Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “CASTRATION”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 217 records · Page 12Linked to original sources
PubMed1979

The effect of subcutaneous injections of melatonin, arginine vasotocin, and related peptides on pituitary and plasma levels of luteinizing hormone, follicle-stimulating hormone, and prolactin in castrated adult male rats.

A sc injection of 2 micrograms arginine vasotocin (AVT) administered every 2 h for a 25-h period starting 1 h after castration of adult male rats caused a 43% reduction (P less than 0.05) in plasma levels of LH compared to diluent-treated castrated controls. In Exp 2, a sc injection of 5 micrograms AVT or diluent was administered to intact or acutely castrated male rats every 3 h for 48 h. After AVT administration, both plasma LH (P less than 0.001) and FSH (P less than 0.05) were significantly reduced, with a concomitant increase in pituitary levels of these gonadotropins. Using the same injection regimen in Exp 3, 250 micrograms melatonin had no effect on plasma or pituitary levels of LH in castrated male rats. In the fourth experiment, neither 1 IU arginine vasopressin nor 1 IU oxytocin had an effect on plasma or pituitary levels of LH, whereas 1 IU of AVT significantly lowered plasma levels of LH (P less than 0.05) and prevented the fall in the pituitary level of this gonadotropin (P less than 0.01) when compared to diluent-treated castrated control rats. Oxytocin (1 IU) significantly inhibited (P less than 0.01) plasma levels of FSH and raised plasma levels of PRL (P less than 0.01) in castrated male rats. No effect on plasma titers of PRL were observed after treatment of castrated rats with AVT in Exp 2 or 4. It is concluded that in acutely castrated male rats, AVT could possibly act either on the hypothalamus and/or the pituitary to affect pituitary and plasma levels of gonadotropins.

Animals↗
PubMed1975

The interaction of castration and photoperiod in the regulation of hypophyseal and serum gonadotropin levels in male golden hamsters.

Luteinizing hormone (LH) and follicle-stimulating hormone (FSH) were measured in intact and castrate adult male hamsters maintained on photostimulatory (LD 14:10) and non-photostimulatory (LD 6:18) light:dark cycles to assess the interaction of photic stimuli and gonadal hormones on pituitary gonadotropin release. Immunoreactive serum LH and FSH levels increased 1.6- and 8-fold respectively, within 3 days after photostimulated hamsters were castrated. In contrast, castration failed to alter serum LH concentration and had only a slight, if any, effect on FSH concentration in hamsters exposed to nonstimulatory photoperiods that induced testicular atrophy. In a second experiment, male hamsters previously maintained on LD 14:10 were castrated, transferred with intact animals to LD 6:18, and killed periodically over 60 days. In intact animals, pituitary content and serum levels of LH and FSH declined substantially during exposure to the non-stimulatory LD 6:18 cycle. In castrated animals, serum LH and FSH levels which had increased 2- and 8-fold in response to the castration eventually declined to about the levels found in the intact initial control animals. In contrast to serum gonadotropins, the increased hypophyseal content of LH and FSH following castration was not reduced during exposure to LD 6:18. Exposure to nonstimulatory photoperiods does not alter the increased hypophyseal LH and FSH content observed after castration. However, our results indicate that exposure to short days renders the hypothalamic-hypophyseal neuroendocrine system governing gonadotropin release relatively insensitive to gonadal steroid hormone feedback.

Animals↗
PubMed1983

Effects of late castration, zeranol and breed group on growth, feed efficiency and carcass characteristics of late maturing bovine males.

