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At least 19 recordsLinked to original sources
PubMed1979

In vivo effect of human chorionic gonadotropin on the migration of inflammatory cells in intact or castrated male and female guinea-pigs: a quantitative histological study. II. Study of castrated males and females.

The effect of purified human chorionic gonadotropin (HCG) on the migration of inflammatory cells into dacron mesh tissue containing live BCG and implanted under the skin of castrated male and female guinea-pigs was investigated. Cell counts have shown that no significant difference appeared between controls and castrated guinea-pigs given HCG. This work suggests that the inhibiting effect of HCG on the mobility of neutrophil granulocytes is closely related to the presence of both male and female gonads.

Animals↗
PubMed1979

A study of the enzyme activity in the seminal vesicles of castrated and hormone-replaced castrated mice.

Castration provokes a time-related decrease in weight, protein, beta-glucuronidase and glucose-6-phosphate dehydrogenase activity of seminal vesicles. A dose-dependent stimulation of these parameters is obtained with 5alpha-DHT. Cryproterone acetate counteracts the stimulatory effects due to androgen. Acid and alkaline phosphatases remain largely unaffected by these treatments.

Acid Phosphatase↗
PubMed1979

Ultrastructure of normals and castrates and the effects of testosterone and ultraviolet (UVL-B) irradiation on scrotal skin of rats.

The ultrastructure of the testosterone dependent epidermal melanocyte system of the scrotal skin of normals and castrates, with and without testosterone replacement therapy, and UVL-B (280-315 nm) radiation in black Long Evans rats is reported. UVL-B increases melanocyte activity, melanosome forming apparatus, (size of Golgi zone and RER, and quantity of cytoplasmic vesicles, dendrites, and stages of melanosomes) in normals and in castrates. Testosterone replacement therapy to castrates is not a prerequisite for stimulation by UVL-B, but it enhances the effects of UVL-B without restoring normalcy as melanosome packaging into complexes predominates. After UVL-B stimulation of normals or castrates, melanocyte dendrites are observed more often. Melanocyte dendrites of skin of castrated rats are observed less often than in normals, but with testosterone replacement therapy, the dendrites become more numerous. Melanosomes donated to keratinocytes are mostly located as singles in normals and as complexes in castrates. After UVL-B, castration, or testosterone replacement therapy, the melanosomes are packaged in keratinocytes in complexes larger than in normals. In the epidermis of long term castrates (9-109 days), non-specific clear cells are observed and Langerhans cells containing melanosomes; we did not observe them in normals. Melanocytes of castrates have a reduced melanosome forming apparatus. The dermis of castrates contains many dermal melanocytes in the superficial dermis with melanosomes in several stages of formation. These cells are not apparent in normals at this location in the dermis. Testosterone replacement therapy and/or UVL-B administered to castrates does not restore the epidermal melanocyte system nor the dermis to precastration ultrastructural appearance; castration has a permanent altering effect as melanosomes are packaged into complexes.

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↗
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↗
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↗
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↗
PubMed1975

In vitro pituitary responsiveness to gonadotropin-releasing hormone (LH-RH) in intact and castrated male and female rats.

The in vitro response of pituitaries isolated from both normal and 18-21 day post-castration male and female intact rats to incremental doses of synthetic gonadotropin-releasing hormone (LH-RH) has been investigated. Intact male pituitaries released luteinizing hormone (LH) maximally at the smallest dose of LH-RH (0.1 ng/ml) whereas intact female pituitaries released LH in a dose-response fashion. FSH release from intact male pituitaries was considerably greater than that from intact female pituitaries. As with LH, intact male pituitaries appeared maximally stimulated at 0.1 ng/ml of LH-RH. Intact female pituitaries did not release FSH until a 10 ng/ml dose of LH-RH was used. Male and female castrate pituitaries were more susceptible to LH-RH-induced LH and FSH release than were their intact counterparts, although this was more pronounced with regard to LH release. In addition castrate male pituitaries were more sensitive to lower doses of LH-RH than were castrate female pituitaries, this being most pronounced regarding LH release. Castrate female pituitaries released less FSH at the 100 ng/ml dose than at the 10 ng/ml dose, possibly indicating inhibition at these higher doses. In addition, pituitary extraction and serum from normal and castrate male and female rats were examined for LH and FSH content. LH content of castrated rat pituitaries of both sexes was considerably greater than that of their intact counterparts, as expected. However, castrate male pituitaries contained significantly less FSH than intact male pituitaries, whereas the opposite was true for the female groups. Serum LH and FSH levels were increased in the castrate groups with no difference between sexes. Serum from intact males contained considerably more FSH than did the serum from intact females.

