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PubMed1995

Degradation of gonadotropin beta-subunits retained in the endoplasmic reticulum of the gonadotropes of castrated rats.

LH and FSH are composed of a common alpha-subunit and a noncovalently associated hormone-specific beta-subunit. Unassociated beta LH and beta FSH can be retained in the cisternae of endoplasmic reticulum (ER). This phenomenon is particularly evident in gonadotropes of castrated animals where beta-subunits are expressed in larger amounts than the alpha-subunit. Because little was known about the fate of the gonadotropin beta-subunits retained in the ER, we carried out immunocytochemical studies on ultrathin frozen sections of anterior pituitaries of castrated rats. After castration, the intracellular levels of the beta-subunits were found to increase more than that of the alpha-subunit. When the subcellular localization of the alpha- and beta-subunits and secretogranin II (a regulated secretory protein present in the secretory granules of gonadotropes of many species) was investigated by double immunoelectron microscopy, both gonadotropin subunits were colocalized in secretory granules with secretogranin II. However, only the beta-subunits, not the alpha-subunit and secretogranin II, were localized in the dilated cisternae of the ER as well as in irregularly shaped vacuoles. Using markers for the endoplasmic reticulum, the prelysosomal compartment and lysosomes (cathepsin D and lgp120), we found that these vacuoles correspond to a degradative compartment with two types of intermediates: 1) one with small amounts of lgp120, and cathepsin D preferentially localized at the periphery of a central dense matrix; and 2) the other with larger amounts of lgp120, and cathepsin D present all over the matrix of the vacuole. These vacuoles do not derive from autophagy because vesicles surrounded by a double or multilamellar membrane containing profiles of ER cisternae together with small amounts of the cytoplasm were never detected. Moreover, they do not correspond to crinophagic bodies because the latter contained beta-subunits as well as alpha-subunit and SgII. Our data indicate that gonadotropin beta-subunits, probably retained as unassociated subunits in the endoplasmic reticulum of castrated rat gonadotropes, undergo degradation in vacuoles that acquire lysosomal enzymes. This process appears different from the classical autophagy, but similar to the nonautophagic pathway for the diversion to lysosomes of the intracisternal granules accumulated in the ER of hyperstimulated thyrotropes.

Animals↗
PubMed1999

A novel gene overexpressed in the prostate of castrated rats: hormonal regulation, relationship to apoptosis and to acquired prostatic cell androgen independence.

We have identified a novel complementary DNA (cDNA) corresponding to a gene overexpressed in the rat ventral prostate after castration. This cDNA displays 89.4% identity with 453 bp of a mouse EST and 81.5% identity with 157 bp of a human EST and was named PARM-1 for prostatic androgen-repressed message-1. The complete cDNA is 1187 bp long and codes for a protein of 298 amino acids that contains four potential glycosylation sites and three half cystinyl residues. The PARM-1 gene was found to be expressed at quite low levels in most rat tissues including those of the urogenital tract. The kinetic of induction of PARM-1 gene in the prostate was highly correlated to the development of apoptosis in the whole organ. Supplementation of castrated animals with androgens reversed both the process of apoptosis and the overexpression of PARM-1 gene. Supplementation with estrogens did not result in an increase in the PARM-1 messenger RNA levels when compared with the castration alone. However, the treatment resulted in a more rapid return to intact levels in the castrated plus estrogen group. When apoptosis of testis and prostate was induced in vivo by hypophysectomy, it was found that PARM-1 was only overexpressed in the prostate. Therefore, PARM-1 seems to be regulated by androgens only in the prostate. Using in situ hybridization and immunohistological techniques, we have shown that PARM-1 gene product is found exclusively in the epithelial cells of involuting prostate. Analysis by flow cytometry of MAT LyLu epithelial cells transiently expressing PARM-1 protein did not allow us to demonstrate a direct effect of PARM-1 gene overexpression on the programmed death of the transfected cells. Treatment of MAT LyLu cells by transforming growth factor-beta induced apoptosis but had no effect on PARM-1 production. However PARM-1 protein has been detected by Western blotting in various cell lines such as MAT LyLu, MAT Lu, and PIF, which are androgen independent. This would suggest that PARM-1 gene product would be a marker for acquired androgen-independence of these tumor cells.

Amino Acid Sequence↗
PubMed1986

Serum luteinizing hormone (LH) biological activity in castrated patients with cancer of the prostate receiving a pure antiandrogen and in estrogen-pretreated patients treated with an LH-releasing hormone agonist and antiandrogen.

