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PubMed1987

Protein bound folates in liver of castrated rats.

The effect of castration and testosterone treatment on the distribution of [3H] radioactive and endogenous bound folates in hepatic cytosolic folate binding proteins (FBP-C) has been studied in rats. The distribution of [3H] radioactive bound folates in these FBP's shows no significant difference in the three experimental group animals. On the contrary a significant decrease in the amount of endogenous bound folates is observed in castrated if compared with control rats, particularly marked for FBP-CI and FBP-CII bound folates. The testosterone treatment of castrated rats partially restores bound folate levels. The decrease of bound folates in castrated rats might be ascribable to a lower availability of longer-chain forms, almost the ones that bind to FBP's; however lower binding protein content and/or lower affinity for ligands cannot be excluded.

Animals↗
PubMed1979

Inhibin activity in ram rete testis fluid: depression of plasma FSH and LH in the castrated and cryptorchid ram.

Ram "rete testis" fluid (RTF) routinely collected throughout the year has been used as a source of inhibin. The mean flow rate and mean concentration of spermatozoa in the fluid remained constant during the first 12 days of cannulation. More than 50 castrated or cryptorchid rams have been treated with low doses of steroid-free RTF over a 25-h blood sampling period. Human serum albumin was injected as a control. RTF depressed both FSH and LH plasma levels although the pattern was different for each hormone. There was no change in prolactin secretion. LH secretion was affected first while FSH remained unchanged in castrated and in cryptorchid rams. Thereafter, the maximum depression of FSH plasma levels occurred at a time when LH started to return or had returned to preinjection levels in the cryptorchid and castrated animals respectively. In the cryptorchid rams, RTF suppressed pulsatile LH secretion which was present before treatment but in the castrated animals, RTF lowered LH plasma levels which were constant and showed no pulsatile changes before treatment. Both FSH and LH inhibitory activities have been found in all active fractions obtained by purification of RTF. These activities are papain-sensitive and active fractions have a high apparent molecular weight (greater than or equal to 100 000) as shown by gel filtration and ultrafiltration. These and other results in the literature have lead to a re-definition of inhibin as a protein factor of gonadal origin able to depress plasma levels of FSH and LH, even at low doses.

Animals↗
PubMedDate not supplied

[Effect of androgens (testosterone, 5 alpha-dihydrotestosterone, 3 alpha, 17-beta androstanediol and 3 beta, 17 beta androstenediol) on the nocturnal activity of N-acetylserotonin methyltransferase and hydroxyindole O-methyltransferase in the pineal body of castrated rats].

To prove the effect of sex steroid hormones on the specificity of the pineal organ metabolism the activity of melatonin-synthesizing enzymes--N-acetylserotonine transferase (AST) and hydroxyindol-O-methyltransferase (HIMT) in the circadian rhythm was studied in castrated animals and in those administered androgens (testosterone 5 alpha-dihydrotestosterone, 3 alpha, 17 beta-androstandiol). Male Wistar rats, aged 30 days, kept for 12 hours under light conditions and for 12 hours in darkness were used in these experiments. Androgens (50 micrograms) were injected to rats two days after castration and 1 to 6 hours before the animals were sacrificed (at 2 a.m.). Activity of the enzymes under study was maximal at night (between 2 and 3 a.m.). Castration of rats weakened the peaks of the AST and HIMT activities by 30 and 40%, respectively. A single androgen administration stimulated the nocturnal rise of both androgens activities in 2 to 4 hours. By physiological activity the androgens were distributed in the following way: 5 alpha-dihydrotestosterone, 3 alpha, 17 beta-androstandiol, testosterone. beta-Epimer of androstandiol produced no effect on AST and HIMT activities in the epiphyses of castrated rats. Experimental data demonstrate that epiphysis serves as the target organ for sex steroid hormones, and that androgens are capable of modulating the melatonin-synthesizing enzymes' activity.

Acetylserotonin O-Methyltransferase↗
PubMed1983

[Effect of testosterone propionate on the induction by 1,2-dimethylhydrazine of angiosarcomas of the renal capsule in castrated mice].

Administration of 1,2-dimethylhydrazine (DMH) produced 83% (15/18) of renal capsule angiosarcomas in CBA mice. Castration that preceded the DMH-treatment reduced tumor incidence to 7% (2/29). Simultaneous administration of DMH and testosterone propionate (TP) to castrated males restored the tumor frequency (100%, 24/24). Castrated males that received TP after the cessation of the DMH treatment developed tumors in 10% (3/31). Combined treatment of castrated females with DMH and TP resulted in the development of angiosarcomas in 92% animals (22/24). It is concluded that TP enhances the stage of sarcomogenesis initiation induced by DMH.

