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PubMed1996

Systemically administered gonadotrophin-releasing hormone enhances copulatory behaviour in castrated, testosterone-treated hyperprolactinaemic male rats.

Hyperprolactinaemic male rats exhibit deficits in copulatory behaviour which can be reversed by a single injection of GnRH. We tested whether systemically administered GnRH can stimulate copulatory behaviour independently of LH-mediated increases in plasma testosterone levels. Gonadectomized, pituitary-grafted adult male Fischer 344 rats bearing implants of 5, 10 or 20 mm capsules of testosterone were administered a single injection of 500 ng GnRH or saline s.c., 30 min prior to copulation tests. Pituitary-grafted castrates displayed copulatory deficits, relative to sham-operated castrates with identical levels of testosterone replacement. Administration of 500 ng GnRH to pituitary-grafted castrates bearing 10 mm testosterone implants significantly increased the proportion of rats that mounted, intromitted and ejaculated during a 30 min test. This treatment also reduced significantly the latency of intromission and ejaculation, and increased significantly the frequency of intromission. The copulatory behaviour of the sexually unresponsive, pituitary-grafted castrates bearing 5 mm testosterone implants, or of the more sexually responsive castrates bearing 20 mm testosterone implants, was not altered significantly by GnRH injections. These results support the hypothesis that copulatory deficits in moderately hyperprolactinaemic rats are due in part to reduced hypothalamic GnRH release, and suggest that GnRH can stimulate sexual behaviour in these animals via mechanisms that are independent of luteinizing hormone-induced testosterone release. However, a threshold level of testosterone (achieved with 10 mm implants) appears to be required for GnRH to elicit this effect.

Animals↗
PubMed1995

The effect of castration on tumor growth rate and cell kinetics in hormone sensitive and hormone insensitive rat prostatic adenocarcinomas.

Cell kinetics were measured in vivo in four experimental rat prostatic adenocarcinomas grown in normal or castrated rats. The aim was to investigate the effect of castration on growth rate and cell kinetics in hormone sensitive and hormone insensitive prostatic carcinomas. We used two anaplastic, hormone insensitive, fast growing tumors (Dunning R-3327-AT1 H and E), as well as two well differentiated, hormone sensitive, slow growing tumors (R-3327-H and R-3327-PAP). DNA ploidy, S-phase transit time (Ts), the labeling index (LI) and potential doubling time (Tpot) was determined by dual parameter flow cytometry, after in-vivo labeling, using bromodeoxyuridine (BUdR) and the tumor doubling time (DT) was determined from growth curves. After castration DT in the hormone sensitive H-subline changed from 21.7 days to 82.0 days, and in the PAP-subline from 22.2 days to 33.2 days. No significant changes in Tpot were observed. In the anaplastic tumors no differences in neither DT nor Tpot were seen. The cell loss factor (CLF) was relatively low in the two anaplastic tumors (0.55-0.59) compared to the well differentiated tumors. The CLF was unaffected by castration in the poorly differentiated tumors, whereas it increased significantly (from 0.75 to 0.92, P = 0.005) after castration in the H-tumor, and showed a non-significant increase in the PAP-tumor. This implies that the decrease in tumor growth in the hormone sensitive tumors is due to an increase in cell death, not a decrease in cell proliferation. These data indicate that CLF is the dominating factor in the reduced growth following androgen ablation in an androgen sensitive tumor. This study suggests that Tpot might be an additional predictor of a tumors proliferating rate and it may provide important information of the human prostatic cancer.

Adenocarcinoma↗
PubMed1997

Potentiating effect of buserelin acetate, an LHRH agonist, on the proliferation of ventral prostatic epithelial cells in testosterone-treated castrated rats.

BACKGROUND: We used buserelin acetate ([D-Ser(But)6] LHRH ), an LHRH agonist and strong blocker of LH secretion, as a treatment for prostatic cancer. It is possible that this LHRH agonist has a proliferative effect on the prostate in addition to suppressing LH secretion. The purpose of this study was to examine the proliferative effect of LHRH agonist on rat prostatic epithelial cells. METHODS: We determined the optimal dose of testosterone necessary to maintain a positive level of proliferating cell nuclear antigen (PCNA) in the ventral prostatic epithelial cells of castrated Wistar rats. Testosterone-treated rats then received various doses of buserelin acetate. Castrated rats without exogenous testosterone also received buserelin acetate. The PCNA positivity was determined by immunohistochemistry with anti-PCNA monoclonal antibody. RESULTS: The optimal dose of testosterone enanthate was 4 mg at 0 and 28 days after castration. Administration of buserelin acetate on day 0 and 28 in doses of 0.16 mg to 1.28 mg significantly increased PCNA positivity in a dose-dependent manner. Administration of buserelin acetate to castrated rats without testosterone also increased PCNA positivity but there was no statistical significance. CONCLUSIONS: Buserelin acetate has a potentiating effect on the proliferation of ventral prostatic epithelial cells of castrated rat in the presence of a physiological level of exogenous testosterone. This effect may slightly influence the result of hormonal therapy by LHRH agonist.

