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PubMed1996

Effect of castration and hormonal supplementation on cholesterol cholelithiasis in the male hamster.

This study examined the effect of castration and dietary hormonal supplementation on cholesterol cholelithiasis in male hamsters. Animals fed a standard lithogenic diet developed cholesterol gallstones (17%) after 6 wk, while castrated hamsters did not form any stones. Addition of a synthetic androgen, methyltestosterone, to the lithogenic diet induced cholelithiasis in castrated animals (50%). The biles of normal and castrated-hormone supplemented hamsters had cholesterol saturation indices of 1.0 and 1.1, respectively, while the bile of the castrated animals remained unsaturated (0.6). The ratio of cholic acid/chenodeoxycholic acid in bile increased after castration, but returned to normal levels following hormonal supplementation. Biliary cholesterol carriers were separated by ultracentrifugation. Animals in the stone-forming groups (normal and castrated-hormone treated) had a significant proportion of their biliary cholesterol in vesicles (44 and 46%, respectively); castrated hamsters had less cholesterol in vesicle form (9%). The molar ratio of cholesterol/phospholipid in vesicles was reduced after castration (0.93 vs. 0.42) and increased by hormonal supplementation (1.89). In conclusion, when compared to normal male hamsters fed a standard lithogenic diet, castration reduced the cholesterol saturation of bile, lowered the vesicular/micellar ratio in bile, and inhibited cholesterol cholelithiasis. Dietary androgen supplementation increased the lithogenicity of bile, resulting in stone formation in castrated animals.

Animals↗
PubMed1999

Quantification of the pain and distress responses to castration in young lambs.

Pain and distress following castration were assessed in lambs using three indicators: behaviour, plasma cortisol and mechanical nociceptive thresholds. Three castration methods: rubber ring (RR), combined ring and Burdizzo clamp (CM) and surgery (SU) were compared. The effects of castration following local anaesthetic pre-treatment (LA) and castration performed under general anaesthetic (GA) were compared to castration performed with no anaesthetic. This gave a 4 x 3 x 3 block design i.e. 36 experimental treatments. Six lambs were allocated to each treatment i.e. 216 lambs were used in all. SU produced the greatest response, followed by RR then CM castration. LA abolished the responses to RR and CM castration but had no effect on the response to SU castration. GA did not reduce the responses to RR and SU but abolished the rise in mechanical nociceptive thresholds and markedly attenuated active pain behaviours in lambs CM castrated without anaesthesia. This suggests that the clamping procedure itself rather than post-castration pain and distress is responsible for the rise in nociceptive thresholds and active pain behaviours in CM castrated lambs.

Anesthesia, General↗
PubMed2000

A survey of the methods used by farmers to castrate calves in New Zealand.

AIMS: To identify the methods used to castrate calves and the age at which castration is carried out on farms in New Zealand. METHODS: A survey was carried out by questionnaire sent to the 14,000 recipients of Meat Matters produced by Meat New Zealand. The questionnaires on return were analysed on a national and regional basis. RESULTS: Of the 3,788 respondents, 74% (2,825) castrated calves on their farms. Of these 2,825 respondents 85% (2,403) used a rubber ring, 18% (512) carried out surgical castration and only a few respondents, 25, used a clamp. The ring was used on calves with an average age of 2.2 months and 93% of calves castrated by ring were castrated during the first 3 months of life. Surgical castration was carried out on calves with an average age of 4.3 months, 54% of them were castrated in the first 3 months of life and 39% during the following 3 months. Respondents from the West Coast (40%), Otago (38%) and Southland (50%) were more likely to use surgical castration than respondents from elsewhere (<17%). Local anaesthetic was used by only 3% (94) of respondents and a similar percentage employed a veterinarian to do the castration. CONCLUSIONS: There are marked regional differences in methodology used for castration of calves. The survey gives a sound basis for future research into humane and cost effective methods.

Journal Article↗
PubMed2004

Effect of time of castration and tumour volume on time to androgen-independent recurrence in Shionogi tumours.