Animals↗
PubMed1984

[Sex differentiated protein pattern in the urine of the rat following castration].

Protein excretion and protein fractions according to their molecular weight (SDS polyacrylamide-gelectrophoresis) were studied in the urine of male and female rats before and after castration. The polyacrylamide-gels were investigated qualitatively as well as quantitatively by densitometry. Male rats excrete considerably more protein in the urine than female rats. The values for the absolute protein quantity in 24-h-urine and the relative proteinuria (mg protein per 24 h and 100 g body weight) are five and three times higher, respectively, in males than in females. After castration proteinuria decreases significantly in both sexes, in males, however, more considerably (by about 75%) than in females (by about 30%), so that there is no significant difference in relative proteinuria between castrated males and females. The electrophoresis method used in this study allows to distinguish at least 10 to 11 protein fractions in the total urinary protein of both sexes within a molecular weight range from about 94.000 d to 14.000 d. Low molecular weight proteins (about 31.000 d to about 14.000 d) represent in both sexes the main part of the urinary protein. Females, however, excrete relatively more high molecular weight proteins (about 94.000 d to 60.000 d; about 25% of total urinary protein) than males (about 15% of total urinary protein). Concerning the relative parts in total urinary protein there are sex differences in all protein fractions, especially, however, in the fraction with a molecular weight of about 19.000 d (males more than 50%, females about 17% of total urinary protein). Castration causes in males more distinct changes in the relative parts of protein fractions in total urinary protein (drastic decrease of the 19.000-d-fraction) than in females. The results can be interpreted among other things in connection with a sex different handling of proteins in the proximal tubule of the rat kidney. The lysosomal catabolism of proteins in the proximal tubule is probably lower in males than in females, thus contributing to a higher proteinuria and a higher excretion especially of low molecular weight proteins in males in comparison with females.

Animals↗
PubMed1980

Effects of castration on 24-hour periodicity of hypothalamo-pituitary gonadotropic function.

Groups of 6 castrated or sham-castrated (controls) adult male rats were decapitated 7 days after the operation at 4 h intervals within a 24 h period. Serum LH, FSH and PRL were measured by radioimmunoassay and GnRH activity in medial basal hypothalamus was estimated by bioassay using donor pituitaries from normal adult rats. Finally, the responsiveness of pooled pituitaries from each experimental group to 5 ng synthetic GnRH was tested in vitro immunoreactive LH in medium being used as the end point. It was found that the castration of male rats results in the abolition of 24 h periodicity of hypothalamic GnRH content. Furthermore, a shift in the occurrence of peak levels (acrophase) and about 100 percent increase of the pituitary sensitivity to GnRH was observed. The castration also resulted in a shift in the acrophase of serum gonadotropins levels. In conclusion, the presented data suggest that the gonadal secretion possibly maintains the circadian periodicity of hypothalamo-pituitary gonadotropic function.

Animals↗
PubMed1981

Differences in the effects of estradiol on dihydrotestosterone induced prostatic growth of the castrate dog and rat.

The treatment of castrate beagles with a combination of estradiol an dihydrotestosterone (DHT) results in the synergistic enhancement of prostatic growth and the experimental induction of benign prostatic hyperplasia. This estradiol synergism can be shown as a greater than 3 fold increase in both prostatic wet weight and total DNA content in castrate dogs treated with both steroids, as compared to those animals treated with DHT alone. In direct contrast to the situation in the dog, there was no evidence of estradiol synergism on prostatic growth when castrate rats were treated with combinations of estradiol and DHT, even if both the ratio and absolute amount of both steroids were experimentally varied over a wide range of values. Regardless of the ratio or absolute dose, estradiol was completely unable to synergize the DHT induced growth of the prostate as well as other sex accessory tissues of the castrate rat. This indicates a fundamental difference between the rat and dog in regard to prostatic growth response to combinations of estradiol and DHT treatment.

Animals↗
PubMed1981

Influence of castration upon the seminal vesicle response to parasympathomimetic drugs.

The influence of castration upon rat seminal vesicle responses to acetylcholine, carbachol and betanechol has been investigated through the determination of the parameters pD2 (the apparent affinity constant), alpha (the intrinsic activity) and rho (the relative responsiveness) of such drugs on vesicles excised from normal and castrated rats. The pD2 and alpha values for carbachol and betanechol and the pD2 value for acetylcholine increased after orchiectomy; the pD2 increase was greater for the first two drugs than for acetylcholine. No significant difference in the values of rho of the acetylcholine receptor system was obtained after castration. Since carbachol and betanechol are not metabolized by cholinesterase, these results may indicate that the reported change in cholinesterase activity following castration is not the only factor to be considered as responsible for the variation in the seminal vesicle pharmacological reactivity. These results suggest that additional experimentation may be necessary to clarify the mode of action of these drugs in this system.