A total of 280 young bulls representing five breed groups with an average age of about 1 yr were assigned to five experimental treatments as follows: (1) emasculator castration at d 0, (2) surgical castration at d 0, (3) intact, (4) intact and implanted at d 0 and 70 with 36 mg of zeranol and (5) intact and implanted at d 0 with 72 mg zeranol. All animals were slaughtered and carcass data were collected after a feeding period of 141 d. Method of castration did not affect rate of gain. Intact males not implanted with zeranol gained 38.6% more (P less than .01) during the 141 d period than castrate males. Intact males from the two zeranol implant treatment groups did not differ from each other in gain, but averaged 11.1% more (P less than .01) during the 141 d period than males from the intact treatment group not implanted. Castrate males required 40.4% more (P less than .01) metabolizable energy (ME) and dry matter (DM)/kg gain than intact males not implanted, but intact males implanted with zeranol did not require less (P greater than .05) ME or DM/kg gain than intact males not implanted. Males castrated at about 1 yr showed a progressive decrease in secondary sex characteristics during the 141 d feeding period, while males from the three intact treatments showed a progressive increase. Zeranol did not have an effect on testicular weight or on aggressive male behavioral characteristics. Castrate males had greater (P less than .01) fat thickness at 12th rib, higher (P less than .01) marbling score and lower (P less than .01) cutability and retail product percentage than the males from the three intact treatments, which did not differ (P greater than .05) from each other in traits associated with carcass composition. The effect of treatment on lean color score, though significant, was not of major importance; all treatments produced meat of acceptable color. The longissimus muscle of castrate males had a finer texture (P less than .01) than longissimus muscle from males from intact treatments, which did not differ from each other (P greater than .05).

Adipose Tissue↗
PubMed1984

Effect of castration on plasma luteinizing hormone concentrations in prepubertal boars.

Mean concentrations and the occurrence of pulsatile release of luteinizing hormone (LH) were determined in 14-wk-old crossbred boars (50.5 +/- 1.5 kg) after bilateral or unilateral castration at 10 wk of age. Blood was collected at 10-min intervals for 5 h. Then gonadotropin releasing hormone (GnRH; 40 micrograms) was given and sampling was continued at 5-min intervals for 1 h. Compared with intact boars, bilateral castration increased (P less than .001) mean LH (982 +/- 56 vs 389 +/- 56 pg/ml), pulsatile releases of LH (7.0 +/- .6 vs 2.0 +/- .6 pulses/5 h) and LH pulse amplitude (617 +/- 29 vs 360 +/- 58 pg/ml). Unilaterally castrated boars did not differ from intact boars in any of the above measures of LH secretion. Testis weight increased more between 10 and 14 wk of age in the unilateral castrates than in the intact boars (432 +/- 42 vs 245 +/- 34%; P less than .05). Thus, compensatory hypertrophy occurred within 4 wk of castration. Plasma testosterone was lower for bilateral castrates than for intact animals (.1 +/- .8 vs 3.6 +/- .9 ng/ml; P less than .05) while unilateral castrates (3.8 +/- 1.0 ng/ml) and intact boars did not differ. Plasma estradiol concentrations in bilateral and unilateral castrates were not different from levels found in intact boars (1.8 +/- 1.8, 8.8 +/- 2.1 and 6.0 +/- 1.8 pg/ml, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1995

Castration therapy rapidly induces apoptosis in a minority and decreases cell proliferation in a majority of human prostatic tumors.

Major differences in the long-term clinical response to castration therapy of prostatic carcinoma suggests intertumoral differences in cellular response and defines a need for identification of patients with an eventually positive outcome as well as those in need of additional treatment. Using morphometry, monoclonal antibodies against Bcl-2, c-myc, Ki-67, and p53 proteins, and an in situ method to visualize apoptotic cells, we examined the short-term response of prostatic tumors to castration in core biopsies from 18 prostatic cancer patients taken the day before and 7 days after castration. At the histological level, 3 tumors seemed practically unaffected by castration. In 15 tumors, castration induced vacuolization of tumor cell cytoplasm and decreases in nuclear area and Ki-67 index. In these 15 tumors, apoptotic index was significantly increased in 6, principally unaffected in 6, and decreased in 3. The 6 tumors responding with an increase in apoptotic index were WHO grade 1 or 2 and negative for p53, c-myc, and Bcl-2 or contained only few Bcl-2- or c-myc-positive tumor cells before therapy. The 12 tumors in which apoptotic index was unaffected or decreased were WHO grade 2 or 3 and immunopositive for one or more of p53, Bcl-2, and c-myc proteins before therapy. The Bcl-2 index was significantly increased in 10 patients. Prostatic tumors may respond in a variety of possibly predictable ways to castration therapy including a decrease in apoptotic index. The magnitude of these responses are not correlated in individual tumors, suggesting that the common classification of prostatic tumors as either androgen dependent (dying after castration) or independent (not responding at all to castration) may be an oversimplification.

