LH to an injection of LRH whereas oxytocin had no effect. A single injection of AVT + LRH significantly augmented the plasma titers of LH compared to levels observed in LRH-treated control rats as did a second injection 1 h later. The administration of cyproterone acetate sc for 2 days by itself had no effect on plasma LH but in conjunction with LRH caused a marked rise in plasma LH compared to intact rats treated with LRH alone. AVT in combination with LRH and cyproterone acetate caused a significant elevation in plasma LH at 60 min post-injection when compared to plasma levels of rats treated with LRH alone or the combination of LRH and cyproterone acetate. It is concluded that acute intravenous injections of AVT augment the LH-releasing activity of LRH; chronic treatment for 48 h, however, with LRH + AVT leads to a significant depression of plasma LH perhaps due to an exhaustion of the releasable pool of LH in the anterior pituitary.

Animals↗

PubMed1977

Specific protein synthesis in isolated epithelium of guinea-pig seminal vesicle. Effects of castration and androgen replacement.

Four intrinsic soluble secretory proteins are synthesized in vitro by isolated seminal-vesicle mucosa from sexually mature guinea pigs. Newly synthesized specific proteins labelled with [(14)C]glycine and [(14)C]lysine were precipitated by using double-antibody immunoprecipitation techniques and their radioactivity was assessed. Rates of synthesis were determined on each of 5 days after castration. By 5 days after castration the wet weight of the epithelium decreased to 42% of intact control values; the absolute amount of specific protein synthesized in vitro after 60min incubation decreased to 28% and the 27500g cytoplasmic protein content decreased to 31%. Thus androgen deprivation leads to a decrease in general protein synthesis in vivo, as well as to a decrease in specific protein synthesis in vitro. Specific protein synthesis comprised 76% of the total protein formed in isolated tissue from animals 5 days after castration as compared with 99-100% in tissue from intact animals. At 72h after an injection of testosterone or dihydrotestosterone, seminal-vesicle epithelium wet weight, cytoplasmic protein content and capability for synthesizing specific proteins in vitro were restored to approx. 70% of normal values. At 72h after onset of therapy with 3alpha-androstanediol, both epithelium wet weight and cytoplasmic protein content had increased significantly, but without a corresponding increase in the capability of the isolated tissue to synthesize specific proteins. The soluble labelled proteins synthesized in vitro by isolated epithelium from intact animals during 60 or 120min incubation were essentially entirely immunoprecipitable, i.e. specific. In contrast, approx. 29% of all soluble protein newly synthesized by isolated epithelium from animals 5 days after castration was acid-precipitable, but not immunoprecipitable, i.e. ;non-specific'. The injection of testosterone into castrated animals inhibited the synthesis of the non-specific fraction by isolated tissue. The effects of castration on the ultrastructure of guinea-pig seminal-vesicle epithelium are also presented.

Androgens↗

PubMed1975

Effect of castration upon hypothalamic luteinizing hormone releasing factor (LH-RF).

The effect of castration upon hypothalamic LH-RF synthesis and content was determined in mature male rats. In each single experiment 20 hypothalami from both normal and 60-day-castrated rats were bisected into symmetrical portions. For the determination of LH-RF synthesis 20 hypothalamic halves were incubated for 120 min. After incubation the tissue was homogenized in medium containing 1 N acetic acid, and centrifuged; 1.0 ml of the supernatant was used to test LH-RF activity. In the other 20 halves, hypothalamic LH-RF content was determined: the samples were homogenized without incubation in 1 N acetic acid, centrifuged, and LH-RF activity was tested in 1.0 ml of the supernatant. LH-RF activity was determined in vivo in ovariectomized rats pre-treated with estrogen-progesterone by measuring, by radioimmunoassay, the LH modifications in serum after the i.v. administration of the extracts. Hypothalamic LH-RF content was significantly higher in control than in castrated rats (p is less than 0.001). After incubation there were no changes in the LH-releasing potency of control hypothalami compared with non-incubated tissue, whereas a significant increase (616%) was found after the incubation of hypothalami from castrated rats. On the other hand, after incubation LH-RF activity was higher (p is less than 0.02) in castrated than in control hypothalami. These results suggest that castration stimulates the release and synthesis of hypothalamic LH-RF in male rats.

