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PubMed1975

Luteinizing hormone release in entire and castrated rams following injection of synthetic luteinizing hormone releasing hormone, and effect of testosterone propionate pre-treatment.

Plasma luteinizing hormone (LH) levels and LH responses to intravenous administration of 100 mug luteinizing hormone releasing hormone (LH-RH) were studied in entire rams, long-term castrated animals (operation performed six months previously), long-term castrated animals treated with testosterone for the two prededing weeks and short-term castrated animals (castrated 3 h before LH-RH injection). LH was measured by radioimmunoassay in samples taken at 5 or 15 min intervals. Basal LH levels were lower in entire rams (0-9 ng/ml) than in long-term castrated animals (6-0 ng/nl). After LH-RH treatment the LH response was much smaller (peak level 9-6 ng/ml), total response 13-3 ng/ml/1 h) and slower (120 min to peak) in entire than in long-term castrated animals (peak level 61-8 ng/ml, total response 141-2 ng/ml/1 h, 29 min to peak). Testosterone treatment after long-term castration depressed the basal LH level and delayed the peak LH response after LH-RH to values similar to those for entire rams. After short-term castration the response to LH-RH was already as great (peak level 70-1 ng/ml, total response 133-6 ng/ml/1 h) as after long-term castration. The latency to peak LH level (82 min) was intermediate between that for untreated and testosterone-treated long-term castrated animals (130 min). Testosterone treatment was considered to have acted on the hypothalamus to depress basal levels. The results provided evidence for the presence of two inhibitory actions of the testis at the pituitary level in the ram: a qualitative delaying action of testosterone and a quantitative inhibitory action of the testis on LH release after LH-RH injection. The latter may also be related to plasma testosterone levels.

Animals↗
PubMed1996

Cell proliferation and apoptosis during prostatic tumor xenograft involution and regrowth after castration.

The biological mechanisms involved in androgen-dependent and -independent prostate cancer growth after castration were analyzed in the LuCaP 23.1 human prostate cancer xenograft model. Athymic mice (n = 82) bearing LuCaP 23.1 xenograft were castrated and tumors were harvested at different time points from day 0 to day 112 post castration. In each group of mice, tumor growth rate (TGR), serum PSA concentration, percentage of tumor cells incorporating bromodeoxyuridine (BUdR index), percentage of apoptotic tumor cells assessed by morphological analysis (apoptotic index), and presence of apoptosis-related DNA "ladder" were analyzed. Castration induced a significant decrease in TGR and serum PSA from day 1 to day 7, and a progressive increase in the 2 parameters from day 14 to day 112, heralding androgen-independent tumor relapse. Meanwhile the BUdR and apoptotic indexes varied as follows after castration: an increase was noted for both at day 3, a significant increase in apoptotic index with a decrease in BUdR index from day 5 to day 14, and a progressive decrease in apoptotic index while BUdR index remained at 50% of the pre-castration value from day 28 to day 112. DNA ladder was present sparsely in tumors grown in non-castrated hosts, universally present in tumors from day 1 to day 28 post castration, and frequent in tumors from day 56 to 112. Castration-induced effects in LuCaP 23.1 tumors were characterized by an increase in number of apoptotic cells and a decrease in proliferative activity. The androgen-independent tumor relapse after castration was associated with a low apoptotic index with no increase in proliferative activity.

Animals↗
PubMed1989

Effect of androgen pretreatments at adulthood on androgen-induced proliferative response of seminal vesicles in neonatally castrated mice.