Animals↗
PubMed2006

Tolerability, efficacy and pharmacokinetics of bicalutamide 300 mg, 450 mg or 600 mg as monotherapy for patients with locally advanced or metastatic prostate cancer, compared with castration.

OBJECTIVE: To evaluate the pharmacokinetics, tolerability and effect on endocrinology of bicalutamide given as once-daily monotherapy at doses of >150 mg to patients with locally advanced (M0) or metastatic (M1) prostate cancer, with efficacy as a secondary endpoint. PATIENTS AND METHODS: Patients were initially enrolled to receive bicalutamide 300 mg in a non-randomized phase, after which further patients were randomized to higher bicalutamide doses (in 150 mg increments) or castration. Overall, 248 patients received bicalutamide at 300 mg (21), 450 mg (95) or 600 mg (42), or castration (90). RESULTS: Systemic exposure to bicalutamide stabilised at a dose of approximately 300 mg, as determined by pharmacokinetic analysis. The tolerability of high doses of bicalutamide was similar to that of the 150 mg dose, with no increase in the incidence of adverse events. Patients receiving bicalutamide had early increases in the mean levels of oestradiol, testosterone and luteinizing hormone, which were maintained throughout the study. Levels of these hormones rapidly decreased in the castration group and remained low. From baseline (first day of treatment) to 12 weeks there was an equivalent reduction in prostate-specific antigen (PSA) levels across all four groups. At a median follow-up of 5 years, there was no significant survival difference between patients who received bicalutamide and those who received castration, either in M0 or M1 disease. CONCLUSION: The low median PSA level (180 ng/mL) of patients with M1 disease might account for the lack of survival difference between the treatment groups. Further studies are needed to assess whether high-dose bicalutamide monotherapy can provide equivalent efficacy to castration in patients with M1 prostate cancer.

Aged↗
PubMed1990

Effects of zeranol implants on post-castration response in calves.

Suckling and yearling calves were surgically castrated and one half of each group implanted with 36 mg zeranol at time of castration. Both treated and control cattle of each class were maintained as a group and evaluated for swelling of the scrotum, inflammation and healing, plasma prostaglandin levels and weight gain. Swelling and inflammation of the scrotum were less in treated suckling calves than in controls at both 7 and 14 d after castration, though this difference was not statistically significant. In yearlings at 7 d after castration, treated cattle had more swelling than controls; however at 14 d, treated cattle had less swelling and inflammation with only one treated yearling having an open scrotal wound versus 6 (P less than .03) in the control group. Plasma prostaglandin levels as indicated by plasma malondialdehyde increased from d 0 to 14; however no significant treatment differences were observed for either age group. Suckling calves treated with zeranol gained 9.79 kg more (P less than .03) than non-treated calves during the 97 d of trial while the yearlings treated with zeranol gained 16.78 kg more (P less than .01) than controls during 102 d. It is concluded from the increased growth and reduced scrotal swelling and inflammation in treated cattle that zeranol implantation could possibly have a beneficial effect in improving the healing process after castration.

Animals↗
PubMedDate not supplied

The influence of castration on the development of prostatic carcinoma in the dog. 43 cases (1978-1985).

Prostatic carcinoma (PC) was diagnosed in 43 dogs at the Michigan State University Veterinary Clinical Center (MSU-VCC) between 1978 and 1985. Of the 43 dogs with histologically confirmed PC, 19 (44.19%) had been castrated at least three years prior to the development of any prostatic disease. Seven of the castrates had been neutered at less than 12 months of age. Fourteen dogs (32.55%) were presented as intact males at the time of diagnosis. The remaining ten dogs (23.62%) had been castrated as treatment for presumptive prostatic disease prior to referral to the MSU-VCC. Dates of castration were known in all cases. In this study, therefore, castration at any age showed no sparing effect on the risk of development of PC in the dog. The etiology of PC in the dog may not be exclusively related to testicular hormones. Work in humans suggests that the adrenal and pituitary glands play a significant role in the disease. Preliminary work in dogs supports that nontesticular androgens exert a significant influence on the canine prostate.