Acetylcholine↗
PubMed1981

Comparative effects and mechanisms of castration, estrogen anti-androgen, and anti-estrogen-induced regression of accessory sex organ epithelium and muscle.

We examined the effects and mechanisms of action of various endocrine manipulations on the epithelium and muscle preparations of the guinea pig seminal vesicle. Castration, which reduced the plasma testosterone level to 10 percent of normal, caused approximately 80 per cent reductions in epithelium wet weight and RNA and DNA contents. Estradiol benzoate effected similar reductions in plasma androgen and epithelial cell function in intact males. Reduction in plasma androgen level accounted for the estrogen-induced epithelial regression; no antiandrogenic effect of estrogen on the epithelium was detectable. All anti-androgens tested, flutamide, spironolactone, and cyproterone acetate, reduced epithelium weight in intact animals. Studies of the mechanism of cyproterone acetate action indicated its effects were attributable solely to an anti-androgenic action on the epithelium. The anti-estrogens, tamoxifen and nafoxidine, had no effect on the epithelium of intact animals when tested alone or in combination with cyproterone acetate. Regression of seminal vesicle muscle occurred only after castration or treatment of intact animals with cyproterone acetate. The action of cyproterone acetate on the muscle was attributable to blockade of the androgenic stimulus. The drug had no effect on plasma testosterone or estradiol levels and had no anti-estrogenic activity. In intact males estradiol reduced plasma testosterone to castrate levels, but did not alter muscle weight and nucleic acid levels. The potential deleterious effects of reduced plasma testosterone on the muscle were surmounted by direct estrogenic stimulation of the tissue. The anti-androgens, flutamide and spironolactone, and the anti-estrogens, tamoxifen and nafoxidine, had no effect on the muscle of intact males. Inasmuch as the regressive effects of castration on the epithelium and muscle can be duplicated in intact animals only by treatment with cyproterone acetate, this particular drug may provide the most effective nonsurgical treatment of prostatic neoplasia.

Androgen Antagonists↗
PubMed1980

[Maturation of gonadotropin function in the growing female rat. Influence of neonatal castration].

Evolution during growth of plasma level gonadotropins, was studied in the normal rat or castrated at birth. 1. In the control animals, plasma level gonadotropins decreased from the 15th to the 25th day then increased progressively to adult age. 2. Neonatal castration induced a new phenomenon: from the 25th to the 45th day, the increase of plasma gonadotropins in the normal rat corresponded with a decrease in the castrated animals; from the 45th day to the 90th day, plasma gonadotropins increased in the castrated and did not change significantly in the normal animals. 3. Ovary hormones affected gonadotropin function; however, as autonomous maturation of this function, independant of gonadal secretions, appeared to exist.

Animals↗
PubMed1978

Castration effects on tumor-specific immunity.

Using 2 immunogenic (3-methylcholanthrene-induced fibrosarcomas in BALB/c x DBA/2 F1 (CD2F1) male mice, we observed initially that the rate of tumor growth might be enhanced by castration. For confirmation, tumor transplantation experiments with over 500 mice were done to compare tumor-specific transplantation immunity in castrate and in control male mice. Inbred mice bearing a 3-methylcholanthrene-induced fibrosarcoma transplant underwent surgical excision of the tumor; specific resistance to subsequent challenges with varying doses of that tumor cell line were compared in castrate and in noncastrate groups of mice. Although castration influenced the rate of tumor growth, it had no apparent effect on tumor-specific immunoresistance. Mechanisms of host-tumor immunorelationships are discussed as they might relate to endocrine therapy of prostate adenocarcinoma.

Adenocarcinoma↗
PubMed1998

Interiority and inner genital space in men: what else can be lost in castration.

The author reassesses castration anxiety in men in light of advances in psychoanalytic theory. Castration anxiety arises when any crucial part of mature psychic life is threatened. As in women, oedipal-level and adult male psychic functioning contains powers rooted in the body-mind that are distinct from those we designate as phallic. The author struggles for a comparable word to represent devalued aspects of higher-level development that are primary, "feminine," essential for psychic mastery, and threatened by loss, i.e., by castration. Defining this aspect of mental life is difficult, but it includes receptivity, groundedness, connectedness to self and others, and tolerance of ambiguity. Without access to this interior and more ambiguous continent, a man is castrated, less than whole. Clinical examples are provided.