Apoptosis↗
PubMed1996

Expression of transforming growth factor-beta 1 in rat ventral prostate and Dunning R3327 PAP prostate tumor after castration and estrogen treatment.

BACKGROUND: In normal prostate, TGF-beta 1 is associated to castration induced apoptosis. Combined castration and estrogen treatment, but not castration alone, induces apoptosis in the Dunning R3327 PAP adenocarcinoma. METHODS: TGF-beta 1 expression in rat ventral prostate (VP) and Dunning R3327 PAP tumor was studied after castration and estrogen treatment, using competitive RT-PCR, in situ hybridization and immunohistochemistry. RESULTS: TGF-beta 1 mRNA level was 6 times higher in the tumor than in the VP. Combined castration and estrogen treatment increased TGF-beta 1 mRNA levels in the tumor from day 3, while castration did not. The TGF-beta 1 expression was located in the epithelial cells. CONCLUSIONS: The Dunning R3327 PAP tumor contains high levels of TGF-beta 1, which are further increased by combined castration and estrogen treatment. However, since this increase is not apparent until day 3, TGF-beta 1 probably does not contribute to the known induction of apoptosis in the tumor at day 1 after combined castration and estrogen treatment.

Adenocarcinoma↗
PubMed2000

Estradiol causes a dose-dependent stimulation of prostate growth in castrated beagle dogs.

BACKGROUND: Previous studies have shown that chronic treatment of castrate dogs with androgen and estrogen results in significant prostate growth. Estrogen treatment of castrate dogs in the absence of androgen has resulted in conflicting data as reported by several authors. The purpose of this experiment was to evaluate the effect of a physiological dose of estradiol on prostate growth in dogs, using ultrasound to study size changes over time. METHODS: Dogs (n = 25) were randomly divided into groups (n = 5) and treated as follows: castration alone (CC), castration plus low dose estradiol (E(2) low), castration plus high estradiol (E(2) high), castration plus estradiol and androstanediol (E(2)A), or no treatment (normal controls, NC). Silastic implants containing 5alpha-androstan-3alpha-17beta-diol (3alphadiol), and/or 17beta-estradiol were used for continous delivery of steroids. Prostate volume was measured by transrectal ultrasonography, and blood was drawn for hormone and sex hormone binding globulin (SHBG) determinations. RESULTS: Results show that serum estradiol and SHBG levels were fairly constant over 12 weeks in all groups. Estradiol-treated groups had mean serum estradiol values of approximately 40 and 60 pg/ml, respectively. Initially, all groups had similar prostate volumes. Over 12 weeks the castrate dogs had a decline in prostate volume, whereas the intact dogs and those treated with E(2) and 3alpha-diol maintained a constant prostate volume. Estradiol treatment caused a large, late onset (week 7), dose-dependent increase in prostate volume relative to the intact group (P < 0.01). At 12 weeks, animals were euthanized and prostates weighed. The mean prostate weights in each group were: NC 14.8 +/- 2. 9, CC 2.4 +/- 0.5, E(2)A 9.7 +/- 2.0, E(2) low 21.7 +/- 4.3, and E(2) high 63.6 +/- 12.6 g (geometric mean +/- SEM). Histologically, prostates of estrogen-treated dogs showed metaplastic squamous epithelium. CONCLUSIONS: These results demonstrate that estradiol causes marked dose-dependent stimulation of prostate growth in the castrate dog.