Age Factors↗
PubMed1996

Cavernosal nerve stimulation in the rat reverses castration-induced decrease in penile NOS activity.

Castration in the rat reduces both the erectile response and penile nitric oxide synthase (NOS) activity, and these effects are prevented by androgen administration. In this study we determined that the decrease of penile NOS in the castrated rat is due to NOS enzyme inhibition rather than to a reduction of its content and that this inhibition may be reversed. Adult rats were either castrated or left intact, and, after 1 wk, electrical field stimulation (EFS) was applied to the cavernosal nerve and the penises were excised either at the peak of erection or after detumescence. Penile NOS activity in the non-EFS castrates decreased by 70% as compared with the intact non-EFS-treated controls, but neuronal NOS content remained unaffected despite changes in regional distribution. NOS activity in the castrated penis was restored to normal values by EFS at the peak of stimulation, and then decreased on detumescence. This was in contrast to the intact controls in which EFS did not stimulate penile NOS activity. These data indicate that androgen depletion in the rat reduces penile NOS activity rather than NOS content and that this enzyme inhibition is reversed by cavernosal nerve stimulation.

Animals↗
PubMed1987

Lymphatic and vascular responses to fluid infusion in castrated and noncastrated sheep.

Estrogen administration produces blood volume expansion and interstitial fluid retention. We decided to study the effect of estrogen withdrawal on blood volume and determine whether oophorectomy has an effect on lymph flow or protein concentration. The rate of left thoracic duct lymph flow averaged 0.041 +/- 0.005 (SE) and 0.071 +/- 0.008 ml X min-1 X kg-1 in castrated (n = 9) and noncastrated (n = 9) female sheep, respectively (P = 0.006). After three serial intravenous infusions of Ringer lactate solution (2% body wt/infusion) the thoracic duct lymph flow in the castrated animals increased 358, 457, and 498% over the base-line rate, compared with increase of 200, 235, and 353% in the nonpregnant ewes. However, with the lower control values in the castrated animals, the lymph flow rate reached the same absolute values as those seen in the noncastrated ewes. Lymph protein concentration and the lymph-to-plasma protein concentration ratio, as well as arterial and venous pressures, were unaltered by oophorectomy. Base-line whole blood volumes were 58.2 +/- 1.9 (n = 9) and 64.8 +/- 2.6 ml/kg (n = 9) in the castrated and noncastrated ewes, respectively (P less than 0.05). Systemic vascular compliance averaged 4.5 +/- 0.7 and 7.1 +/- 1.7 ml X kg-1 X mmHg-1 in the castrated and noncastrated ewes, respectively (P less than 0.05), whereas interstitial fluid compliance values were 12 and 32 ml X kg-1 X mmHg-1, respectively. The capillary filtration coefficients were not different in the two groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2006

Castration prevents suppression of MHC class II (Ia) expression on macrophages after trauma-hemorrhage.

Several studies indicate that cell-mediated immune responses, i.e., macrophage (MPhi) cytokine release capacities, myosin heavy chain (MHC) class II (Ia) expression, etc., are suppressed after trauma-hemorrhage in male mice. Testosterone has been shown to be responsible for the depression of MPhi cytokine responses in males after trauma-hemorrhage. Antigen presentation via MHC class II plays a key role in initiating and maintaining cell-mediated and humoral immune responses. It remains unknown, however, whether testosterone has any effect on MHC class II after trauma-hemorrhage. To study this, male C3H/HeN mice were castrated or sham castrated 2 wk before trauma (midline laparotomy) and hemorrhage (Hem; blood pressure 35 +/- 5 mmHg for 90 min and resuscitation) or sham operation. Four hours thereafter, MHC class II (Ia) expression was measured using flow cytometry. The results indicate that MHC class II (Ia) expression on peritoneal and splenic MPhi was significantly suppressed in male mice after trauma-hemorrhage. Prior castration, however, prevented the depression in MHC class II (Ia) expression on peritoneal and splenic MPhi after trauma-hemorrhage. Castration did not affect MHC class II (Ia) expression in MPhi from sham-castrated mice. Thus testosterone depresses MHC class II (Ia) expression on peritoneal and splenic MPhi after trauma-hemorrhage in males. Because MHC class II is necessary for an adequate immune response, our results suggest that depletion of male sex steroids or blockade of androgen receptors using agents such as flutamide might prevent immunosuppression via maintaining MHC class II (Ia) expression after trauma and severe blood loss.