Adult↗
PubMed1999

Early castration-induced upregulation of transforming growth factor beta1 and its receptors is associated with tumor cell apoptosis and a major decline in serum prostate-specific antigen in prostate cancer patients.

BACKGROUND: The mechanism behind castration-induced apoptosis in prostate cells is unknown, but data from other species suggest that transforming growth factor beta1 (TGF-beta1) may be involved. METHODS: By using quantitative RT-PCR and immunohistochemistry, expression of TGF-beta1 and its receptors type I and II (RI and RII) was studied in normal and tumor areas of core biopsies taken before and 2-11 days after castration therapy. The TGF-beta responses were related to changes in apoptotic index and to changes in serum prostate-specific antigen (PSA). RESULTS: In normal prostate tissue, apoptosis was generally increased by castration, and apoptosis was accompanied by an increase in TGF-beta1 and RII mRNA levels (P < 0.05). In tumors, apoptosis was seen only in 44% of the cases and in these, but not in the others, TGF-beta1, RI, and RII mRNA levels were increased (P < 0.05). In the patients showing a prognostically favorable PSA response (nadir PSA <5 ng/ml), but not in the others, RI and RII mRNA levels were significantly upregulated (P < 0.05). CONCLUSIONS: Short-term upregulation of TGF-beta1 and its receptors is associated with apoptosis in human prostate and prostate cancer, and possibly with a favorable clinical outcome after castration therapy.

Apoptosis↗
PubMed1999

Expression of gonadotropin-releasing hormone receptor mRNA in the rat ventral prostate and dunning R3327 PAP adenocarcinoma before and after castration.

BACKGROUND: Continuous administration of gonadotropin-releasing hormone (GnRH) agonists in prostate cancer patients results in involution of the tumors due to suppression of androgen production. In addition to the effect of GnRH at the hypothalamic-pituitary level, experiments in vitro on breast, ovary, and prostatic cells have shown an inhibition of cell proliferation, indicating the presence of local GnRH receptors (GnRH-R). The aim of the present study was to investigate the expression of GnRH-R mRNA in the normal rat ventral prostate (VP) and Dunning R3327 PAP adenocarcinoma and to evaluate the effects of castration on receptor mRNA expression. METHODS: RNA was prepared from ovaries, pituitaries, VP, and Dunning tumors from both intact and castrated animals. GnRH-R mRNA levels were quantified by a competitive reverse transcription-polymerase chain reaction (RT-PCR) method. RESULTS: GnRH-R mRNA was detected in normal VP and Dunning tumors. Normal VP showed lower amounts of GnRH-R mRNA compared to Dunning tumors. An elevation of mRNA expression was observed 7 days after castration in Dunning tumors. CONCLUSIONS: GnRH-R mRNA was found in both VP and Dunning tumors, indicating the presence of a local GnRH system. Normal VP showed lower amounts of GnRH-R mRNA when compared to malignant tissues. GnRH-R mRNA levels were elevated in Dunning tumors following castration.

Adenocarcinoma↗
PubMed1986

Variations in sexual dimorphism in the skulls of rats subjected to malnutrition, castration, and treatment with gonadal hormones.

Two groups of weanling rats were subjected to malnutrition, one with periodic injections of testosterone (males) and the other with estradiol (females). Two other groups (castrated males or castrated females) received normal feedings. In control animals, the relative weights (mg/gm body weight) of testes, seminal vesicles, and ovaries were greater than in malnourished rats. However, relative weights of those organs in hormone-treated, malnourished animals were greater than in those subjected to malnutrition alone and still greater than in controls. Normal sexual cranial dimorphism (SCD) was decreased 16% by male castration, 23% by malnutrition, and 83% by estradiol treatment in malnourished females. On the other hand, normal SCD was increased 20% by female castration and more than 200% by testosterone treatment in malnourished males. All monosexual comparisons corroborated the bisexual range of distances found. Testicular but not ovarian secretions seemed to influence sexual cranial dimorphism. Malnutrition delayed SCD because of a deficiency of testosterone level in stressed males. It is suggested that estradiol in females may counteract sexual cranial development and that its inhibitory effect may be additive to the testosterone deficit evoked by malnutrition.

Animals↗
PubMed1991

Immunocytochemical localization of cathepsin D in rat ventral prostate: evidence for castration-induced expression of cathepsin D in basal cells.