Anabolic Agents↗
PubMed2004

Histological structure of antlers in castrated male fallow deer (Dama dama).

Antlers are periodically replaced cranial appendages that, except for the reindeer, are grown only by male deer. The annual antler cycle is controlled by seasonal fluctuations of sex steroid concentrations in the blood, and accordingly castration of male deer causes deviations from normal antler growth. The present study investigated antler histology of castrated fallow bucks (Dama dama). Castration in early spring was followed by casting of the hard antlers carried by the bucks and the growth of a new set of antlers, which remained in velvet permanently. In the following year, numerous bony protuberances developed from the original antler surface. Further growth of these protuberances, which were formed by subperiosteal intramembranous ossification, led to a marked increase in antler diameter in the affected areas. Compared to antlers of intact bucks, the antlers of the castrates showed histological signs of immaturity, suggestive of a reduced bone remodeling and an impairment of the mineralization process. These changes point to the dependence of the above processes on a stimulation by higher levels of sex steroids. Two years after castration, the antlers also developed integumental thickening and showed an initial formation of skin outgrowths. Cystic structures were present in the skin, which were often filled with a presumably sebaceous and/or keratinous material. Formation of intradermal bone or cartilage was not observed in the antlers of the castrated fallow bucks. The histological structure of the skin outgrowths suggested that they were caused by a hypertrophy of the dermal component of the velvet. Due to the localized bone overgrowth, resulting from the periosteal bone apposition onto the original antler surface, skin-lined infoldings originated, which reached deep into the newly formed bone. Our study revealed no indication of invasive/destructive bone growth in the antlers, i.e., of a penetration of the newly formed bone tissue into the pre-existing bone. The hypertrophic bone growth in the antlers of the castrates is compared with other forms of periosteally derived hypertrophic bone formation, including osteomas, in the mammalian skeleton. It is discussed whether the skin and bone outgrowths of the antlers of castrated fallow bucks may be classified as benign tumors.

Animals↗
PubMed2005

Characterization of the autochthonous transgenic adenocarcinoma of the mouse prostate (TRAMP) as a model to study effects of castration therapy.

BACKGROUND: In order to learn more about short- and long-term effects of castration therapy, relevant model systems for prostate cancer are required. In this study, we examined whether the transgenic adenocarcinoma of the mouse prostate (TRAMP) tumor response to castration in C57BL/6 mice mimics that seen in patients. METHODS: Transgenic animals were examined before and 3 days after castration, at the ages of 17, 24, and 36 weeks. Moreover, 24-weeks old animals were castrated and followed for 6 months. Immunohistochemistry (IHC) and stereology were used to evaluate epithelial cell proliferation and death, blood vessel volume, androgen receptor (AR) expression, and transgenic expression of SV40 large T. RESULTS: Cancer developed preferentially in the dorso-lateral prostate lobe. Tumor burden and incidence of metastases increased with age. The majority of tumors were well differentiated, while poorly differentiated, large tumors and macroscopic metastases developed in 8% of the animals. Well and moderately differentiated tumors responded to castration with cessation of proliferation and induction of apoptosis. Poorly differentiated tumors and metastases did not respond. Castration prevented local tumor growth for at least 6 months in 82% of the cases. Although, 45% of the treated animals developed wide-spread metastatic disease suggesting that castration may enhance growth of distant metastases. CONCLUSIONS: The C57Bl/6 TRAMP tumor in several ways mimics how prostate cancer in patients responds to castration both in the short and long term, but some differences may also exist. This model can preferably be used to elucidate how this treatment works, and to test how it can be improved by additional therapies.

Adenocarcinoma↗
PubMed2006

Castration rapidly decreases local insulin-like growth factor-1 levels and inhibits its effects in the ventral prostate in mice.