Androgen Antagonists↗
PubMed1998

Complete androgen blockade versus chemical castration in advanced prostatic cancer: analysis of an Italian multicentre study. Italian Leuprorelin Group.

OBJECTIVES: In spite of a great amount of data, the hormonal treatment of advanced prostatic carcinoma (CaP) still remains controversial. As a relevant amount of dihydrotestosterone is present within the prostate tissue after castration, complete androgen blockade (CAB), with inhibition of the activity of both testicular and adrenal androgens, has been advocated as up-front treatment of advanced CaP. However, many controlled studies have failed to demonstrate a benefit for CAB in comparison with simple surgical or chemical castration. The present study was performed to bring additional data for a worldwide meta-analysis of all phase III trials comparing castration and CAB. METHODS: This is a centrally controlled phase III study in which chemical castration with leuprorelin acetate depot was compared with leuprorelin plus flutamide in stage C and D CaP. Two hundred and forty-one eligible and evaluable patients with histologically proven CaP were recruited for the study (120 treated with castration and 121 with CAB). The diagnostic and staging workup consisted of blood chemistry, general condition assessment, prostate-specific antigen (PSA), abdominal sonography and computed tomography scan, and whole-body isotopic bone scan. End points of the study were survival, time to treatment failure, and time to progression. The patients were followed every 6 months with PSA and sonography. RESULTS: At a cut-off analysis performed in December 1996, when the mean follow-up period was 43.7 +/- (SD) 24.1 months, no statistical differences in terms of time to treatment failure, time to progression, and death rate could be detected. Also considering the common risk factors, such as basal PSA, haemoglobin, alkaline phosphatase, and Gleason score, the outcome did not show any clear advantage for CAB. CONCLUSIONS: This study appears to confirm that the advantages of first-line CAB in CaP are at best marginal. The final analysis will be performed when the follow-up period has reached 5-years, but it seems unlikely that the present results will change.

Aged↗
PubMed1988

Transfer from long to short days reduces the frequency of pulsatile luteinizing hormone release in intact but not in castrated male golden hamsters.

In the golden hamster, prolonged exposure to short days (i.e. less than 12.5 h of light/day) induces testicular regression that has usually, but not always, been reported to be accompanied by a decrease in mean serum luteinizing hormone (LH) levels. As LH appears to be released in a pulsatile pattern in most mammalian species, we hypothesized that individual variations in serum LH levels over time may obscure significant changes in pituitary LH release in hamsters exposed to short photoperiods. Therefore, we examined the effects of short day exposure on pulsatile LH release in castrated and intact golden hamsters. Intact and castrated male golden hamsters were maintained on long days (light:dark 14:10 h) or transferred to short days (light:dark 6:18 h). Nine to eleven weeks after transfer, animals from all four groups were fitted with intra-atrial cannulas and bled at 10-min intervals for 6 h. Exposure to short days inhibited LH release in the intact male hamsters. All 6 of the males maintained on long days had pulsatile LH release while only 1 of the 4 intact males maintained on short days showed a pulse of LH during the 6-hour bleeding session. All of the castrates on short days had pulsatile patterns of LH release that were similar in amplitude and frequency to those of the castrates on long days. Castrates on long days had significantly greater LH pulse frequency and amplitude than intacts on long days. From these data we conclude that the pulsatile nature of pituitary LH release in the golden hamster mandates frequent sampling over several hours for accurate determination of serum LH levels and for determining the effects of photoperiod on pituitary gonadotropin release.

Animals↗
PubMed1989

Comparison of the effects of castration and streptozotocin-induced diabetes mellitus on contractile responses of the rat vas deferens.

Contractile responses of androgen-sensitive smooth muscles such as the vas deferens and seminal vesicles are highly dependent upon the endocrine status of the animal. Although diabetes mellitus produces disturbances in reproductive function, including decreased serum androgen levels, the effects of diabetes on the contractile function of androgen-dependent urogenital smooth muscles have not been conclusively established. The present study compared the effects of streptozotocin-induced diabetes with those of castration on the contractile responses of rat vasa deferentia. Diabetes and castration produced significant decreases in serum testosterone levels, accompanied by significant decreases in vas deferens weights. Contractile responses of vasa deferentia from diabetic rats to carbachol, ATP, and phenylephrine were significantly increased, and responses to nerve stimulation were decreased. Similar results were obtained with vasa deferentia from castrated rats. Castration produced significant increases in contractile responses of vasa deferentia to carbachol and phenylephrine and decreased responses to nerve stimulation. The data suggest that both castration and diabetes produce a denervation-like supersensitivity which is specific for receptor-mediated processes.

