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 109 records · Page 6Linked to original sources

Behavioural responses of piglets to castration: the effect of piglet age.

It has long been assumed that neonatal animals are less sensitive than older animals to pain, and this reasoning has been used to recommend that routine surgical procedures be performed at an early age. In this study we tested if vocal and other behavioural responses to castration increase with piglet age. Piglets (n=84) from 14 litters were assigned to one of six treatment groups: castration or sham castration at 3, 10 or 17 days of age. During the procedure castrated piglets produced high-frequency calls (>1000Hz) at more than three times the rate of piglets in the sham-castrate group. The rate of low-frequency (<1000Hz) calls was also higher for piglets in the castrate group. The rate of high-frequency calling was lower for the youngest pigs but there was no relationship between age and the effect of treatment for any of the vocal responses measured (i.e. no age by treatment interaction). During the first 2h after castration, castrated piglets spent more time sitting or standing and less time lying. During the subsequent 22h, castrated piglets spent marginally more time at the udder and less time lying down. Older piglets missed more nursings. However, the effect of castration did not vary with the age of the piglet for any measure. We conclude that while the factors affecting both the shams and the castrates (e.g. distress due to restraint) may vary with age, the pain of castration is not affected by age within the range of ages that we tested.

Journal Article↗

Later onset of apoptosis in the bulbourethral glands after castration compared to that in the seminal vesicles.

Androgens affect many different target organs within the male reproductive tract to stimulate their development and secretory cytodifferentiation, and to maintain structure and function in adulthood. Castration causes regression of these organs via apoptosis. However, not all organs of the reproductive tract are equally sensitive to androgen withdrawal. The effects of castration on the mouse seminal vesicles (SVs) and bulbourethral glands (BUGs) were compared in terms of protein and DNA contents, epithelial apoptosis, and proliferative response of epithelial cells to androgen. Castration induced similar, marked decreases in protein contents in the SV and BUG by 2 days after castration which reached a minimum at 16 days post castration. Both organs underwent a decrease in DNA content, but the kinetics of this decline differed. In the SV, DNA content was significantly decreased by 4 days whereas in the BUG this did not occur until 16 days post castration. By day 16 both organs had regressed to roughly the same degree. The apoptotic index in the epithelium reflected this difference in timing as well. Apoptotic index of the SV epithelium was highest on day 3 after castration and declined thereafter. On the other hand, the apoptotic index in the BUG didn't begin to increase until 7 days after castration and became maximal on day 12. Daily injections of testosterone propionate (TP) from day 8, 16, or 30 after castration all increased epithelial labelling index in the SVs to a similar degree. However, the TP-induced increase in the epithelial labelling index in the BUG beginning on day 8 after castration was considerably less than that in BUGs receiving TP treatment from day 16 or 30 after castration. Thus, the proliferative response of the epithelium depended upon prior apoptosis in the gland, with the timing being delayed in the BUG as compared with the SV. The present results indicate that castration induces epithelial apoptosis and reduction in glandular DNA content considerably later in the BUG than in the SV though reduction in protein content in the BUG fell simultaneously with that in the SV.

Animals↗

An evaluation of calf castration by intra-testicular injection of a lactic acid solution.

This experiment evaluated intra-testicular injection of a sclerosing drug, lactic acid, for castration of bulls. Its use was compared in 58 Brahman cross calves (50 to 128kg) with the general practice of open surgical castration. Chemical castration appeared to be more painful than surgical castration, though post-operative swelling and pain appeared similar for both methods. Chemical castration took 3 times longer than surgical castration (58 sec v 20 sec; P less than 0.01). Scrotal necrosis occurred in 25% of chemically-castrated calves and appeared due to drug leakage from the testes under the high pressure of injection. Healing time for chemical castrates was approximately twice that for surgical castrates. Five chemically-castrated calves (18%) retained one testis. Though all 5 were rendered sterile, each maintained androgenesis. This led to secondary male behaviour which caused management problems. Castration method did not influence post-operative growth. It is concluded that lactic acid administration is not a suitable alternative to the open surgical technique for castration of Brahman cross calves.

Animals↗

Castration induces luteinizing hormone (LH) secretion in hypophysectomized pituitary-grafted rats receiving pulsatile LH-releasing hormone infusions.