OBJECTIVE: To use the androgen-dependent Shionogi tumour model in mice to help define the effects of the timing of androgen ablation on the development of androgen resistance in prostate cancer, as the timing of androgen ablation remains controversial. MATERIALS AND METHODS: Groups of nine mice were castrated at 1, 3, 6, 10 and 14 days after tumour inoculation, with a similar-sized group of mice castrated before tumour inoculation serving as a control. The time of first palpable tumour recurrence and tumour volume was monitored after castration. RESULTS: All mice were observed for > or = 80 days after castration. Only mice castrated at 10 and 14 days had palpable tumour at the time of castration. Mice castrated at 14 days had the highest rate of early tumour recurrence (all nine) while mice castrated before inoculation or at 1 and 3 days afterward had a significantly lower rate of tumour recurrence (four of nine; P < 0.01). Mice castrated at 14 and 10 days had tumour recurrence significantly earlier than mice in the other groups. When calcium-channel blockers were administered to inhibit apoptosis, all mice had a similar time to recurrence and time to death regardless of the time of castration. CONCLUSIONS: Large tumour volume and corresponding delay in castration reduced the time to androgen-independent tumour recurrence and survival. Earlier androgen ablation, at the time of subclinical (impalpable) disease, significantly delayed the rate and time to androgen-independent recurrence compared with delayed therapy when the tumour burden was high.

Androgens↗
PubMed2000

Morphologic and biochemical changes in male rat lung after surgical and pharmacological castration.

The morphology of the rat lung was studied by light microscopy in different situations: after surgical and pharmacological castration and after administration of testosterone to the castrated rat to determine if the androgen is required to maintain the normal morphology of the lung. We also determined the effect of flutamide on the phospholipid composition of both the surfactant and microsomes of the lung. Rats were separated into five groups: I - control non-castrated rats, II - castrated rats sacrificed 21 days after castration, III - castrated rats that received testosterone daily from day 2 to day 21 after castration, IV - castrated rats that received testosterone from day 15 to day 21 after castration, and V - control rats injected with flutamide for 7 days. The amount of different phospholipids in the surfactant and microsomes of the lung was measured in group I and V rats. At the light microscopy level, the surgical and pharmacological castration provoked alterations in the morphology of the lung, similar to that observed in human lung emphysema. The compositions of surfactant and microsomes of the lung were similar to those previously reported by us for the surgically castrated rats. These results indicate that androgens are necessary for the normal morphology as well as for some metabolic aspects of the lung.

Androgen Antagonists↗
PubMed1985

In-vivo activity of the LH-releasing hormone pulse generator in castrated and intact male rats.

The in-vivo LH-releasing hormone (LHRH) output from the mediobasal hypothalamus of conscious freely moving sham-castrated, acutely castrated (immediately after castration) and long-term castrated (greater than 20 days after castration) adult male rats has been studied. Five rats in each of the three conditions were perfused for an 8-h period (11.00-19.00 h). One animal in each condition was perfused for a 24-h period. In the sham-castrated and acutely castrated, but not in the long-term castrated rats, apparently random surges of LHRH output (greater than 5.6 pmol/l), separated by periods of non-detectable activity, were observed throughout the perfusion period. The LHRH output of the long-term castrated rats was characterized by an extremely low overall mean release and markedly attenuated pulse amplitudes, with both parameters significantly lower than those of the sham-and acutely castrated rats. These results indicate that the raised blood levels of LH in long-term castrated rats do not appear to be the consequence of high amplitude and high overall release of LHRH.

Animals↗
PubMed1996

Effect of castration method and the provision of local anesthesia on plasma cortisol, scrotal circumference, growth, and feed intake of bull calves.