Male mice were castrated on days 0 and 60 after birth. The majority of the neonatally castrated mice were pretreated with androgen; the mice were given daily injections of testosterone propionate (TP; 4 or 8 micrograms/g body wt) for 20 or 30 days starting from day 60. Daily injections of TP (4 micrograms/g body wt) to examine androgen-induced proliferation were started from day 30 or 60 after the end of TP pretreatments or from day 60 after castration; on various days after starting TP injections, the weight and the incorporation of 5-[125I]iodo-2'-deoxyuridine into the whole seminal vesicles were determined as indices for proliferation. The seminal vesicles of neonatally castrated adult mice were characterized by long duration of androgen-induced proliferation (greater than 20 days) with a low peak (neonatal castration type), whereas the seminal vesicles of adult castrated mice were characterized by short duration of proliferation (10 days) with a high peak (adult castration type). In neonatally castrated adult mice, the neonatal castration type of androgen-induced proliferation was changed largely to the adult castration type when pretreatment with 8 micrograms/g body wt of TP had been given for 30 days. However, this effect gradually disappeared when the mice had been pretreated with decreasing amounts of TP for a shorter period. The present findings suggest that the defect in the androgen-induced proliferative response of mouse seminal vesicles induced by the absence of neonatal and prepubertal testicular androgens can be compensated by androgens given in adulthood, if enough androgen is given for a sufficiently long time.

Animals↗
PubMed1989

Increase in epithelial cell growth by hyperprolactinemia induces delay of castration-induced involution of mouse seminal vesicle.

Male (C57BL/6 x DBA)F1 hybrid mice were castrated on day 60 after birth; two pituitaries from 60-day-old female mice were immediately grafted under the capsule of the left kidney in half of the castrated mice to induce hyperprolactinemia. The seminal vesicles in the absence of androgen treatment were examined 15, 22, 30 and 60 days after castration with or without grafting. Significant increases in the weight (1.3-1.4-fold), DNA content (1.2-1.3-fold) and labeling index of epithelial cells (4-10-fold) of the seminal vesicles were found in mice with pituitary grafts compared to mice without grafts on days 15-30 after castration but not on day 60 after castration. Such stimulatory effects of hyperprolactinemia on mouse seminal vesicle cells were also observed on day 15 after castration plus adrenalectomy. Cell loss from the seminal vesicles was found to be similar in castrated mice with and without the grafts. The present findings demonstrate that hyperprolactinemia induces an increase in DNA synthesis of epithelial cells in the seminal vesicles until 30 days after castration and results in a significant delay of castration-induced involution of the weight and DNA content of the seminal vesicles for 1 month. However, the delay with increased epithelial cell growth by hyperprolactinemia disappeared 60 days after castration.

Adrenalectomy↗
PubMed1989

Effect of castration on plasma luteinizing hormone in postpubertal boars.

Two experiments were conducted to test the working hypothesis that mean plasma concentrations of luteinizing hormone (LH) increase as a result of an increase in the frequency and amplitude of the pulsatile releases of LH in postpubertal boars after removal of gonadal steroid hormones by castration. It was further hypothesized that these changes in secretion of LH would be the result of changes in sensitivity of the pituitary to gonadotropin releasing hormone (GnRH). In Experiment 1, plasma LH was monitored in 10 postpubertal crossbred boars (13 to 14 mo old and weighing 159 +/- 6.0 kg) at 12-min intervals for 6 h before and 1 h after GnRH (375 ng/kg of body weight) on Days -1, 7, 14, 21 and 29 relative to castration. In Experiment 2, plasma LH was monitored in four castrated and five intact postpubertal boars (11 to 12 mo old and weighing 150 +/- 5.1 kg) after each of three doses of GnRH (94, 188 and 375 ng/kg) were administered to each animal. Sample collection occurred 5 wk after castration. Mean LH and frequency of pulsatile releases of LH increased as a result of castration (P<0.0001), with changes evident by Day 7 after castration. However, the amplitude of the LH pulses increased minimally after castration (P<0.10). The response to exogenous GnRH increased throughout Experiment 1 (P<0.0001), even though the amplitude of the pulsatile releases of LH (response to endogenous GnRH) did not change. Castrated animals in Experiment 2 had a greater response of LH to GnRH stimulation than intact boars (P<0.05). The dose-response curve of castrated animals was not parallel (P<0.001) to that of intact boars, and indicated that sensitivity of the pituitary to GnRH had increased in the absence of gonadal steroids. Thus, the hypotheses stated above can be accepted with the exception that castration may have a minimal effect on LH pulse amplitude. Based on the results of these experiments, we suggest that gonadal steroid hormones modulate both the size of releasable stores of LH and pituitary sensitivity to GnRH in boars.