Animals↗

PubMed1979

Administration of gonadal steroids to the castrated male rat prevents a decrease in the release of gonadotropin-releasing hormone from the incubated hypothalamus.

The influence of testosterone on gonadotropin-releasing hormone (GnRH) secretion was assessed indirectly by altering the serum testosterone concentration of male rats and measuring GnRH release from their incubated hypothalami 1 wk later.GnRH release from hypothalami of castrated rats was 13.4+/-1.2 (SE) pg/h, compared to 35.3+/-3.8 pg/h from hypothalami of intact rats (P < 0.001). GnRH release from the hypothalami of castrated rats treated with testosterone propionate, 100 or 500 mug daily, was 25.0+/-3.4 pg/h and 27.9+/-3.6 pg/h, which is significantly greater (P < 0.05 and P < 0.01, respectively) than that from hypothalami of castrated rats treated only with sesame oil.A similar decrease in GnRH release from hypothalami of hypophysectomized rats and prevention of this decrease by treating the hypophysectomized rats with testosterone propionate is evidence that the observed effects of testosterone are not mediated via luteinizing hormone and(or) follicle-stimulating hormone secretion. Treatment of castrated rats with either dihydrotestosterone propionate or estradiol benzoate also prevented the decrease in GnRH release from the hypothalami of castrated rats. We conclude that testosterone, dihydrotestosterone, and estradiol all prevent the decrease in GnRH release from hypothalami of castrated rats treated with these steroids. The possibility exists that these steroids may also maintain GnRH secretion in vivo.

Animals↗

PubMed1977

Differential response of luteinizing hormone-releasing hormone in the basal hypothalamus and the preoptic area following anterior hypothalamic deafferentation and/or castration in male rats.

Serum LH, FSH and LHRH concentrations and the LHRH content in the medial basal hypothalamus (MBH) and the preoptic area (POA) were measured by radioimmunoassay in male rats 33 days after anterior hypothalamic deafferentation (AHD) and/or castration. In castrate rats following AHD, there was a significant decrease in serum LH, FSH, and LHRH concentrations, whereas, in intact rats, serum LH was elevated in AHD over the sham AHD rats. Castration and AHD each caused a significant fall in the LHRH levels in the MBH; the decline was more pronounced in rats undergoing both castration and AHD. In contrast, deafferentation in intact and castrate rats resulted in the accumulation of LHRH activity in the POA. These studies support the suggestion that a) a substantial amount of LHRH normally found in the MBH of intact and castrate male rats originates in the rostral regions and, b) the LHRH-containing neural elements within the MBH have the competence to respond to a loss in the circulating testicular steroids.

Animals↗

PubMed1976

Prolactin binding sites in the male rat liver following castration.

Specific binding sites for prolactin (PRL) have been detected in membrane preparations from the liver of the male rat following castration. The magnitude of the increased binding following castration varied with the age of the animals and with the time after castration. The effect of castration did not appear to be PRL mediated, since increases or decreases of serum PRL levels after pharmacological agents had no effect on PRL binding. The pituitary, however, seems to have a critical role in mediating the increase in PRL binding. Adrenalectomy did not influence the extent of binding of PRL after castration. Testosterone administration, however, completely prevented the increased PRL binding which followed castration. These studies suggest that testosterone has a modulating effect on hepatic PRL binding sites. The maintenance of such binding activity requires not only PRL, but also a functioning pituitary.

Adrenal Glands↗

PubMed1976

Effect of unilateral and bilateral castration and cryptorchidism on serum gonadotrophins in the rat.