To determine the effects of castration of calves, with or without local anesthesia, on plasma cortisol, scrotal circumference, ADG, and ADFI, 56 Friesian bulls (5.5 mo of age; mean +/- SE BW = 173 +/- 2 kg) were randomly assigned to each of seven treatments: 1) control (CON); 2) s.c. injection of .1 mg of a human serum albumin-GnRH conjugate with DEAE-dextran adjuvant (HSA-GnRH); 3) burdizzo castration without local anesthetic (BURD); 4) burdizzo castration following local anesthetic administration (BURD + LA); 5) surgical castration without local anesthetic (SURG); 6) surgical castration following local anesthetic administration (SURG + LA); and 7) local anesthetic administration alone (LAA). Blood samples for cortisol analyses were taken via jugular catheter from -2 to 10 h and at 24, 48, and 72 h relative to treatment. Average daily feed intakes were recorded for 5-d periods and calves weighed at 7-d intervals before and after treatment. Local anesthetic alone had no effect (P > .10) on any variable. The HSA-GnRH calves had elevated (P < .05) plasma cortisol from 2 to 6 h compared with CON calves. Peak plasma cortisol was elevated (P < .01) in BURD, BURD + LA, SURG, and SURG + LA compared with CON calves. The SURG calves (46.0 ng/mL) had higher (P < .03) peak cortisol than BURD (31.4 ng/mL) and SURG + LA (35.4 ng/mL) calves. There was no difference in peak cortisol between BURD and BURD + LA (26.5 ng/mL) calves. The ADG from d 0 to 7 was reduced (P < .05) in calves in BURD + LA, SURG, and SURG + LA treatments (-.01, -.83 and -.24 kg, respectively) compared with CON calves (.54 kg). The ADFI were reduced (P < .05) in BURD and BURD + LA calves during d 1 to 5 and in BURD + LA, SURG, and SURG + LA calves during d 6 to 10 compared with CON calves. The scrotal circumferences of BURD and BURD + LA calves were greater (P < .05) than those of CON calves for 7- and 35-d periods post-castration, respectively. Castration induced increases in cortisol and decreases in ADG and ADFI. Surgical castration induced a greater plasma cortisol response than burdizzo castration, and the administration of local anesthetic reduced the cortisol response of surgical castrates but was less effective for burdizzo castrates.

Anesthesia, Local↗
PubMed1999

Castration induces acute vasoconstriction of blood vessels in the rat prostate concomitant with a reduction of prostatic nitric oxide synthase activity.

PURPOSE: Previous studies demonstrating a rapid and drastic reduction of blood flow to the rat prostate gland resulting from castration caused us to consider the influence of castration on the state of vascular constriction and on the activity of the vascular tone-regulating factors (nitric oxide synthase and cyclic GMP) in the rat prostate. MATERIALS AND METHODS: Sections of ventral prostate glands obtained from intact and castrated rats were analyzed for the mean areas within smooth muscle-coated blood vessels using a computerized microscopic image analysis system. Nitric oxide synthase (NOS) levels were measured in prostatic extracts from unoperated or castrated rats using an enzyme assay system that measures conversion of 3H-L-arginine to citruline. Cyclic GMP levels were measured in prostatic extracts from unoperated or castrated rats using a competitive radioimmunoassay system. RESULTS: The mean area within ventral prostate smooth muscle-coated blood vessels was reduced 39% at 24 hours after castration (p = 0.039) and 47.7% at 48 hours after castration (p = 0.039). NOS activity measured in prostatic extracts was reduced 38% at 24 hours (p = 0.0012) and 51.6% at 36 hours after castration (p = 0.0001) compared with the control group of noncastrated rats. Finally, prostatic cGMP levels were reduced 55.8% (p = 0.0018) at 36 hours after castration when compared with controls rats. CONCLUSION: Within 24 hours after castration, the lumenal areas of smooth muscle-coated blood vessels in the rat prostate gland were found to be significantly reduced. This vasoconstriction was associated with a significant reduction of prostatic NOS activity as well as a reduction in the prostatic levels of the NOS co-factor, cGMP. Thus, acute vasoconstriction is a prominent early event associated with rat prostate regression in response to castration and likely contributes to the regression of the tissue.

Animals↗
PubMedDate not supplied

Influence of castration and testosterone propionate on prostatic and seminal vesicular lipids in mature monkeys.