Adenosine Triphosphate↗
PubMed1985

Further regression of seminal vesicles of castrated guinea pig by administration of cyproterone acetate.

It has been established that a low level of secretory activity persisted in seminal vesicles of guinea pigs long after castration and that this may be due to a higher extratesticular androgen level in this animal. A RIA study revealed that the normal serum testosterone concentration of the guinea pigs was comparable to that of the rats, but the basal serum testosterone level after castration was ten times higher than rats under a similar condition. It was also shown that cyproterone acetate did not significantly lower the basal serum testosterone concentration in the castrated guinea pigs. The higher basal serum testosterone level is believed to be responsible for the slow and incomplete regression of this gland in the guinea pigs. There was a significant reduction in wet weight of the seminal vesicles after the treatment of castrated guinea pigs with cyproterone acetate. Ultrastructural study showed that there were both qualitative and quantitative changes in the cytoplasmic organelles. The Golgi apparatus further reduced in size and in the number of associated vesicles and vacuoles. There was a marked decrease in the number and size of secretory granules and lysosomes and an increase in the degree of undulation of the basement membrane. Accumulation of lipid droplets and glycogen was commonly observed. All these morphological evidences showed that further regression of the castrated guinea pig seminal vesicles can be achieved by cyproterone acetate treatment.

Animals↗
PubMed2005

Effect of testosterone replacement or duration of castration on baroreflex bradycardia in conscious rats.

BACKGROUND: In this study, we tested the hypothesis that 17beta-estradiol contributes to testosterone-mediated restoration of baroreflex-mediated bradycardia in short-term (3 weeks) castrated rats. Further, a reported increase in serum testosterone after long-term (6 weeks) castration constituted a basis for testing the hypothesis that a spontaneous increase in serum testosterone or androstenedione in this model causes a commensurate increase in baroreflex-mediated bradycardia. RESULTS: Testosterone (1 week) replacement enhanced baroreflex-mediated bradycardia in short-term castrated rats without changing 17beta-estradiol level. A spontaneous recovery of baroreflex-mediated bradycardia occurred following long-term castration, although circulating testosterone and androstenedione remained suppressed. CONCLUSION: The data suggest: 1) 17beta-Estradiol does not contribute to testosterone restoration of the baroreflex-mediated bradycardia in short-term castrated rats. 2) The long-term modulation of baroreflex-mediated bradycardia occurs independent of androgens, or the baroreflex mechanism may become adapted to low levels of circulating androgens.

Animals↗
PubMed1986

Dissimilarities between the uterine estrogen receptor in cytosol of castrated and estradiol-treated rats.

The estrogen receptor (ER) in its native state appears oligomeric and can be dissociated by salt into a monomer with a mol wt of 50,000-80,000. Lower molecular weight fragments have also been observed but are considered to result from ER proteolysis by tissue proteases. Three-month-old Sprague-Dawley rats have been studied after castration, estradiol treatment (3 days at 25 micrograms/day), or during the normal estrus cycle. The uterine cytosol was labeled with [3H]estradiol, and the [3H]estradiol-receptor complexes were studied by sucrose gradient centrifugation, gel filtration, diethylaminoethyl (DEAE)-Trisacryl and phosphocellulose chromatography, and kinetic experiments. In low salt buffer in presence of molybdate (20 mM), uterine ER of castrated and treated rats could not be differentiated by sucrose gradient centrifugation (9.9S), gel filtration (7.7 nm), or DEAE-Trisacryl and phosphocellulose chromatography, but the dissociation rate at 23 C was lower for castrated than for treated rats (t1/2 = 45 and 27 min, respectively). In high salt buffer (0.4 M KCl) in presence of molybdate (20 mM), no difference was apparent by sucrose gradient centrifugation (3.7S) or gel filtration (3.4 nm), but again the dissociation rate at 23 C was lower for castrated than for treated rats (t1/2 = 102 and 45 min, respectively). In high salt buffer in presence of molybdate and ammonium thiocyanate (0.5 M), differences were observed by sucrose gradient centrifugation (3.6 and 3.2S), gel filtration (3.2 and 2.6 nm), and dissociation rate assays at 10 C (t1/2 = 24 and 12 min) for castrated and treated rats. The calculated wts were 50,000 and 35,000, respectively. Protection from limited proteolysis by molybdate, contained in all buffers used, plus various protease inhibitors, particularly leupeptin, as well as mixing tissues before homogenization, suggested that the 35,000-dalton monomer was not a product of protease action formed after cell breakage. ERs covalently labeled with [3H]tamoxifen aziridine also showed different entities of 62,000 and 47,000 mol wts, respectively, on denaturing polyacrylamide gels. In vitro activation and transformation were demonstrated for the two types of [3H]estradiol-receptor complexes by sucrose gradient centrifugation analysis and affinity for phosphocellulose and purified nuclei. Finally, it has been shown that both entities coexisted in different proportions during the diestrous (1:2) and proestrous (1:1) phases of the estrus cycle; only the low mol wt component was present during the estrous phase.