Animals↗
PubMed1979

Testosterone-induced cell proliferation in the accessory sex glands of mice at various times after castration.

The proliferative response to testosterone in the accessory sex glands (seminal vesicle and coagulating gland) of castrated pale Balb/c mice has been examined by pulse and continuous thymidine-labelling experiments, and by the fraction of labelled mitoses technique. Progressive reductions in cellularity followed castration, and by varying the time elapsing between castration and the initiation of testosterone treatment, it was clear that the size of the response depended upon the number of cells in the tissue, relative to the normal complement. Interpretation of FLM data was difficult in periods where proliferative rates changed rapidly. We have attempted to explain the cell kinetic events by postulating a G0 compartment, form which cells are stimulated to enter the proliferative cycle before subsequently returning to an out of cycle state. It was thought unlikely that substantial changes in cell cycle time occurred. In both the accessory sex glands, the overall form of the continuous thymidine labelling curves showed that most proliferative cells entered DNA synthesis in a shorter time after stimulation at 14 days after castration than they did at 3 days after castration. The data were not consistent with cells moving deeper into G0 with time after castration. In the seminal vesicle almost all epithelial cells were potentially proliferative by 3 days after castration. In the coagulating gland only 30% were potentially proliferative at 3 days, increasing to 85% at 14 days after castration. However, such proportional increases represented much smaller changes in terms of absolute numbers of cells, because of a concomitant decline in cellularity from 3 to 14 days after castration.

Animals↗
PubMed1977

Myocardial lesions in rats fed rapeseed oil. II. Effects of castration.

The effects of castration on the incidence of myocardial lesions in rats were investigated in an experiment which included two factors: sex (entire males, castrated males, entire females and castrated (ovariohysterectomized) females) and diets (5% corn oil, 20% corn oil, and 20% Brassica napus var. Zephyr rapeseed oil). For 16 weeks, each of the 12 groups of 30 Sprague-Dawley rats, housed 2 per cage, were fed ad libitum the test oils incorporated in a semisynthetic diet. At each weighing, the mean body weights for each diet were highest in entire males followed by castrated males, castrated females, and entire females with all differences significant (P less than 0.05). The results indicated that castration did not influence cardiac fatty acid composition. The incidence of myocardial lesions in entire and castrated females and in castrated males was similar while significantly more entire males developed lesions (P less than 0.001). Rats fed a diet containing 20% Zephyr rapeseed oil showed a significantly (P less than 0.001) higher incidence of heart lesions than did rats fed diets containing 5% or 20% corn oil. Similarly, significantly (P less than 0.05) more rats fed the 20% corn oil diet had lesions than rats fed the 5% corn oil diet. The involvement of androgens in the formation of myocardial lesions is suggested, since castration significantly lowered the incidence in males but not in females.

Animals↗
PubMed1979

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

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

Animals↗
PubMed1975

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

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

Animals↗
PubMed1975

Effect of castration on the smooth muscle cells of the internal sex organs of the rat: influence of the smooth muscle on the sympathetic neurons innervating the vas deferens, seminal vesicle and coagulating gland.