The effect of castration and administration of testosterone propionate (TP) has been studied in mature monkeys in relation to prostatic and seminal vesicular lipids to castrates on prostatic and seminal vesicular lipids were studied in mature monkeys. Castration decreased prostatic total lipid, total phospholipids and total glyceride glycerols. Among neutral lipid classes only diacyl glycerol was decreased due to castration. Similarly among phospholipid classes, phosphatidyl choline and ethanolamine were decreased. A marked decrease in the seminal vesicular total lipid, total phospholipids, total cholesterol and total glyceride glycerol were observed due to castration. Mono and diacyl glycerols and phosphatidyl choline and ethanolamine also registered a significant decrease after castration. Administration of TP to castrates brought back all the lipid classes to normal level which showed a decrease due to castration. However, TP treated to castrates on both seminal vesicles and prostates had no effect on other classes of lipids which were unaltered by castration. The present study reveals that lipid metabolism in the male accessory sex organs is under androgenic control. Nevertheless, the influence of testicular androgen is specific to different classes of lipids as a number of phospholipids and neutral lipid classes were resistant to castration or administration of TP.

Animals↗
PubMed1979

The effect of long-term castration on the histochemically demonstrable catecholamines in the hypogastric ganglion of the rat.

The effect of long-term castration on the hypogastric ganglion of the rat was studied using the formaldehyde-induced fluorescence (FIF) method. After castration the fluorescence intensity was lower and the size of the adrenergic neurons was smaller than in normal or in testosterone-treated castrated rats. The fluorescence profile of the ganglia of castrated rats differed from the profiles of control or testosterone-treated castrated rats. Vacuolated neurons were seen in the hypogastric ganglion of controls but not in the ganglia of castrated animals. After long-term castration the size of the ventral prostate was drastically reduced. The density of adrenergic nerves was similar in castrated, normal and testosterone-treated castrated rats. It is concluded that long-term castration has an effect on adrenergic neurons by decreasing the FIF and by producing other morphological changes. The effect can be reversed by testosterone treatment.

Adrenergic Fibers↗
PubMed2003

Effect of castration on acetyl salicylic acid metabolism in rabbits.

OBJECTIVES: The biotransformation of acetyl salicylic acid (ASA) differs within species, and gender differences have been documented and attributed to the effect of sex hormones. Castration remains a standard therapy for men with advanced prostate cancer. We studied the effect of castration on the metabolism of ASA in rabbits to find out whether the metabolism of ASA is adversely affected after castration. METHODS: ASA in doses of 12.5, 25, and 50 mg/kg body weight was given intravenously to male and female prepubertal and adult rabbits, castrated adult male rabbits, and castrated male rabbits given testosterone (3 animals per group). Blood samples were collected at 0, 10, 30, 60, 120, and 180 minutes. The high-performance liquid chromatography method was used for the quantitation of salicylic acid (SA) in serum. The percentage of SA not metabolized was determined by comparing the serum level at 10 and 180 minutes for each group. RESULTS: At a dose of 50 mg/kg in the adult rabbits, the mean +/- SD of SA in serum at 10 and 180 minutes was 146.54 +/- 29.54 microg/mL and 19.12 +/- 5.93 microg/mL for males, 158.25 +/- 6.70 microg/mL and 33.24 +/- 2.78 microg/mL for females, 229.72 +/- 47.85 microg/mL and 44.33 +/- 5.64 microg/mL for castrated male rabbits, and 170.88 +/- 12.03 microg/mL and 68.1 +/- 37.54 microg/mL for castrated male rabbits given testosterone, respectively. Also, at 180 minutes, the percentage of SA not metabolized in adult male rabbits was 12.82% +/- 1.65% compared with 21.04% +/- 2.14% (P <0.01) in adult females, 19.53% +/- 1.73% (P <0.01) in castrated adult male rabbits, and 38.95% +/- 19.48% (P <0.001) in castrated male rabbits given testosterone. At all doses of ASA, the serum SA concentration in male and female prepubertal rabbits was not significantly different for each time point. CONCLUSIONS: These results indicate that male rabbits are able to metabolize ASA faster than are females. After castration, this ability is significantly decreased. If these experimental results are confirmed in humans, men who are undergoing hormonal manipulation for advanced prostate cancer and who require high-dose ASA, such as in the treatment of stroke or rheumatoid arthritis or as an antioxidant, may need lower doses to reduce the possible toxic effects of ASA.

Androgen Antagonists↗
PubMed2001

Castration-induced reduction of vascular endothelial growth factor expression in benign human prostate tissue is lost in advanced prostate cancer.