The effects of unilateral and bilateral cryptorchidism and castration on serum concentrations of testosterone, FSH and LH in adult male rats were examined. The results provide no evidence for compensatory growth or development of the remaining scrotal testes up to 32 days after unilateral castration, although the scrotal testis of unilaterally cryptorchid rats showed enlargement when compared with those of control rats (P less than 0 - 05) at 32 days. Unilateral treatments had few significant effects on serum hormones, but testosterone was increased on day 4 (P less than 0 - 05) in unilaterally cryptorchid rats and on day 32 (P less than 0 - 05) in unilaterally castrated rats, compared with controls, and FSH levels were higher in unilaterally castrated rats on day 16 (P less than 0 - 05). Bilateral cryptorchidism caused an increase in serum FSH within 4 days (P less than 0 - 05) and in serum LH by 8 days (P less than 0-05) after surgery, with both hormones reaching levels double those found in control rats (P less than 0 - 01) by day 16, while testosterone levels were maintained at or above control values. Bilateral castration resulted in a marked decrease in testosterone levels (P less than 0 - 01) and a sharp increase in serum gonadotrophins. FSH had nearly doubled (P less than 0 - 01) and LH had increased fourfold (P less than 0 - 01) 4 days after castration, their levels reaching 773% (LH) and 287% (FSH) of control values by 32 days (P less than 0 - 01). The observations support the hypothesis of a separate, testosterone-independent feedback system of the testis on the hypophysis.

Animals↗

PubMed1977

Effect of neonatal castration on the content of hypothalamic LHRH, pituitary LH and plasma LH in developing male rats.

The content of hypothalamic LHRH and concentration of LH in pituitary and plasma were measured on day 5, 7, 10, 14, 17, 22, 25, 30, 45, 52 and 60 in male rats which were bilaterally castrated on day 2. The levels of plasma LH were significantly higher in all the groups of castrated rats than in normal male rats of corresponding ages. The concentration of plasma LH did not rise progressively but showed day to day fluctuation apparently due to alteration of sexual differentiation of the hypothalamus. The concentration of pituitary LH was significantly lower in neonatally castrated rats compared to normal male rats except on days 17, 25 and 30. The content of hypothalamic LHRH declined initially following castration, but from day 17 onwards significantly higher levels of hypothalamic LHRH were maintained in neonatally castrated rats than in intact control. Initial decline in the content of hypothalamic LHRH may be because of stimulation of release of LHRH which exceeds maximal rate of synthesis and subsequent increase in the content of hypothalamic LHRH may be due to enhanced LHRH synthesis as a result of castration.

Aging↗

PubMed1979

[Studies on the kinetics of the RNA metabolism in the prostate of normal and castrated rats (author's transl)].

In the prostate of adult Wistar rats the RNA/DNA quotient of the whole organ as well as the amount of RNA and DNA in the nucleus was measured at different times after castration. Furthermore the half-life time for the turnover of the RNA in the nucleus and the cytoplasm was determined for normal and castrated rats with the aid of pulse labelling using [5(-3)H]uridine. A mathematical model was developed to analyze the experimental results. This model enabled us to make differentiated statements on the heterogeneous nuclear RNA (hmRNA) and the remaining RNA in the nucleus. The evaluation of the experimental values gave the following results: 1. By deprivation of androgens the uptake of [3H]uridine into the prostate is lowered. 2. The amount of DNA in the morphologically intact nucleus remains constant at least up to the 12th day after castration. 3. 6 days after castration the amount of hmRNA decreases to 1/10 and that of cytoplasmic RNA to 1/4. 4. The half-life time for the decrease of the whole nuclear RNA is 3.7 d and that of the cytoplasmic RNA 1.7 d. 5. The half-life time for the turnover of hmRNA is 16 min and that of cytoplasmic RNA about 2 days. 6 days after castration the half-life times are unchanged. The experimental results suggest that the observed decrease of nuclear RNA following castration can mainly be attributed to a reduced synthesis of hnRNA, while the decrease of cytoplasmic RNA is first of all caused by an increase in RNA degradation.

Animals↗

PubMed1979

Serum sex hormone binding globulin and testosterone binding after estradiol administration, castration, and their combination in men with prostatic carcinoma.