Journal Article↗
PubMed1998

Castration reduces olfactory bulb norepinephrine transporter function as indicated by responses to noradrenergic uptake blockers.

It has been demonstrated that castration alters the functioning of the olfactory bulb (OB)-norepinephrine (NE) system. In the present experiment, we examined one of the mechanisms by which castration modulates the OB-NE system by comparing NE uptake activity between intact and castrated male rats as studied using an in vitro superfusion technique. To accomplish this goal, NE output from the OB of intact and castrated male rats in response to infusion with two different drugs which alter NE uptake functions, tomoxetine and talsupram, were tested. Overall, NE outputs in response to tomoxetine were significantly higher in the castrated than in intact rats and both groups were significantly greater than non-infused controls. For the talsupram infusion group, NE outputs from the castrated, but not intact rats, were significantly greater than controls. No statistically significant differences were detected between the castrated and intact rats. These results demonstrate that castration alters the NE uptake activities in response to these noradrenergic uptake blockers and suggest that one mechanism by which castration alters OB-NE functioning is through reducing the uptake activity of NE within the OB. Such findings have important implications for olfactory-based learning and memory/recognition processes which are believed to involve the OB-NE system and are altered following castration.

Adrenergic Uptake Inhibitors↗
PubMed1999

Influences of surgical castration on the thymus of male rats.

In previous studies, we have shown that castration of Sprague-Dawley rats enhances thymic weight through puberty whilst sex steroids reduce the castration-induced hypertrophy. In the current study, we have confirmed that castration enhances thymic growth compared to age-matched intact controls. In addition, immunoassays were used to measure thymosin alpha1 and thymosin beta4 levels in sera from intact and castrate rats. Castrate animals displayed greater sera levels of thymosins compared to sera from intact animals. To test whether the enhanced thymic weight and increased levels of thymosins observed post-castration were able to influence immune function of castrate animals, concanavalin A was used in the 3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenyl tetrazolium bromide assay to examine lymphocyte and thymocyte responses from both intact and castrate male rats. Responses of cells isolated from castrate rats demonstrated that lymphocytes and thymocytes were stimulated at low levels of concanavalin A (1.56-3.13 microg/ml for lymphocytes and 1.56 microg/ml for thymocytes) compared to the same cell types isolated from intact rats. Concentrations of concanavalin A ranging from 6.25 to 200 microg/ml produced no significant differences in response from intact and castrate animals.

Animals↗
PubMed1999

Effects of adrenocorticotrophin (ACTH) and progesterone on luteinising hormone (LH) secretion in recently castrated rams.

The goal of the present study was to determine whether ACTH and progesterone have any effect on LH secretion and pulse frequency in recently castrated rams. Six 2-year-old Corriedale rams were castrated in the winter. The day before castration, blood samples were taken in order to establish the precastration LH levels. The rams were divided into an untreated group (group U: n = 2) and a treated group (group T: n = 4). The first treatment consisted of the i.v. administration of 0.5 mg of ACTH on day 20 post-castration, immediately after the first sample had been taken. During the second treatment, subcutaneous progesterone implants were given to group T for 5 days. Control samplings were performed one week before each treatment. Prior to castration, the testosterone levels were low, while after castration they were below the detection limit of the assay. Cortisol and progesterone concentrations were basal before castration in all of the animals and after castration in group U and also in the control samplings for group T. ACTH treatment caused a significant increase in both cortisol and progesterone levels for 3 h (P < 0.001). Progesterone implants raised progesterone levels in group T, but cortisol levels remained basal. Before castration, all animals had low LH levels and hardly any pulse activity was seen. After castration, both the number of LH pulses and the mean LH production increased significantly in all of the animals (P < 0.01). During the ACTH trial, LH pulse frequency was significantly reduced for the first 4 h following ACTH administration (P = 0.013), however, no such differences occurred in the prior control period. No effect was seen on mean LH concentration during the ACTH treatment. Progesterone treatment did not have any effect on either the number of LH pulses nor on LH concentrations (P > 0.05).