An in vivo isolated pituitary paradigm was used to examine the extent to which negative feedback actions of testicular hormones are exerted directly at the level of the anterior pituitary gland. Hypophysectomized male rats received single anterior pituitary transplants under the kidney capsule. On the next day each hypophysectomized, graft-bearing (H/G) animal was fitted with a concentric atrial catheter system which allowed for intermittent infusions of LHRH (250 ng/5 min.h) and chronic blood sampling. On the fifth or sixth day of infusions, blood samples were obtained 2 h before sham-castration (n = 6) or castration (n = 5) and at every 2-h interval for 24 h thereafter. For comparison, blood samples were similarly obtained from a group of normal pituitary-intact male rats before and after sham-castration (n = 5) or castration (n = 5). Plasma LH and PRL levels in all animals were determined by RIA. In the H/G sham-castrate rats, LH levels remained constant throughout the 24-h postsurgery period. By contrast, plasma LH concentrations in the H/G castrate rats increased steadily for 18 h, reaching a plateau at levels 2- to 3-fold higher than pretreatment values. The absolute amounts of immunoreactive LH, and the trajectory of the LH rise in the H/G castrates closely resembled those in the normal castrates during the initial 20 h after castration; at subsequent time points, however, these similarities were not apparent, as LH levels in normal castrates continued to rise, while those in H/G castrates did not. PRL levels were not significantly different in H/G rats compared to those in their pituitary-intact counterparts. We conclude from these studies that most of the acute (less than 20 h) effects of castration on LH secretion can be accounted for by pituitary escape from direct negative feedback suppression. At longer times after orchidectomy, however, the continued postcastration rise in LH secretion may increasingly depend upon additional hypothalamic input. It is hypothesized that this added input consists of an acceleration of LHRH pulse frequency.

Animals↗

Control of gonadotropin secretion in the ovine fetus. III. Effect of castration on serum follicle-stimulating hormone levels during the last trimester of gestation.

Gonadal involvement in fetal FSH regulation was examined by studying FSH levels in 13 female (7 castrate and 6 sham control) and 13 male (8 castrate and 5 sham control) chronically catheterized ovine fetuses operated upon in utero at 106-115 days gestation (term = 147 days). These fetuses had been studied previously for pulsatile LH secretion every 2-7 days over a 2- to 38-day period until fetal delivery or death. From each study day, 3 1-h spaced blood samples (1.5-2.0 ml) were taken for FSH determination by RIA (NIH FSH-S8 standard), and the results were averaged. The overall mean was then calculated for each fetus. In female fetuses, there was no significant difference in mean serum FSH levels between castrates [53.4 +/- 5.0 ng/ml (+/- SEM)] and controls (52.5 +/- 14.4 ng/ml). In contrast, serum FSH levels in the eugonadal males were significantly (P less than 0.001) lower (23.4 +/- 8.0 ng/ml) than those in castrate males (56.9 +/- 7.1 ng/ml, a value comparable to those observed in both female groups). Mean serum FSH levels declined significantly (P less than 0.001) in castrate fetuses of both sexes after 125 days (61.5 +/- 5.6 vs. 42.4 +/- 7.7 ng/ml in females; 64.1 +/- 6.1 vs. 51.5 +/- 8.6 ng/ml in males). In the males, the FSH decline did not reach sham control levels, which remained unchanged with advancing gestation. Moreover, mean serum FSH levels were significantly higher in a group of 4 male fetuses (62.2 +/- 13.7 ng/ml) castrated at 121-130 days gestation compared to values in 3 age-matched sham castrate controls (22.1 +/- 2.6 ng/ml; P less than 0.001). The increment in serum FSH levels in castrate compared to sham castrate male fetuses demonstrates an important role for the fetal testis in FSH regulation from 106 days gestation until term. The lack of a detectable castration effect on the relatively high serum FSH levels in eugonadal females indicates that the fetal ovary does not play a similar role and suggests that in females, FSH is secreted in a functionally castrate mode. The decline in FSH levels after 125 days in castrate fetuses of both sexes may result at least in part from the previously reported coincident rise in circulating levels of feto-placental sex steroids and/or PRL.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

Effects of castration on problem behaviors in male dogs with reference to age and duration of behavior.