We measured serum sex hormone binding globulin (SHBG) binding capacity, the index of testosterone binding to SHRG, and the serum concentrations of testosterone, 5 alpha-dihydrotestosterone, and estradiol in 16 patients treated for advanced prostatic carcinoma in order to evaluate the effectiveness of various therapeutic regimes in reducing total and biologically active androgen in blood. Polyestradiol phosphate (Estradurin, 80 mg im as a monthly injection) treatment alone is not as efficient as castration in reducing serum testosterone and 5 alpha-dihydrotestosterone. There was no clear difference between the castration and combination treatment (castration followed by polyestradiol phosphate administration) groups in this respect. It is apparent that Estradurin treatment alone and in combination with castration results in small but significant increases in SHBG binding capacity, whereas this parameter did not alter after castration alone. All three forms of treatment resulted in relatively similar significant increases in the index of testosterone binding to SHBG. The rather mild effect of Estradurin on the parameters measured may be attributable to the binding of the exogenous estradiol to SHBG, which thus greatly reduces its biologic activity. We concluded that castration is clearly more effective in reducing the amount of biologically active testosterone than Estradurin and the combination of these treatments has little influence on further reducing total or biologically active circulating testosterone.

Aged↗

PubMed1976

Androgen metabolism by rat epididymis. 3. Effect of castration and anti-androgens.

The in vivo and in vitro metabolism of 3H-testosterone by rat epididymis and the changes in epididymal weight have been studied after castration and treatment with anti-androgens. The utilization of 3H-testosterone was greatly reduced after castration as was the formation of 5alpha-reduced 17 beta-hydroxy metabolites. The formation of the 17 -keto metabolites was unaffected. Castration had no effect on the ratio between water and ether soluble radioactivity. Administration of testosterone propionate, necessary for giving normal stimulated prostate weight (150 mug/day), restored the metabolism of testosterone to approximately normal values. Estradiol benzoate and progesterone inhibited metabolism of testosterone in vitro and greatly reduced the formation of DHT (17 beta-hydroxy-5alpha-androstan-3-one) and 3 alpha-diol(5 alpha-androstane-3 alpha-17 beta-diol) by experiments both in vivo and in vitro. No effect of cyproterone acetate could be demonstrated on either the in vitro or in vivo metabolism of testosterone. Castration for 14 days reduced the epididymal weight to about 30% of that found in intact animals. Administration of testosterone propionate restored the epididymal weight to about 80% of normal. Estradiol benzoate and cyproterone acetate given to intact rats led to a decrease in the epididymal weight. Progesterone had no such effect. In 14 days castrated rats receiving testosterone propionate all three anti-androgens reduced the weight of the epididymis. In conclusion, our results show that the metabolic conversion of testosterone in epididymis to DHT and 3 alpha-diol is dramatically dependent on the hormonal status of the animal; castration or treatment with anti-androgens causes a reduced formation of the "active" androgens whilst testosterone replacement treatment restores the metabolism of testosterone to normal.

Androgen Antagonists↗

PubMed1976

Effects of castration and androgen-substitution on the morphology of the epididymal epithelium of the Japanese monkey, Macacus fuscatus, as revealed by scanning electron microscopy.

The caput epididymidis from castrated and androgen-supplemented, castrated Japanese monkeys was observed with the scanning electron microscope. The experimental findings were compared with the normal structures in control animals. The epididymal lumen of control animals was lined by a tall, pseudostratified columnar epithelium possessing long, slender stereocilia which were densely arranged in a tuft-like form. After castration, the epididymal epithelium was decreased in height to one-fifth of controls. The stereocilia were also considerably reduced in length and in number, resulting in a flattened epithelial surface with polygonal boundaries. Frequent projection of a long, single cilium from an epithelial cell into the lumen was also a prominent feature in the epididymal ducts of the castrated animals. Administration of testosterone to the castrated animals resulted in almost complete recovery of the epididymal epithelium as well as regeneration of the stereocilia which regained a tuft-like arrangement.