Adrenocorticotropic Hormone↗
PubMed1990

Urokinase- and tissue-type plasminogen activators are suppressed by cortisol in the involuting prostate of castrated rats.

The effects of cortisol on the inhibition of cell-death processes and suppression of plasminogen-activator (PA) activity during involution of the rat ventral prostate gland were investigated to determine the principal type of PA activated by castration and inhibited by this hormone and whether the mechanism responsible for decreased PA activity involved reductions in enzyme synthesis or increased activity of a PA inhibitor. By using the technique of fibrin-agarose zymography, three bands of PA activity were detected at 4 and 7 days after castration: a major band with a molecular mass of approx. 30 kDa and two minor bands of 48 kDa and 64 kDa. Both the 30 kDa and 48 kDa activities were inhibited with anti-[urokinase-type PA (u-PA)] IgG. The 64 kDa activity was inhibited by anti-[tissue-type PA (t-PA)] IgG. In addition to retarding prostatic involution, daily administration of cortisol to the castrated animals suppressed all three bands of PA activity. A comparison of the pattern of total PA activity and of e.l.i.s.a. estimates of u-PA concentration during the castration-induced rise and after cortisol inhibition indicated a near perfect correlation between the two parameters. Northern-blot analysis using prostatic polyadenylated RNA revealed that the level of u-PA mRNA was highest at 4 and 7 days after castration and that cortisol treatment repressed u-PA mRNA to a level similar to that in non-castrated controls. Neither Northern hybridizations nor reverse zymography detected RNA transcripts or activity corresponding to the PA inhibitor PAI-1 in any of the prostate samples. Western-blot analysis revealed that, although the amount of arginine esterase A, another prostatic proteinase, also increased after castration, the rise in concentration of this protein was not blocked by glucocorticoid administration. Together our findings indicate the following: (1) the predominant form of PA activity induced in the prostate after castration and inhibited by cortisol is a 30 kDa form of u-PA. Although less prominent, t-PA and a 48 kDa form of u-PA follow a similar pattern of induction and inhibition; (2) changes in u-PA activity in response to castration and cortisol treatment are due to alterations in the level of u-PA mRNA and protein rather than in the activity of PAI-1; (3) not all castration-induced proteinases in the prostate are inhibited by cortisol.

Animals↗
PubMed2005

Effect of alendronate administration on bone mineral density and bone strength in castrated rats.

Castration of male rats leads to increased bone turnover and osteopenia. This study was conducted to examine the effects of the aminobisphosphonate alendronate on castration-induced bone changes. Bisphosphonates are drugs that inhibit bone turnover by decreasing the resorption. Since they suppress bone remodeling, they may also prevent the repair of microdamage and decrease bone strength. Although the mechanical properties of bones are directly related to the determination of fracture risk, bisphosphonate effects on the related variables have scarcely been investigated. Twenty-four male Wistar rats at two months of age were castrated or sham-operated to evaluate the effects of long-term administration (six months) of sodium alendronate at a dose of 1 mg/kg/day. The bones were tested mechanically by a three-point bending test in a Mini Bionix (MTS) testing system. High bone remodeling seen in castrated rats expressed by increased TrACP and B-ALP was suppressed by alendronate administration. Bone from castrated rats was characterized by a reduction in bone density as well as ash, calcium and phosphate content. Castration significantly altered mechanical properties of bone and femoral cortical thickness. When castrated rats were treated with high dose of alendronate, the changes in bone density resulting from castration were entirely prevented, and mechanical analysis revealed preserved mechanical strength of femur and cortical thickness. We conclude that castration induces cortical bone loss associated with high bone turnover in the male rat, and this bone loss can be prevented by alendronate through the inhibition of osteoclastic activity, while preserving the mechanical properties of bone. These results document the efficacy of alendronate, even at high doses, in preventing bone loss, loss of bone mechanical strength, and the rise in biochemical bone turnover indicators due to castration in rats, and raises the possibility that a alendronate could be equally effective in humans.

Acid Phosphatase↗
PubMed2005

The welfare significance of the castration of cattle: a review.