OBJECTIVE: To determine whether 9 problem behaviors in adult male dogs were affected by castration and to examine the influence of age and duration of problem behavior on behavioral effects of castration. DESIGN: Cohort study. ANIMALS: 57 male dogs > 2 years old at the time of castration that had > or = 1 of the targeted problem behaviors. PROCEDURE: Data were collected by telephone contact with owners to identify dogs that had > or = 1 problem behavior before castration and to estimate the improvement (ie, decrease) in the objectionable behaviors after castration. Problem behaviors of interest included urine marking in the house, mounting, roaming, fear of inanimate stimuli, aggression toward human family members, aggression toward unfamiliar people, aggression toward other dogs in the household, aggression toward unfamiliar dogs, and aggression toward human territorial intruders. RESULTS: Effects of castration on fear of inanimate stimuli or aggression toward unfamiliar people were not significant. For urine marking, mounting, and roaming, castration resulted in an improvement of > or = 50% in > or = 60% of dogs and an improvement of > or = 90% in 25 to 40% of dogs. For remaining behaviors, castration resulted in an improvement of > or = 50% in < 35% of dogs. Significant correlations were not found between the percentage of improvement and age of the dog or duration of the problem behavior at the time of castration. CLINICAL IMPLICATIONS: Castration was most effective in altering objectionable urine making, mounting, and roaming. With various types of aggressive behavior, including aggression toward human family members, castration may be effective in decreasing aggression in some dogs, but fewer than a third can be expected to have marked improvement. Age of the dog or duration of the problem behavior does not have value in predicting whether castration will have a beneficial effect.

Aggression↗

Influence of castration on the response of the rat vas deferens to fluoxetine.

Antidepressant drugs such as desipramine and fluoxetine increase norepinephrine (NE) contractile response in rat vas deferens by inhibiting neuronal amine uptake. Fluoxetine, unlike other antidepressants, also inhibits calcium fluxes, which results in an inhibition of maximal NE effect. Since the contractile response of the reproductive tract is under the influence of testosterone, the effect of fluoxetine could be modified according to the endocrine status of the animal. In the present study we evaluated the influence of castration and testosterone replacement (1 mg per 100 g body wt.) on the peripheral action of fluoxetine. Castration was followed by a decrease in vas deferens weight and the appearance of spontaneous activity. Testosterone replacement reversed these effects. Concentration-response curves to NE and calcium were obtained in the absence and the presence of fluoxetine in vasa deferentia from normal, castrated and testosterone-treated castrated rats. After castration the effect of fluoxetine on vas deferens contractility was markedly altered. The spontaneous activity that appears after castration was prevented by fluoxetine and the stimulatory effect on NE-induced contractions was not observed. In contrast, the inhibitory action of fluoxetine on maximal NE effect was increased. Testosterone replacement restored vas deferens response to NE in the presence of fluoxetine. Fluoxetine did not modify the binding parameters of [(3)H]prazosin in vasa deferentia from normal or castrated animals. Cocaine shifted the NE concentration-response curve to the left in all groups, suggesting that the changes in fluoxetine effect following castration were not the result of an alteration of the neuronal uptake mechanism. The nitric oxide synthase inhibitor l-NMMA did not modify vas deferens response to NE in castrated animals either in the absence or presence of fluoxetine. An increased sensitivity to the inhibitory effect of fluoxetine was observed in the calcium concentration-response curves in vasa deferentia from castrated rats, an effect that was reversed by testosterone replacement. The results suggest that the alteration in the responsiveness of vasa deferentia from castrated rats to calcium could be responsible for increased sensitivity to the inhibitory effect of fluoxetine. It is concluded that vas deferens contractile response is testosterone dependent and that this behaviour modifies the effect of drugs such as fluoxetine that have dual effect on contractility.

Adrenergic alpha-Antagonists↗

Pituitary androgen receptors and the resistance of long-term castrated rams to the androgenic control of luteinizing hormone (LH) secretion.