BACKGROUND: The mechanisms by which castration induces prostate involution are largely unknown. METHODS: Early responses to castration in mouse ventral prostate (VP) were explored by quantitative microscopy, cDNA array expression, quantitative RT-PCR, and Western blot analysis. As several changes occurred in the insulin-like growth factor (IGF) system this was studied in more detail. Laser micro-dissection was used to localize sites of IGF-1 and IGF-1 receptor (IGF-R1) production. IGF-1 protein levels and IGF-R1 mediated signaling via insulin regulated substrate 1 and 2 (IRS-1 and 2) were examined. IGF-1 was injected into the VP in intact, and castrated mice and effects studied 1 day later. RESULTS: IGF-1 and IGF binding protein 2 (IGFBP-2) mRNA were rapidly reduced whereas IGFBP-3 and IGF-R1 mRNA were increased after castration. IGF-1 was principally produced in the stromal compartment, while IGF-R1 was produced in both epithelial and stromal cells. IGF-1 and IRS-1 protein levels were decreased 1 and 3 days after castration, respectively, while IRS-2 was unchanged. Inactivating phosphorylation of IRS-1 at serine 307 was increased 1 day after castration, and activating phosphorylation at tyrosine 612 was decreased 2 days later. These changes were accompanied by decreased cell proliferation and increased cell death in the glandular and vascular compartment. Local injection of IGF-1 increased vascular density and epithelial cell proliferation in intact mice, but had no effect in castrated animals. CONCLUSION: Decreased IGF-1 levels and action may mediate some of the key features of castration-induced prostate involution.

Animals↗
PubMed1988

Activation of a Ca2+-Mg2+-dependent endonuclease as an early event in castration-induced prostatic cell death.

Previous studies have demonstrated that castration-induced androgen withdrawal results in the fragmentation of prostatic DNA into nucleosomal oligomers, and this process comprises an early event in the activation of programed cell death in the rat ventral prostate. This DNA fragmentation could be due to changes in the chromatin conformation increasing its sensitivity to preexisting nucleases and/or to increases in the activity of the nucleases themselves. However, comparative kinetic analysis of in vitro DNA fragmentation induced by exogenous nucleases did not reveal any differences in the sensitivity of prostatic chromatin between intact and castrated rats. In contrast to these negative findings, using [3H] DNA as an exogenous substrate, it was shown that within the first day following castration there was a twofold increase in a Ca2+-Mg2+-dependent nuclease activity without a concomitant increase in other nuclear nucleases. This Ca2+-Mg2+-dependent nuclease activation occurred coincidental with the initial increase in nuclear DNA fragmentation following castration and preceded the enhanced appearance of morphological changes characteristic of dying cells (i.e., apoptosis), as well as the major increase in prostatic DNA loss. These results suggest that castration-induced androgen deprivation leads to a sequential activation of a Ca2+-Mg2+-dependent nuclease leading to the fragmentation of the genome into discrete nucleosomal-sized fragments of DNA, subsequently followed by the fragmentation of the nucleus itself (i.e., apoptosis) and eventually with the complete digestion of the nucleosomal oligomers into component nucleotides (i.e., DNA loss). Since the castration-induced nuclease is dependent upon calcium ions for maximal activity, a potential role of intracellular calcium in the early events activating prostatic cell death was investigated. Acute disturbances in intracellular calcium homeostasis within the ventral prostate by means of a potent calcium influx blocker, nifedipine, simultaneous with castration, resulted in a significant delay in the biochemical and morphological changes associated with prostatic cell death (i.e., prostatic weight loss, prostatic DNA loss, and DNA fragmentation). These results point to a potential role of intracellular calcium levels in the mechanism of activation of castration-induced death of the androgen-dependent epithelial cells in the ventral prostate.