Castration is an ancient husbandry procedure used to produce docile cattle for draught work, to reduce unwanted breeding, and to modify carcass quality. All the physical methods used to castrate cattle have side-effects and cause pain. The plasma cortisol response to castration using Burdizzo clamps and, by inference, the acute pain experienced, is less than that caused by surgical, rubber-ring or latex-band castration. The cortisol response may be influenced by the age of the animal castrated, but this has not been well defined. Local anaesthesia virtually eliminates the cortisol response, and thus the acute pain, caused by rubber-ring or latex-band castration, but needs to be combined with a systemic analgesic such as the non-steroidal anti-inflammatory drug ketoprofen to eliminate the cortisol response to Burdizzo or surgical castration. When used alone, ketoprofen sometimes reduces the cortisol response to Burdizzo or surgical castration but may need to be accompanied by local anaesthesia to eliminate the pain-induced behaviour seen during the castration process itself. Thus, pharmacological methods are available to virtually eliminate the acute pain experienced by calves during the 12 h following castration. The use of these methods is an additional cost for farmers and may be limited by the availability of drugs for farmers to use and the scarcity of veterinarians in farm animal practice.

Anesthetics, Local↗
PubMed1995

The effect of long-term castration on the neuronal and physiological responses to acute or repeated restraint stress: interactions with opioids and prostaglandins.

Sixty min supine restraint stress induced a marked, but transient, hypothermic response in intact male rats, which tended to recover towards pre-stress levels or slightly overshoot during the later stages of restraint. Castration reduced the initial hypothermia but increased overshoots. Baseline (pre-stress) core temperature was also higher in castrated than intact rats, but the reduction in stress-induced hypothermia was still present even when this difference had been taken into account. The hypothermic response was not altered during the course of 10 sessions of daily repeated restraint in either intact or castrated rats. Castration did not alter cardiac responses to restraint. Both intact and castrated rats showed marked tachycardia during the initial 12 min of restraint, followed by a gradual fall towards baseline values. Repeated restraint accentuated the second phase of the cardiac response, without modifying the initial tachycardia, in both intact and castrated animals. The response of blood corticosterone levels to the first period of restraint was unaltered by castration but the attenuation observed after 10 sessions of stress was more complete in castrated rats. The neuronal c-fos response 60 min after the last of the series of repeated restraints was less in the hypothalamic paraventricular nucleus, medial amygdala, and locus coeruleus compared with that following the first session, but not in the lateral septum or the bed nucleus of the stria terminalis. Castration did not change the c-fos profile following the same number of restraint sessions. Castration depleted completely the vasopressinergic innervation in the lateral septum, diagonal band of Broca and medial amygdala.(ABSTRACT TRUNCATED AT 250 WORDS)

Acute Disease↗
PubMed1999

Acute cortisol responses of lambs to ring castration and docking after the injection of lignocaine into the scrotal neck or testes at the time of ring application.

OBJECTIVE: To test whether injecting lignocaine into the scrotal neck 5 to 10 s before or into both testes immediately after ring castration and docking wound significantly reduce the plasma cortisol response to castration and docking. DESIGN: A physiological study with controls. PROCEDURE: Lambs were given one of six treatments: control handling, injection of lignocaine into scrotal neck, injection of lignocaine into both testes, ring castration and docking, ring castration and docking after lignocaine was injected into the scrotal neck, and ring castration and docking before lignocaine was injected into both testes. Blood samples were taken before and regularly after treatment and analysed for plasma cortisol concentrations. RESULTS: The plasma cortisol concentrations of lambs castrated and docked after lignocaine had been injected into the scrotal neck were significantly lower between 20 and 60 min after treatment than in lambs castrated and docked without local anaesthesia. Injecting lignocaine into the testes after ring application did not significantly reduce the cortisol response to ring castration and docking. CONCLUSIONS: Lignocaine injected into the scrotal neck 5 to 10 s before ring castration will reduce the cortisol response and by inference the pain associated with ring castration.

Anesthesia, Local↗
PubMed2001

Effects of surgical or banding castration on stress responses and behaviour of bulls.