OBJECTIVE: To determine the role of vascular response in the castration-induced regression of benign and malignant human prostate tissue, as recent studies show that castration rapidly decreases blood flow and induces endothelial cell death, which may be important for subsequent epithelial cell death and involution of the glandular tissue of the prostate. MATERIALS AND METHODS: The expression of vascular endothelial growth factor (VEGF) and its receptors was analysed using the quantitative reverse transcriptase-polymerase chain reaction, in benign and tumour areas of core biopsies taken before, and approximately 1 week after castration therapy. The castration-induced VEGF response was related to therapy-induced changes in tumour cell apoptotic index and subsequent response in serum prostate-specific antigen (PSA). In another set of patients, serum VEGF was quantified by enzyme-linked immunosorbent assay before, and at 3--6 months after castration therapy. RESULTS: VEGF mRNA was down-regulated after castration in benign prostate tissue (P < or = 0.05), whereas in tumour tissue, VEGF levels were reduced in some of the patients but unchanged or increased in others. In most patients whose tumour tissue responded with VEGF reduction, there was a corresponding increase in tumour cell apoptosis. Serum VEGF levels were not significantly changed after castration. Almost all patients responded with a substantial reduction in serum PSA after castration. CONCLUSION: Castration reduces VEGF mRNA expression in benign prostate tissue and generally in those prostate tumours where castration also induces tumour cell apoptosis. This suggests that a therapy-induced down-regulation of VEGF could be important for tumour cell death.

Apoptosis↗
PubMed1976

Cell proliferation in the prostate complex of the castrate mouse.

Cell proliferation during 100 h of continuous androgen challenge was studied in the seminal vesicle and coagulating gland of Balb/c mice castrated 3 days or 14 days prior to the first daily injection of 250 mug testosterone propionate. Continuous labelling with [3H] thymidine indicated that the seminal vesicle was almost totally responsive to androgen, as early as 3 days after castration, whereas the androgen sensitivity of the coagulating gland increased from 30% at 3 days after castration to 85% at 14 days after castration. In both tissues the magnitude of the proliferative reaction could be related to the extent of cell loss prior to stimulation. The duration of the pre-replicative phase in the response of the seminal vesicle to androgen was 20-25 h both at 3 and 14 days after castration. In the coagulating gland the pre-replicative phase was 40 h at 3 days after castration and 20 h at 14 days after castration. The maximum uptake of [7alpha-3H] testosterone administered to mice 3 days after castration was significantly greater (P less than 0-01) in the seminal vesicle compared to the coagulating gland. At 14 days the seminal vesicle and coagulating gland exhibited a similar capacity for uptake. The in vivo metabolism of [7alpha-3H] testosterone was studied by thin layer chromatography 30 min and 120 min after administration. A high proportion of the radioactivity extracted from all the tissues was associated with highly polar steroids. At 3 days after castration, the seminal vesicle, 2 h after administration of radioactive testosterone, retained a much higher proportion of radioactivity associated with dihydrotestosterone than did the coagulating gland. The localization of steroid in mice 3 days after castration was studied by dry-mount autoradiography at intervals up to 2 h after the injection of [1,2,6,7(n)-3H]-testosterone. A heavier deposition of silver grains was observed over autoradiographs of the seminal vesicle. In the seminal vesicle the grains were primarily located over nuclear areas whereas in the coagulating gland the grains were diffusely distributed over both nuclear areas and over cytoplasmic areas.

Animals↗
PubMed1983

Effect of castration and testosterone substitution on the urinary output of gamma-glutamyl transpeptidase and of N-acetyl-beta-D-glucosaminidase of male rats with renovascular hypertension.

The effect of castration of male rats with experimental renal hypertension ('two-kidney Goldblatt hypertension') was studied on the height of the hypertension and on the urinary output of gamma-glutamyl transpeptidase (gamma GT) and of N-acetyl-beta-D-glucosaminidase (NAG). Castration was carried out immediately after clamping one renal artery. Some of the castrates received testosterone substitution from the 3rd postoperative week onwards. Uncastrated hypertensive males served as controls. The experiments were carried out 8-18 weeks after eliciting high blood pressure. Hypertension as well as enzymuria were less expressed in castrates than in uncastrated males or in testosterone-substituted rats. In all animals studied the gamma GT excretion rate showed a positive correlation with the blood pressure. The output of gamma GT and of NAG as well as the specific gamma GT activity of the renal membrane fraction was lower in castrates than in uncastrated males or in substituted castrates. In uncastrated males and in testosterone-substituted castrates the daily NAG output showed a direct correlation with the renal hydroxyproline content. No such correlation was found in castrated males. The kidneys of castrates and of testosterone-substituted castrates contained less hydroxyproline than those of uncastrated males.