Luteinizing hormone (LH) responses of short-term (24 h) and long-term (6 mo) castrated rams to testosterone replacement therapy were investigated. Testosterone filled Silastic capsules which maintained physiological concentrations of testosterone in blood (approximately 3.2 ng/ml) prevented the post-castration rise in serum LH of short-term castrated rams but failed to effectively reduce the established elevated serum LH levels in long-term castrated rams. The LH response to exogenous LHRH was also suppressed in the short-term castrated rams, whereas the response was increased in direct proportion to basal LH levels in long-term castrates. The possibility that a change in pituitary androgen receptors may explain the resistance of long-term castrates to testosterone feedback was examined. For this purpose, a cytosolic androgen receptor binding assay was developed using tritiated methyltrienolone (R 1881) as the labeled ligand and dextran-charcoal to separate free and protein-bound steroid. Stable, high affinity (Kd = 0.3-1.5 nM), saturable binding of R 1881 was demonstrated in pituitary cytosol from both intact and castrate rams. Relative binding specificities in intact rams, however, suggested partial binding to a progestin-binding component, whereas receptor binding in long-term castrates was androgen specific. For this reason, androgen receptor binding was studied after addition of triamcinolone acetonide to occupy apparent progestin binding sites. We observed no differences in either androgen receptor concentration (4.10 +/- 0.70 versus 3.23 +/- 0.45 fmol/mg protein; Mean +/- SD) nor ligand affinity at 0 degrees C (Kd = 0.66 +/- 0.34 versus 0.40 +/- 0.08 nM) in 6 mo compared to 24-h castrate rams. These data indicate that the inability of androgens to suppress gonadotropin secretion in long-term castrate rams is unlikely to be related to specific changes in pituitary cytosol androgen receptors.

Animals↗

Some pre- and postjunctional effects of castration in rabbit isolated corpus cavernosum and urethra.

Pre- and postjunctional effects of castration were investigated in isolated corpus cavernosum (CC) and prostatic and preprostatic urethral preparations obtained from rabbits that had been castrated surgically 14 days before investigation. Preparations obtained from untreated animals were used as controls. Castration did not change the relaxing effects of SIN-1 (NO donor) or papaverine in CC preparations contracted by noradrenaline (NA). Electrical field stimulation of CC preparations contracted by NA or endothelin-1 produced frequency-dependent and tetrodotoxin-sensitive relaxations. As compared with controls, the electrically induced relaxations were increased in preparations from castrated animals. Pretreatment with prazosin increased the electrically induced relaxations in CC from untreated rabbits, but had no effect on preparations from castrated animals. In CC preparations incubated with 3H-NA, castration significantly reduced the electrically evoked release of 3H. L-NOARG, an inhibitor of NO synthase, had no effect on 3H-efflux. In prostatic, but not preprostatic, urethral preparations contracted by NA, the relaxant effects of SIN-1 and vasoactive intestinal polypeptide were significantly smaller following castration. Furthermore, castration significantly reduced electrically evoked relaxations in prostatic urethral preparations contracted by NA, while in preprostatic urethra, no such effect was seen. Castration or L-NOARG had no effect on the electrically induced release of 3H-NA in either of the urethral tissues. The results suggest that the hormonal changes caused by castration may modulate the functional effects in vitro of some parts of the urogenital tract. In penile erectile tissue, the relaxations induced by electrical field stimulation are increased, probably for the most part through a decrease in the neuronal release of NA. In prostatic urethra, on the other hand, electrically evoked relaxations are decreased, possibly as a result of an impaired ability of the smooth muscle itself to respond to relaxant agents. In preprostatic urethra, castration has no obvious functional effects. The physiological consequences of these findings in the in vivo situation remain to be established.

Animals↗

Influences of sex, castration, and androgens on the eumelanin and pheomelanin contents of different feathers in wild mallards.

In mallards the bright nuptial plumage of the drake represents the neutral, sex hormone-independent coloration of the species that both sexes eventually exhibit after castration. We compared the pheo- and eumelanin contents of feathers from the head, breast, flank, and under-tail coverts in five groups of mallards after the post-nuptial molt in summer: intact hens, intact drakes, castrated drakes, castrated drakes injected with testosterone during the spring, and castrated drakes injected with 5 alpha-dihydrotestosterone during the spring. In the head feathers and under-tail coverts, the gonadal hormones of the intact birds and the testosterone injections into castrates significantly reduced the eumelanin content, tended to increase the pheomelanin content, and, thereby, changed the melanin type from eumelanic in the untreated castrates to mixed melanic in the other three groups. The eumelanin contents of the flank feathers did not differ among the groups, but the pheomelanin contents at this site was significantly elevated in the two intact groups and the testosterone-treated compared to the uninjected castrates. Again, the melanin type changed from eumelanic in the castrates to mixed melanic in the other three groups. The high pheomelanin content of the breast feathers in the castrated birds was significantly reduced in the hens, intact drakes, and testosterone-injected castrates with a concomitant tendency for elevated eumelanin contents. At this site, a change occurred from pheomelanic to mixed melanic. 5 alpha-dihydrotestosterone was clearly less effective than testosterone in affecting the melanin contents in castrates and resulted in an intermediate coloration.(ABSTRACT TRUNCATED AT 250 WORDS)

Androgens↗

Diminished role of LHRH in the control of gonadotroph morphology and function in the long-term castrated male rat.