OBJECTIVE: To compare the effects of surgical and latex banding methods of castration in 14- and 9-month-old bulls. DESIGN: Two randomised, controlled experiments. PROCEDURE: In Experiment 1, following administration of local anaesthetic, 14-month-old bulls were castrated by either surgical or banding methods, or left entire. Behavioural, plasma cortisol, plasma haptoglobin and bodyweight responses were recorded. A group of steers from the same mob was used as an additional comparison for bodyweight data. In Experiment 2, following administration of local anaesthetic, 9-month-old bulls were castrated by either surgical or banding methods and cortisol, haptoglobin and bodyweight responses were recorded. Entire bulls from the same group were used as an additional comparison for bodyweight data. RESULTS: In Experiment 1, surgical castrates exhibited more leg stamping and tail swishing than banded or entire animals in the hours after castration. Surgical castrates in both experiments also showed an increase in plasma haptoglobin, which resolved after 4 days. Plasma cortisol was generally not affected by castration. Surgical castrates grew more slowly than entire bulls, but faster than banded animals, in the 56 days after treatment. In Experiment 1, after 56 days, the bodyweights of surgical and banded castrates were not different from the bodyweights of the steers. Fourteen-month-old banded cattle developed persistent wounds above the latex band which remained for several weeks after scrotal dehiscence, but this did not occur in the 9-month-old animals. CONCLUSION: The banding procedure produced fewer acute effects, but a greater suppression of growth than surgical castration and induced prolonged wound formation in the older age group, suggesting that this procedure may not be as suitable for yearling cattle.

Age Factors↗
PubMed1994

Castration-induced decrease in the activity of medial preoptic and tuberoinfundibular GABAergic neurons is prevented by testosterone.

We recently determined that castration specifically decreased GABA turnover in discrete rostral and mediobasal hypothalamic structures. This study aimed to investigate whether testosterone could stimulate GABAergic neuronal activity in these hypothalamic GABAergic neurons in the castrate rat, and to compare the effects of episodic testosterone replacement with the constant levels provided by subcutaneous testosterone implants. Animals were divided into 4 experimental groups: intact, 48 h castrate, 48 h castrate+testosterone capsules (2 x 30 mm Silastic implants, 1.57 mm ID, 3.18 mm OD) and 48 h castrate+testosterone injections (100 micrograms/injection s.c., every 8 h). GABA concentrations were measured in 4 microdissected brain regions either before or 60 min after inhibition of the GABA degrading enzyme, GABA transaminase, by injection of aminooxyacetic acid (AOAA, 100 mg/kg i.p.). The rate of GABA accumulation in the tissue following injection of AOAA was used as an index of GABAergic neuronal activity. Castration resulted in a 10-fold increase in serum LH concentrations compared with intact rats. Either mode of testosterone administration completely prevented this castration-induced LH rise. In the diagonal band of Broca at the level of the organum vasculosum of the lamina terminalis, the medial preoptic nucleus and in the median eminence, GABA turnover was significantly reduced by castration to approximately 50% that of intact rats. Either testosterone implants or testosterone injections prevented this castration-induced decrease in GABA turnover, such that the turnover rates were not significantly different from intact rats. There was no effect of castration with or without testosterone replacement in the cingulate cortex.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1999

Early effects of castration on the vascular system of the rat ventral prostate gland.

Recent studies have found that blood flow to the rat ventral prostate gland is drastically reduced at an early time after castration. These observations caused us to reevaluate the effects of castration on the various cell populations of the ventral prostate, especially those in the prostatic vascular system. Sections of ventral prostate glands obtained at different times after castration were analyzed using the TUNEL (terminal deoxynucleotide transferase-mediated dUTP nick END labeling) staining method to quantify apoptosis in different cell types. The results of this analysis showed a significant increase in TUNEL staining of prostate endothelial and (nonendothelial) stromal cells as early as 12 h postcastration that continued to 24 h after castration. In contrast, TUNEL labeling of prostate epithelial cells was not significantly increased compared with control values until 72 h after castration. The use of dual immunohistochemical staining procedures (anti-CD31 for endothelial cells or antismooth muscle actin for smooth muscle cells combined with TUNEL labeling) allowed us to confirm that the TUNEL-positive vascular cells at these early times after castration were endothelial in nature, whereas smooth muscle cells surrounding the prostate glands or portions of the afferent vascular endothelium were rarely TUNEL labeled. Electron microscopic evaluation of ventral prostate tissues at 48 h after castration provided further morphological evidence for the occurrence of apoptosis in prostate endothelial cells. Finally, the Lendrum-Fraser histochemical procedure used to identify fibrin leakage in tissues with vascular damage was applied to sections of the ventral prostate gland. This stain revealed diffuse fibrin accumulation in periglandular areas outside the capillaries and blood vessels in prostates from 24-h castrated rats, but not in prostates of sham-operated rats. Our results confirm an early effect of castration on the vascular system of the rat ventral prostate identified by increased apoptosis of endothelial cells and vascular leakiness. As these changes temporally precede the loss of epithelial cells, we propose that they may be causal rather than incidental to regression of the rat ventral prostate after castration.