Animals↗
PubMed1991

Effect of castration, DES, flutamide, and the 5 alpha-reductase inhibitor, MK-906, on the growth of the Dunning rat prostatic carcinoma, R-3327.

Male rats bearing implants of the Dunning rat prostatic carcinoma, R-3327, were used in a 42-day study to determine the effect of castration or orally administered flutamide (FL), DES (diethylstilbestrol) or the 5 alpha-reductase inhibitor, MK-906, on the growth of this androgen-responsive cancer. The rate of growth and final weights of the tumor and the ventral prostate (VP) were all reduced (P less than 0.05) by castration. Flutamide (25 mg/kg/day) significantly decreased tumor and VP weights in intact rats and castrates given 100 micrograms/day (SC) of testosterone propionate (TP) or dihydrotestosterone propionate (DHTP). It also significantly retarded tumor growth rate in TP- or DHTP-treated castrates and was marginally effective in intact animals. DES (100 micrograms/kg/day) reduced (P less than 0.05) tumor and VP weights of intact rats but did not significantly affect tumor growth rate or weight in castrates given TP or DHTP. These results indicated that the effect of DES on tumor growth is caused by its inhibition of the secretion or release of the gonadotropins necessary for testicular androgen production. MK-906 (25 mg/kg/day) affected neither the gross nor the histomorphology of the tumor in intact rats or castrates given TP or DHTP. Further, it caused no histological changes in the testes of intact rats. It did, however, significantly reduce VP weight in intact animals and TP-treated castrates but not in those given DHTP. This illustrates that the anti-androgenicity of MK-906 stems from its inhibition of DHT formation. The failure of MK-906 to influence tumor growth in the TP-treated castrates strongly suggests that the R-3327 tumor can respond to testosterone directly. If that is true, then its growth is unlikely to be affected by a pure 5 alpha-reductase inhibitor such as MK-906. In ancillary experiments, tumors from MK-906-treated animals were found to have reduced levels of DHT and, when assayed in vitro, to have a reduced capacity to convert [3H]-T to [3H]-DHT.

5-alpha Reductase Inhibitors↗
PubMed1992

Effects of castration on LH-RH patterns in intrahypophysial microdialysates.

A microdialysis system was used to monitor LH-RH patterns in the extracellular fluid of the adenohypophysis of testes-intact and short-term castrate rats. Male rats received guide cannulae implants fitted with stylets that extended into the anterior pole of the anterior pituitary gland. At the same time, animals were either castrated or received sham surgeries. On day 4 following surgeries, microdialysis probes were inserted into the guide cannulae and artificial CSF was pumped through the system at a flow rate of 2.5 microliters/min. Continuous samples were obtained from each animal over 5- or 10-min intervals throughout 4-7 sessions. Placements of probe tips were verified by histological examination of stained tissue sections. In vitro tests of microdialysis probe performance revealed an exchange rate of 4% at the 2.5 microliters/min flow rate. In vivo patterns of LH-RH in microdialysates obtained from sham-operated and castrate rats were pulsatile, as determined by the computer algorithm ULTRA. Pulses of LH-RH occurred at a higher frequency (P less than 0.05) in the castrates (1.30 +/- 0.26 pulses/h, n = 6) versus the sham-castrates (0.87 +/- 0.06 pulses/h, n = 11). Mean LH-RH pulse amplitude (castrates delta 0.24 +/- 0.03 pg, testes-intact delta 0.42 +/- 0.06 pg) and mean LH-RH levels (castrate 0.37 +/- 0.04 pg/10 min, intact 0.48 +/- 0.06 pg/10 min), however, were not significantly changed by castration (delta = difference between trough and peak LH-RH value of an LH-RH pulse).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1993

Testosterone is required for the stimulatory effects of 8-OH-DPAT on sexual behavior in castrated male rats.