Acetylglucosaminidase↗
PubMed1982

Pituitary receptor sites for gonadotropin-releasing hormone: effect of castration and substitutive therapy with sex steroids in the male rat.

To examine the role of pituitary gonadotropin-releasing hormone (GnRH) receptors (pit GnRH-R) in the regulation of gonadotropin secretion, male rats were orchidectomized and then selectively received substitutive therapy with sex steroids. Pituitary content of GnRH-R was determined by saturation analysis, using radioiodinated [D-Trp6,(N-Et)Pro5,des-Gly10]GnRH as tracer. Castration produced a rapid and sustained increase of the number of GnRH-R, which doubled after 2 days, and after 10 days the pituitary content of GnRH-R was 258 +/- 23 fmol/pituitary compared to 103 +/- 12 fmol/pituitary for sham-operated control animals. No change of the affinity constant (Ka) was observed (Ka = 1.13 +/- 0.08 X 10(10) M-1; n = 14). Plasma LH increased 5- to 10-fold and FSH-2- to 3-fold after castration, and hypothalamic GnRH content was depleted by 30-60%. Immediate substitution of castrated rats with testosterone propionate (250 micrograms daily) prevented the increases of both plasma gonadotropins and of GnRH-R. Treatment of acutely castrated rats for 7 days with testosterone propionate (50-200 micrograms), 5 alpha-dihydrotestosterone propionate (25-400 micrograms), or estradiol benzoate (2 micrograms) prevented the rise in pit GnRH-R in a dose-related manner and normalized the other parameters studied except that plasma FSH remained slightly elevated. In contrast, when substitutive therapy was started 8 days after castration or later, the 7-day treatment with sex steroids reduced plasma gonadotropins, but pit GnRH-R remained elevated, and hypothalamic GnRH content remained depleted. These results indicate that the marked increase of gonadotropin secretion after castration is mediated at least in part, by an increase in the number of pit GnRH-R. Sex steroids were able to reverse all castration-induced endocrine changes in acutely castrated rats, but in long term castrated animals their action at higher centers to normalize hypothalamic GnRH content, and indirectly, to reduce pit GnRH-R content, was either delayed or ineffective. Thus, the rapid feedback action of sex steroids in long term castrated rats may be predominantly exerted at the pituitary level.

Animals↗
PubMed1984

Effects of castration and sex steroids on the thyroid response to thyrotropin.

There is a profound difference in the incidence of thyroid disease between males and females. We have investigated the possibility of a direct effect of sex steroids on the thyroid gland by investigating thyroid function in castrate animals. The rate of thyroid hormone release was estimated by measuring the rate of hydrolysis of labeled thyroglobulin from mouse thyroid glands in vitro. The thyroid glands were labeled in vivo with 131I and then cultured for 20 h in the presence of mononitrotyrosine, an inhibitor of iodotyrosine and deiodinase. The rate of hydrolysis of labeled thyroglobulin was measured as the percentage of radioactivity released as iodotyrosines and iodothyronines into the gland and the medium at the end of incubation. TSH was injected at varying intervals before death in some cases. The basal rates of thyroglobulin hydrolysis were similar in intact and castrate mice, but TSH-stimulated rates were significantly higher in both male and female castrates. Daily treatment of castrates for a week with estradiol or testosterone decreased the rate of thyroglobulin hydrolysis to that seen in intact mice, but dihydrotestosterone was without effect. (Bu)2cAMP added in vitro increased the rate of thyroglobulin hydrolysis in both intact and castrate mice, but the stimulation was significantly greater in the castrates. Basal and TSH-stimulated cAMP levels in the thyroid were similar in castrate and intact mice. There was no difference in thyroidal incorporation of iodine by intact and castrate mice in either presence or absence of TSH. These data suggest the following. 1) Castration results in significantly greater sensitivity to TSH with respect to thyroid hormone secretion. Thyroid hormone synthesis, basal or TSH-stimulated, is, however, unaltered. 2) Estradiol inhibits TSH-stimulated hormone release in castrates. Testosterone has a similar effect, possibly through aromatization to estradiol. 3) The effect of sex hormones is likely to be exerted at a post-cAMP step specific for hormone secretion.