It was found in previous studies that the neurotransmitter control of the secretion of LHRH and LH differs between long-term castrated and ovariectomized rats. One interpretation of these data was that there was a reduced 'positive drive' in the male, and the question was raised 'how do the gonadotrophs of long-term castrated rats maintain a high level of LH secretion?'. In the present series of experiments, evidence for a reduced dependence of the gonadotrophs upon LHRH stimulation is provided. Although sensitivity to native LHRH was not completely lost in long-term castrated rats, two potent LHRH antagonists (D-pyroglu1,D-Phe2,D-Trp3,6)-LHRH and (N-acetyl-3,4-dehydro-Pro,p-fluoro-D-Phe2,D-Trp3,6)-LHRH, were found to inhibit LH secretion in short-term castrated and long-term ovariectomized rats, but not in long-term castrated rats. Neither blockade of axonal transport with colchicine nor immunoneutralization of LHRH with an antiserum against LHRH (both administered 48 h before blood sampling) produced reductions in serum concentrations of LH in long-term castrated rats, although these treatments significantly suppressed LH levels in short-term castrated animals. Chronic (6-day) infusions of the second LHRH antagonist (up to 450 micrograms/day) neither reduced LH secretion nor altered the morphology of the 'castration cells' in the pituitaries of long-term castrated rats. Chronic treatment with testosterone (15 days), however, reversed these parameters to some extent, and when the testosterone treatment was coupled with chronic infusions of the LHRH antagonist, significantly lower serum levels of LH and reductions in the size of the castration cells were observed. These data thus indicate that castration cells may function autonomously, without the need for LHRH, and that testosterone in some way restores the dependency on LHRH and/or the responsiveness to LHRH of these cells.

Animals↗

Influence of castration and estrogen replacement on sexual behavior of female-oriented, male-oriented, and asexual rams.

An experiment was conducted to determine whether exogenous estradiol-17beta (E2) could restore sexual behavior in castrated rams. The protocol consisted of three sequential 6-wk periods during which rams were studied while 1) intact, 2) bilaterally castrated, or 3) implanted s.c. with two 7.6-cm silastic implants each containing 309+/-16 mg of E2. Rams (classified as female-oriented [FOR, n = 7], male-oriented [MOR, n = 7], or asexual [n = 7]) were subjected to 30-min sexual behavior tests every 2 wk during the ensuing 18 wk. Rams were observed for mounts and ejaculations using two ovariectomized, estrous ewes and two intact males secured in stanchions. Behavioral data were analyzed using the signed rank test, but asexual rams showed no sexual behavior and therefore were not evaluated statistically. Jugular blood was collected prior to castration and at the end of the 18-wk period, and testicular venous (n = 21) and arterial (n = 8) bloods were collected immediately prior to castration. Radioimmunoassay was used to quantify systemic levels of estrone (E1), E2, and testosterone (T) and testicular serum concentrations of oxytocin (OT). Mounting behavior of MOR and FOR declined after castration (P < .05 and P < .10, respectively). Castration reduced the number of ejaculations by FOR (P < .05), but not by MOR (P > .10). Mounting behavior of castrated MOR and FOR was not affected by E2 treatment relative to that observed if castrated only (P > .10). Treatment of asexual rams with E2 did not stimulate sexual behavior in these rams. There were no marked differences (P > .10) among ram groups with regard to serum concentrations of E1, E2, or T prior to castration (overall mean +/- SE, 12.8+/-.7, 7.6+/-.5, and 2,670+/-780 pg/mL, respectively) or any difference (P > .10) in systemic concentration of E1 or E2 among ram groups after rams were implanted with E2 (overall mean +/- SE, 9.7+/-.7 and 9.0 +/-.7 pg/mL, respectively). Serum concentrations of E2 after implantation of the steroid did not differ from those present while rams were intact (P > .10). Testicular venous and arterial serum concentrations of OT were low and did not differ within or between rams. These results suggest that restoration of E2 concentrations to physiological levels in castrated adult rams (regardless of sexual orientation) cannot stimulate or reestablish sexual behaviors to levels observed prior to castration.

Animals↗

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↗

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↗

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↗

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↗

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↗

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↗