The stimulatory effects of 8-OH-DPAT (8-hydroxy-2-(di-n-propylamino)tetralin) on male sexual behavior in the absence and presence of testosterone were investigated. Male rats (n = 12) were castrated and tested for sexual behavior (15 min, with an estrous female) up to 1 year after castration. Castration caused an abrupt decrease (50%) in the number of intromissions before first ejaculation, and the number remained stable for about 8 weeks. Between 8-12 weeks after castration, when ejaculation frequency was low, 0.2 or 0.4 mg/kg 8-OH-DPAT had no effect on ejaculation frequency, but significantly decreased the number of intromissions before first ejaculation. In weeks 17-18 after castration, 0.4 mg/kg 8-OH-DPAT no longer affected copulatory behavior. A 5-mm testosterone-filled Silastic capsule (implanted at week 19 after castration) resulted in subnormal plasma testosterone levels (mean 4.4 nmol/l) and did not fully restore male copulatory behavior. Administration of 8-OH-DPAT (0.2 and 0.4 mg/kg) was followed by an increase in ejaculation frequency and a decrease in ejaculation latency. Five months later, when plasma testosterone levels were very low (mean 0.6 nmol/l), 8-OH-DPAT (0.4 mg/kg) significantly increased the mean number of intromissions and ejaculations and decreased the number of intromissions before first ejaculation, intromission latency and ejaculation latency (borderline). The present results suggest that testosterone is required for the activating effects of 8-OH-DPAT on sexual behavior in castrated male rats, tested 17-52 weeks after castration.

8-Hydroxy-2-(di-n-propylamino)tetralin↗
PubMed1986

Proliferative response of seminal vesicle cells to androgen and estrogen in neonatally castrated mice.

Proliferation and death of androgen- and estrogen-responsive cells in seminal vesicles were compared between neonatally and adult (on Day 60 after birth) castrated mice. Daily injections of either testosterone propionate (TP) or estradiol-17 beta (E2) were started on Day 90 after birth; the incorporation of 5-[125I]iodo-2'-deoxyuridine ([125I]IdUrd) into the whole seminal vesicles was used as an index for proliferation. Although the peak of [125I]IdUrd uptake was observed 3 days after starting TP injections in both neonatally and adult castrated mice, the peak was lower and the period of proliferation was much longer in the former than in the latter. When TP injections were stopped, the fraction of surviving cells that synthesized DNA on Day 3 of TP injections was much larger in neonatally than adult castrated mice. The difference was attributed to the presence of TP-induced proliferation of fibromuscular cells in the neonatally castrated mice but not in the adult castrated mice; only the fibromuscular cells but not epithelial cells survived after stopping TP injections. Although injections of E2 increased the proliferation of epithelial cells but did not the weight of seminal vesicles in adult castrated mice, the same procedure increased the proliferation of both epithelial and fibromuscular cells and the weight in neonatally castrated mice. The E2-induced fibromuscular cells seemed to survive in the presence or absence of E2. The present results seem to indicate that androgen- and estrogen-induced proliferation of fibromuscular cells is irreversible in seminal vesicles of neonatally castrated mice and that the depletion of androgen in the seminal vesicle during neonatal and prepubertal periods is at least in part compensated by the administration of androgen, even after 90 days of age.

Androgens↗
PubMed1989

Comparison of residual C-19 steroids in plasma and prostatic tissue of human, rat and guinea pig after castration: unique importance of extratesticular androgens in men.