Animals↗
PubMed1976

Effect of active and passive immunization with luteinizing hormone-releasing hormone on serum luteinizing hormone and follicle-stimulating hormone levels and the ultrastructure of the pituitary gonadotrophs in castrated male rats.

The effect of active and passive immunization with luteinizing hormone-releasing hormone (LHRH) on serum LH and follicle-stimulating hormone (FSH) levels and the ultrastructure of the pituitary gonadotrophs was investigated in castrated male rats. Two weeks after castration, the animals were immunized with Glu1-LHRH conjugated with human serum albumin (hSA), immunized with hSA only, or left uninjected. Immunogens were administered every 2 weeks. Four weeks after the initiation of immunization with hSA-Glu1-LHRH, 2 out of 4 rats showed parallel decreases in serum LH and FSH levels associated with a rise of serum antibody titer to LHRH. Serum LH and FSH levels remained suppressed throughout the experiment in these rats. On the other hand, both LH and FSH levels in hSA-immunized rats or non-immunized rats remained elevated, and typical castration cells containing large vacuoles were found in the pituitary. Although castration cells existed in the pituitary of rats which produced antibody to LHRH by active immunization, these cells were markedly degranulated, and secretory granules were scarce in the cytoplasm. In another experiment, rats were injected iv with one ml sheep anti-LHRH gamma-globulin (anti-LHRH) or normal sheep gamma-globulin (NSG) every 2 days for 3 weeks, starting one day after castration, when serum LH and FSH levels were already elevated. All the animals which received anti-LHRH showed a decrease in both serum LH and FSH levels, which remained low throughout the study, in a range comparable to those in intact normal male rats. On the other hand, in the animals which received NSG, both LH and FSH levels remained high or increased further throughout the experiment, and the pituitary contained numerous castration cells. Castration cells were completely absent from the pituitaries of rats treated with anti-LHRH, suggesting that castration cells are formed as a result of increased secretion of LHRH. Some FSH gonadotrophs in these castrated rats were atrophic. It was difficult to distinguish the LH gonadotrophs in rats which were either actively or passively immunized with LHRH; however, they seem not to have contributed significantly to the development of castration cells. In any case, antibody to the LHRH decapeptide drastically affected both LH and FSH cells, providing additional evidence for the concept that LHRH represents the physiological LHRH and FSHRH.

Animals↗
PubMed1976

The effects of castration on body composition, adipose tissue cellularity and lipid and carbohydrate metabolism in adult male rats.

Gonadal hormones affect body composition, food intake, weight gain and serum lipids in numerous species including man. In this study, mature male Sprague-Dawley rats were castrated or sham-operated at 16 weeks of age. During the 6-week observation period with weekly records of food intake and weight gain, these parameters were significantly lower in the castrated group. The decrease in food intake in this group could not account for the difference in body weight between the groups, indicating a lower feed utilisation in the castrates. At sacrifice accessory reproductive organs, the levator ani muscle, thymus and adrenals were dissected for determination of organ weight and histology, revealing significant reductions in the accessory reproductive organs and levator ani of the castrates. The thymus was significantly heavier in the castrated animals. No differences were found in the adrenals. Two of the sham-operated animals had signs of accidental functional castration. The proportion of body cell mass and total lipid of the carcass was the same in both groups. Significant reductions in adipocyte weights were found in the epididymal depots of the castrated rats. Blood samples taken at sacrifice in pentobarbital anaesthesia were analysed for glucose, insulin, triglycerides, cholesterol, FFA, glycerol and protein. Statistically significant reductions in triglycerides and protein were recorded in the castrated animals without any significant changes in the other parameters studied. The results are discussed with reference to the age of castration and the importance of the reduced food intake in castrated animals.

Adipose Tissue↗