Actins↗
PubMed2002

Castration induces apoptosis in the mouse epididymis during postnatal development.

The effect of castration on apoptosis in the mouse epididymis during postnatal development was examined. The weight of the epididymis slowly increased from day 0 (day of birth) to day 20 after birth, followed by a rapid increase thereafter. Castration on days 0, 5, 10, 20, 30, 40 and 60 increased apoptotic indices (percentages of apoptotic cells) of epithelia of the caput (head), corpus (body), and cauda (tail) epididymis, their apoptotic indices reaching maximal levels on day 2 after castration with the exception of a maximal apoptotic index on day 4 in the tail after castration on day 60. The maximal levels of apoptotic indices of the head, body and tail after castration on days 0, 5, 10 and 20 were significantly lower than those after castration on days 40 and 60. DNAs extracted from the epididymides 2 days after castration on days 0, 5, 10 and 60 showed a ladder pattern on agarose gel electrophoresis, which is a characteristic of apoptosis. When testosterone propionate (10 microg/g body weight) was injected twice a day into mice which had been castrated on day 10, 30 or 60, the increases in apoptotic indices of the head, body and tail of the epididymis were completely inhibited. The weights of the paired epididymides 6 days after castration on days 0, 5, 10, 20, 30, 40 and 60 were significantly lower than those of sham-operated mice, indicating the secretion of androgen by the testes from birth to adulthood. The present results indicated that androgen deprivation caused by castration induces apoptosis in the epithelium of the epididymis of mice from birth to adulthood, and suggested that a proportion of epithelial cells, the survival of which is dependent on the testes, is smaller in the epididymides during a slow growth stage than in the epididymides after this stage.

Animals↗
PubMed1992

Cerebrospinal fluid and blood concentrations of luteinizing hormone, follicle stimulating hormone and prolactin following castration of adult male rats.

Comparative levels of LH, FSH, and PRL in the serum and cerebrospinal fluid (CSF) of adult male rats were studied at different periods following castration. Intact and sham-operated animals served as controls. Blood and CSF were collected at 1, 3, 7, 14, 21, 28, 35 and 46 days following castration. The CSF was collected via cisterna-magna puncture, while the blood was collected from abdominal aorta. Serum gonadotropins increased progressively beginning day 1 post-castration to reach maximum by day 35 or 46 post-castration. Sham operation and castration did not affect mean CSF, LH and FSH levels compared to intact controls. Analysis of the temporal pattern of serum and CSF gonadotropin levels following castration revealed significant positive correlation between CSF and serum LH (r = 0.58) and FSH (r = 0.64) levels respectively. The data suggest that CSF gonadotropins may be derived from systemic circulation. Serum PRL levels were not affected by castration, but CSF PRL levels were significantly reduced at days 28, 35 and 46 post-castration compared to intact controls. CSF PRL levels showed negative correlation with serum LH and FSH levels but failed to show a correlation with serum PRL levels. Hypothalamic norepinephrine turnover rate increased at days 28, 35 and 46 post-castration. Hypothalamic dopamine contents and turnover rates were reduced at days 21 and 28 post-castration. It is suggested that CSF PRL may have a role in the regulation of serum gonadotropins.

Animals↗