The concentrations of dehydroepiandrosterone (DHEA), its sulfate (DHEAS), androstenedione (A-dione), testosterone (T) and dihydrotestosterone (DHT) have been measured before and after castration in men and two animal models, namely the rat and the guinea pig. In adult men, the pre-castration levels of plasma DHEAS and DHEA were measured at 1839 +/- 320 and 2.4 +/- 0.5 ng/ml, respectively, while in both animal models, the concentrations of these two steroids were below 0.3 ng/ml. Orchiectomy in men reduced plasma T and DHT levels from 2.9 +/- 0.1 and 0.60 +/- 0.10 to 0.42 +/- 0.21 and 0.05 +/- 0.01 ng/ml (P less than 0.01), respectively, while there was no significant effect observed on DHEAS, DHEA and A-dione levels. By contrast, castration in the rat reduced the low levels of circulating DHEA and A-dione below the detection of the radioimmunoassay (RIA) used. In castrated guinea pig, a small quantity of plasma A-dione (0.07 +/- 0.02 ng/ml) was measured while DHEA was undetectable. Moreover, in the rat and guinea pig, plasma T and DHT levels became undetectable. Following administration of the antiandrogen Flutamide for two weeks in the castrated rat and guinea pig, prostate weight was not further reduced, thus indicating that there is no significant androgenic activity left following castration of these two species. In fact, castration in the rat and guinea pig caused a decrease in prostatic levels of DHT from 4.24 +/- 0.351 and 9.42 +/- 1.43 ng/g, respectively, to undetectable levels. In men, on the other hand, the prostatic DHT levels were only inhibited from 5.24 +/- 0.59 to 2.70 +/- 1.50 ng/g, respectively. As expected, when Flutamide was administered to the rat and the guinea pig, the levels of prostatic steroids remained undetectable while, in men, the DHT content in the prostate was further reduced to undetectable values. In summary, the plasma levels of DHEAS, DHEA, delta 4-dione are markedly different between men and both animal models used and furthermore, measurements of prostatic levels of androgens suggest that the high plasma levels of these steroids are likely responsible for the presence of important amounts of DHT in human prostate after castration.

Aged↗
PubMed1988

Retention of masculine sexual behavior following castration in male B6D2F1 mice.

The reduction of masculine sexual behavior following castration varies widely among genotypes. In contrast to the loss of sexual behavior by castrated males of other strains, males of the B6D2F1 genotype retain the ejaculatory reflex for many weeks after castration. The present study examined this retention phenomenon. Masculine sexual behaviors were measured before and after castration or sham operation in male C57BL/6J, DBA/2J, and B6D2F1 mice. Castrated C57BL/6J and DBA/2J males showed a rapid decline in copulatory behavior. In contrast, 30% of the B6D2F1 males continued to ejaculate 25 weeks after castration. Regardless of whether or not sexual behaviors were retained, levels of plasma testosterone and hypothalamic nuclear estrogen receptors were reduced by castration. These results suggest that the intra- and inter-strain differences in the retention of sexual behavior following castration are not due to differences in levels of steroid hormones. Further, some B6D2F1 males retain the ability to copulate in the absence of gonadal hormone levels required for the maintenance of sexual behavior in other genotypes.

Animals↗
PubMed1988

Peripubertal castration of male rats, adult open field ambulation and partner preference behavior.

The validity of the hypothesis put forward earlier, that testicular secretions during puberty have an organizing effect on open field ambulation was examined. Male rats were castrated or sham-operated at days 21, 43 or 70. At the age of 17 weeks the males were tested in an automated, octagonal open field (3 consecutive days, 3 min/day) for locomotor activity. Male rats castrated at day 21 or day 43 ambulated more than sham-castrated controls. Males castrated at day 70 did not differ from sham-castrated controls. It thus appears that pubertal testicular secretion(s) organize adult open field locomotor activity in male rats. From 18 weeks of age partner preference behavior was tested in the same open field apparatus with one adjacent cage containing an ovariectomized female and an opposite one containing an ovariectomized female brought into heat. The females in the adjacent cages were separated from the experimental males in the octagonal cage by wire mesh. Peripubertally castrated males did not show a clear-cut partner preference, whereas the intact males preferred the vicinity of the estrous female. There were no differences among the males castrated either before, during or after puberty. Testosterone treatment (crystalline T in silastic capsules) caused peripubertally castrated males to prefer the estrous female. Thus, adult partner preference behavior does not seem to be organized by peripubertal testicular androgens.

Animals↗