Animals↗

PubMed1976

Effects of castration, testosterone and immobilization on the activities of choline acetyltransferase and cholinesterase in rat limb muscles.

Thirteen months after castration of male rats the weight of their soleus muscles was lowered to 82% and their choline acetyltransferase (ChAc) activity to 83% of control values. The administration of testosterone lasting 5 weeks increased the weight of the soleus muscles of castrated animals by 19% and their ChAc activity bu 37%. Changes in the activity of cholinesterase occurring after castration and testosterone treatment were not statistically significant. It is assumed taht the effect of testosterone on the activity of ChAc was mainly due to an increase in the functional activity of the motoneurones innervating the muscle. Rapid developmental increase of ChAc activity was observed in the muscles of intact rats between the age of 48 and 82 days. During this period of development the activity of ChAc rose faster than the weight of the muscles. Testosterone had no effect on the weight and ChAc activity of the soleus and extensor digitorum longus muscles of non-castrated rats after 1 week's administration; after 5 weeks' administration the weight of the muscles and their ChAc activity were diminished. After the soleus muscles of non-castrated rats had been immobilized for 10 days, their ChAc activity was 56% and their weight 51% of control values. The administration of testosterone did not alter the effect of immobilization on the ChAc and weight of the muscle.

Acetyltransferases↗

PubMed1975

Effects of coincubation of the pituitary and hypothalamus of intact and castrate male rats and the influence of LH-RH on pituitary 5 alpha-reductase activity1,2.

Pituitary 5 alpha-reductase activity in intact male rats increases after the pituitary is incubated with the hypothalamus. Incubating the pituitary of castrate rats with the hypothalamus of intact rats relatively inhibits pituitary 5alpha-reductase activity. Coincubation of the pituitary and hypothalamus of castrate rats, or the pituitary of intact with the hypothalamus of castrate males, does not elicit changes in pituitary 5alpha-reductase activity. Different amounts of LH-RH in the incubation medium can modify 5alpha-reductase activity, i.e., activate it in the intact pituitary and inhibit it in the castrate pituitary. Hypothalamus from intact rats, which according to SHIN et al. [1974] is 'rich' in LH-RH, induces changes in pituitary 5alpha-reductase activity. The LH-RH-'poor' hypothalamus of castrate rats does not cause changes in this enzyme activity. The results suggest that there is a very close relationship between LH-RH and 5alpha-reductase activity in the pituitary.

Animals↗

PubMed1977

Gonadotropin secretion in cryptorchid and castrate rams and the acute effects of exogenous steroid treatment.

Gonadotropin secretion in cryptorchid and castrate rams and the acutve been determined. Rams made cryptorchid at 6 weeks of age had increased serum levels of luteinizing hormone (LH) and follicle stimulating hormone (FSH) when determined at 9 months of age. These levels approached those of the castrate animal; and yet serum levels of testosterone (T) were unchanged. Even though mean serum LH concentrations were elevated sixfold to eightfold over those of intact ram levels, a temporal relationship between this hormone and T was observed similar to that reported in the intact ram. Intramuscular injections of dihydrotestosterone had no effect on circulating levels of LH or FSH in either cryptorchid or castrate rams, whereas T effectively reduced these gonadotropins in castrate but not in cryptorchid rams. Only estradiol-17beta (E2) was effective in both cryptorchid and castrate rams. Estradiol was a potent inhibitor of LH secretion; however, its effect on FSH levels was less dramatic. This suggests that testicular products other than E2 may be important in the regulation of FSH production and/or release. Importantly, the inhibition of LH secretion lasted less than 12 h; whereas, the negative effects of E2 on FSH secretion lasted 72 to 144 h. In conclusion, results from this study show that T is not the single factor responsible for regulation of LH and FSH secretion in male sheep. Estradiol may be an important regulator of gonadotropin secretion, but 5alpha-reduction plays no apparent role in this process.

Animals↗