Animals↗
PubMed1988

Activation of programmed cell death in the rat ventral prostate after castration.

The rapid involution of the rat ventral prostate after castration is an active process initiated by removal of the inhibitory effects of androgen on prostatic cell death. The present studies demonstrate that after castration-induced androgen deprivation a series of temporally discrete biochemical events are activated which result in the rapid programmed death of the subset of androgen-dependent cells within the rat ventral prostate. These biochemical steps involve 1) rapid loss of nuclear androgen receptor retention; by 12 h after castration, androgen receptors are no longer detectable in ventral prostatic nuclei; 2) an initial fragmentation of nuclear DNA into low mol wt (less than 1000 basepairs) nucleosomal oligomers which lack intranucleosomal break points; and 3) eventual complete digestion of these nucleosomal oligomers into component nucleotides. Additional studies demonstrate that activation of a Ca2+-Mg2+-dependent endonuclease is associated with this DNA fragmentation. By 4 days after castration, maximal DNA fragmentation is obtained, with 15% of the total nuclear DNA extractable as low mol wt fragments. Proteolytic enzymes are apparently not involved initially in this process, suggesting that DNA fragmentation is a discrete event in, rather than a result of, cell death. Flow cytometric analysis of nuclear DNA content demonstrated that each day after castration, a subpopulation of androgen-dependent cells in rat ventral prostate fragmented all of their genomic DNA, as opposed to the whole population of cells fragmenting an increasing portion of their DNA daily.

Animals↗
PubMed1992

Increase in ubiquitin-immunoreactive nuclei in rat pituitary luteinizing hormone cells after castration.

Immunocytochemical detection of ubiquitin in the nucleus of rat LH cells and the effects of castration and testosterone replacement on the occurrence of immunoreactive ubiquitin in the nucleus were investigated. Immunoreactive ubiquitin occurred in certain nuclei, mostly belonging to identified LH cells. The concentration of testosterone in blood was altered by castration and implantation of testosterone into castrated rats, and the occurrence of ubiquitin was examined weekly for the following 4 weeks. In castrated rats, the proportion of LH cells with ubiquitin-immunoreactive nuclei was high throughout the experiment. In castrated rats implanted with testosterone, on the contrary, the proportion remained significantly lower. Ubiquitin may be involved in the cellular activity of LH cells in the rat pituitary.

Animals↗
PubMed1993

Luteinizing hormone-releasing hormone (LHRH) in rat prostate: characterization of LHRH peptide, messenger ribonucleic acid expression, and molecular processing of LHRH in intact and castrated male rats.

Continuous administration of LHRH agonist suppresses the pituitary-gonadal axis, achieving chemical castration. Thus, LHRH agonist has been used as an alternative (to surgical castration) for the treatment of steroid-dependent prostate cancer. However, recent reports have demonstrated that LHRH agonist had a direct inhibiting effect on prostate cancer cell proliferation and that cancerous prostate tissue contained a LHRH-like peptide. In this paper we are reporting for the first time that the normal rat ventral prostate contained immunoactive and bioactive LHRH as well as its precursor molecule, pro-LHRH. Our investigation showed that the LHRH concentration in prostate increased 2 weeks after castration from 1.68 +/- 0.09 to 3 +/- 0.2 pg/mg tissue (P < 0.001). At the same time, the concentration of pro-LHRH decreased from 149 +/- 6.5 to 68 +/- 6.8 pg/mg tissue (P < 0.001). Furthermore, intact rat prostate expressed LHRH mRNA, which increased 13-fold 2 weeks after castration. In summary, the prostate of intact Sprague-Dawley rats has the capacity to produce the LHRH precursor and process it to the mature decapeptide, and this production/processing increases significantly after castration.

Animals↗