Cathepsin D (EC3.4.23.5) is an aspartyl endopeptidase involved in lysosomal proteolysis. Its functional role is uncertain. This study was undertaken to determine the cellular and subcellular distribution of cathepsin D in the normal rat ventral prostate and its possible role in the castration-induced atrophy of the gland. Cathepsin D was localized immunohistochemically to perinuclear lysosomes in secretory cells, in capillary endothelial cells, and, occasionally, in stromal cells of the untreated animal. Castration resulted in an increased number of cathepsin D-positive cells in the stroma within 24 hr. By 48 hr after castration autophagolysosomes formed in secretory cells and apoptotic bodies appeared in the epithelium. Although apoptotic bodies generally contained immunoreactive cathepsin D, a subpopulation of larger apoptotic bodies, which commonly rested on the basement membrane and contained multiple inclusions, were more variable in cathepsin D expression. The induction of cathepsin D in dendritic cells basally oriented in the epithelium was noted at 4 days of castration. These cells had a phagocytic phenotype, were distributed periodically along the basement membrane, and were not found in ductal epithelia. Treatment with actinomycin D or hydrocortisone to reduce the rate of regression of the ventral prostate blocked the appearance of these cathepsin D-positive, basally oriented epithelial cells. Our data indicate that this cathepsin D-positive, phagocytic cell differentiates from a cell resident in the prostatic epithelium. We suggest that it differentiates from basal cells in the secretory tubuloalveolar portion of the gland and that it is involved in the destruction of regressed secretory cells.

Animals↗
PubMed1991

Gonadotropin-releasing hormone mRNA in the rat: distribution and neuronal content over the estrous cycle and after castration of males.

The decapeptide gonadotropin-releasing hormone (GnRH) stimulates release of luteinizing hormone (LH) and follicle-stimulating hormone (FSH) from the anterior pituitary. In the present study we used a 51-base oligonucleotide probe and in situ hybridization to study the neuronal content of GnRH mRNA at several time points in the estrous cycle and 7 days after castration of male rats. GnRH mRNA containing cells were found in the medial septum (SEPT), the vertical and horizontal limbs of the diagonal band of Broca (DBB), and throughout the preoptic area (POA) from the organum vasculosum of the lamina terminalis (OVLT) to its caudal merger with the anterior hypothalamus. The number of neurons producing detectable quantities of GnRH mRNA was not different either among females killed at 0700 h proestrus, 1000 h estrus, or 1900 h of diestrus 1 or between intact male rats and male rats killed 1 week after castration. We did, however, detect a significant difference in the number of GnRH mRNA producing neurons between males and females (P less than 0.05), where females had 20% more labeled cells. We detected no significant difference in the relative copy number of GnRH mRNA molecules (grains per labeled cell) either over the estrous cycle or between intact and castrate males. However, females overall had 24% more grains per labeled cell than males (P less than 0.05). These results suggest that gonadal steroid regulation of GnRH both over the estrous cycle and after short-term castration of males is mediated primarily by cellular processes subsequent to GnRH gene regulation. Furthermore, these results suggest that biosynthetic activity of GnRH is higher in females than in males.

Animals↗
PubMed2005

Neuropeptide Y in the forebrain of the adult male cichlid fish Oreochromis mossambicus: distribution, effects of castration and testosterone replacement.

We studied the organization of the neuropeptide Y (NPY)-immunoreactive system in the forebrain of adult male cichlid fish Oreochromis mossambicus and its response to castration and testosterone replacement by using morphometric methods. Immunoreactivity for NPY was widely distributed in the forebrain, and the pattern generally resembled that in other teleosts. Whereas immunoreactivity was conspicuous in the ganglia of nervus terminalis (NT; or nucleus olfactoretinalis), a weak reaction was detected in some granule cells in the olfactory bulb and in the cells of area ventralis telencephali pars lateralis (Vl). Moderately to intensely immunoreactive cells were distinctly seen in the nucleus entopeduncularis (NE), nucleus preopticus (NPO), nucleus lateralis tuberis (NLT), paraventricular organ (PVO), and midbrain tegmentum (MT). NPY fibers were widely distributed in the forebrain. Castration for 10/15 days resulted in a drastic loss of immunoreactivity in the cells of NE (P<0.001) and a significant decrease (P<0.01) in their cell nuclear size. However, cell nuclei of the NT neurons showed a significant increase in size. A highly significant reduction in the NPY-immunoreactive fiber density (P<0.001) was observed in several areas of the forebrain. Although testosterone replacement reversed these changes, fibers in some areas showed supranormal responses. Immunoreactive cells in Vl, NPO, NLT, PVO, and MT and fiber density in some other areas did not respond to castration. We suggest that the NPY-immunoreactive elements that respond to castration and testosterone replacement may serve as the substrate for processing the positive feedback action of the steroid hormone.

Androgens↗