Wet weights of vas deferens, seminal vesicle and coagulating gland were reduced by almost 80 to 90% 10 weeks after castration. Endogenous norepinephrine content and dopamine-beta-hydroxylas activity of these tissues were also reduced to the same degree. One week after castration there was approximately a 50% loss in the weight of all three organs. However, this was accompanied by an equal reduction in norepinephrine content and dopamine-beta-hydroxylase activity only in the vas deferens. Two weeks later the degree of reductions in wet weight, norepinephrine content and dopamine-beta-hydroxylase activity was almost identical for all three organs. Treatment of 40-day castrate rats with testosterone (10 mg/kg s.c.) not only restored the wet weights of the internal sex organs to normal but their norepinephrine content and dopamine-beta-hydroxylase activity as well. Castration of immature rats (10-14 days old) resulted in retardation of growth of the vas deferens and seminal vesicle by 90-95%, and similar reductions in norepinephrin content and dopamine-beta-hydroxylase activity, when compared to the tissues of control littermates on the 90th postoperative day. Histological examination of normal and castrate rats indicated that, along with a reduction in epithelial cells, the smooth muscle cells of the vas deferens, seminal vesicle and coagulating gland was markedly reduce in size as well. Administration of testosterone completely reversed these changes. Furthermore, deoxyribonucleic acid content of the seminal vesicle and coagulating gland was reduced by 50% after castration and then restored to control level after testosterone treatment. Taken together, it seems that atrophy of the internal sex organs following castration is a combined effect of reduction in size and number of smooth muscle cells. Therefore, it is concluded that any alteration in the size of smooth muscle cells or loss of such cells of the internal sex organs indirectly influences their sympathetic nerves in such a manner that norepinephrine concentrations, and thereby the density of innervation, are maintained at normal levels.

Animals↗
PubMed1979

Fine structural studies of rat seminal vesicle in castrated and intact animals following estrogen treatment.

The effect of estradiol and/or testosterone upon secretion by seminal vesicle in castrated and intact rats was assessed in young adult Sprague-Dawley rats, using light microscopy (LM), transmission (TEM) and scanning (SEM)electron microscopy. Hormones were injected daily for ten days beginning ten days after castrations were performed. The normal rat seminal vesicle, as revealed by SEM, was characterized by a large saccular lumen with highly folded walls. Cell surfaces were covered with microvilli, or occasionally displayed a protruding, ruffled surface, sparsely covered with short microvilli. Cytology was normal in testosterone-treated animals. Estradiol treatment of castrated animals stimulated secretion by seminal vesicle epithelial cells as evidenced by the presence of normal secretory bodies, the presence of RER, and moderately hypertrophied Golgi complexes. These glands were not heavier than were glands from castrated, untreated animals, although the epithelial cells were significantly taller. Secretion was maintained in intact animals treated with estradiol, although glands were smaller and epithelial height was reduced. Estradiol and testosterone treatment in combination did not appear to have an additive effect on secretion, weight of the gland, or epithelial height. The following results support the hypothesis that estrogen-induced prolactin synthesis and release may be involved in the mechanism by which estradiol effected stimulation of seminal vesicle epithelium. Prolactin-treated, castrated animals exhibited focal areas of stimulated epithelium. In hypophysectomized animals (untreated controls), the seminal vesicle epithelium retained some secretory bodies and secretory fluid in the glandular lumen; epithelial height was taller than that in castrated controls. Estrogen treatment reduced the epithelial height to that of castrated controls; there was no evidence of secretion. This suggests that in the absence of anterior pituitary hormones, including prolactin, the stimulatory effect of estradiol on seminal vesicle epithelium was nullified. In adrenalectomized/castrated animals, estradiol treatment stimulated secretion in seminal vesicle epithelium just as in non-adrenalectomized/castrated animals. This indicates that the adrenal gland plays a non-essential role in the action of estrogen on seminal vesicle epithelium.

Adrenal Cortex Hormones↗
PubMed1975

The effects of castration and androgen replacement on song, courtship, and aggression in zebra finches (Poephila guttata).

Castration of adult male zebra finches (Poephila guttata, Estrildidae) reduces their singing rate and the tempo of song, but castrates continue to sing song identical in form to preoperative song. Injection or implantation of testosterone propionate (TP) but not of vehicle alone reverses the changes produced by castration. Castration or partial castration also reduces the frequency of courtship, copulation, and aggression. Androgen (TP) replacement reverses these changes, but control injections do not. The persistence of song after castration contrasts with the abolition of song by castration in other birds, and this may be related to the natural history of zebra finches.

Aggression↗