We recently reported almost complete disappearance of serum LH biological activity in previously untreated patients with advanced prostatic cancer receiving combined therapy with a LHRH agonist and a pure antiandrogen. This decrease in LH bioactivity was most likely responsible for the fall of circulating testosterone to castration levels during such treatment. Since patients previously treated with high doses of estrogens or orchiectomy before receiving combined therapy had a less favorable response to the new treatment, we measured serum LH levels by RIA and the mouse interstitial cell bioassay in these 2 groups of patients. Serum samples were obtained from 14 men with advanced prostatic cancer treated from 9-41 months (24 +/- 9 months) with diethylstilbestrol before receiving 500 micrograms/day LHRH agonist ([D-Trp6]LH/RH ethylamide) in combination with 3 daily oral doses of 250 mg pure antiandrogen flutamide and from 21 men castrated for at least 9 months (32 +/- 26 months) before receiving the antiandrogen alone. In previously castrated patients, both bio- and immunoactive LH serum levels were elevated and did not change during at least 3 months of antiandrogen treatment. In estrogen-pretreated men, however, bioactive LH concentrations declined from 1.2 +/- 0.5 (+/- SEM) to 0.04 +/- 0.01 ng/ml after 1 month of combined treatment and remained low thereafter, while serum LH levels, measured by RIA, did not significantly decline (1.4 +/- 0.5 vs. 0.9 +/- 0.1 ng/ml on days--2 and 30, respectively). This decrease in LH biopotency caused the biological to immunological activity ratio to fall from 0.5 +/- 0.2 before the onset of the combined therapy to 0.05 +/- 0.01 after 3 months. Thus, estrogen pretreatment did not prevent the ability of the LHRH agonist-antiandrogen combination to decrease serum LH biological activity. Moreover, the absence of an effect in castrated patients receiving antiandrogen alone indicates that the LHRH agonist, and not flutamide, was responsible for the effects of the combined therapy.

Aged↗
PubMed2006

Empirical support for optimal virulence in a castrating parasite.

The trade-off hypothesis for the evolution of virulence predicts that parasite transmission stage production and host exploitation are balanced such that lifetime transmission success (LTS) is maximised. However, the experimental evidence for this prediction is weak, mainly because LTS, which indicates parasite fitness, has been difficult to measure. For castrating parasites, this simple model has been modified to take into account that parasites convert host reproductive resources into transmission stages. Parasites that kill the host too early will hardly benefit from these resources, while postponing the killing of the host results in diminished returns. As predicted from optimality models, a parasite inducing castration should therefore castrate early, but show intermediate levels of virulence, where virulence is measured as time to host killing. We studied virulence in an experimental system where a bacterial parasite castrates its host and produces spores that are not released until after host death. This permits estimating the LTS of the parasite, which can then be related to its virulence. We exposed replicate individual Daphnia magna (Crustacea) of one host clone to the same amount of bacterial spores and followed individuals until their death. We found that the parasite shows strong variation in the time to kill its host and that transmission stage production peaks at an intermediate level of virulence. A further experiment tested for the genetic basis of variation in virulence by comparing survival curves of daphniids infected with parasite spores obtained from early killing versus late killing infections. Hosts infected with early killer spores had a significantly higher death rate as compared to those infected with late killers, indicating that variation in time to death was at least in part caused by genetic differences among parasites. We speculate that the clear peak in lifetime reproductive success at intermediate killing times may be caused by the exceptionally strong physiological trade-off between host and parasite reproduction. This is the first experimental study to demonstrate that the production of propagules is highest at intermediate levels of virulence and that parasite genetic variability is available to drive the evolution of virulence in this system.

Animals↗
PubMed1997

Stronger suppression of serum testosterone and FSH levels by a synthetic estrogen than by castration or an LH-RH agonist.

Serum levels of LH, FSH and testosterone (T) were measured by radioimmunoassays in 36 patients with advanced prostate cancer before and during androgen ablation therapies. Both leuprolide acetate (LH-RH agonist: LHRH-A) and diethylstilbestrol diphosphate (DES-DP) administration decreased serum LH significantly to an undetectable level (LHRH-A: P < 0.01, DES-DP: P < 0.05). LHRH-A and DES-DP diminished serum FSH to 20% of the pre-treatment level (P < 0.005) and to an undetectable level (P < 0.001), respectively. LHRH-A and DES-DP decreased serum T to the castration level and an undetectable level, respectively (P < 0.001). Serum levels of the same 3 hormones before and after DES-DP administration were measured in 8 patients who received DES-DP after LHRH-A treatment or castration because of relapse of the disease. DES-DP lowered serum FSH further than LHRH-A to an undetectable level (P < 0.005) and diminished T further than previous treatments to an undetectable level (P < 0.05 vs. LHRH-A, P < 0.01 vs. castration). These results suggest that 1) DES-DP is able to reduce T production from extra-testicular site(s), and achieve the minimal serum T level, and 2) this DES-DP action appears to be one of the mechanisms of the effectiveness of the estrogen on refractory prostate cancer after castration or LHRH-A. In addition, basal (independent of LH-RH) FSH secretion in elderly men is about 20% of total FSH secretion and DES-DP inhibits the basal FSH secretion at the level of the pituitary.

Aged↗
PubMed1985

Regulation of gonadotrophin secretion in male mice from birth to adulthood. Response to LRH injection, castration and testosterone replacement therapy.

Plasma LH and FSH concentrations were determined by radioimmunoassay in male mice from birth to adulthood after LRH injection, castration and testosterone replacement therapy. Except at birth for LH, LRH significantly increased circulating levels of both gonadotrophins at all stages studied. It is suggested that a change in the pituitary LH response to LRH occurs around puberty and perhaps represents the time of initiation of pubertal processes. At all stages studied (except the infantile stage for LH) castration resulted in a significant rise in circulating LH and FSH levels. The magnitude of LH response to castration increased with age but not that of FSH. Testosterone replacement therapy, inducing supra-physiological circulating testosterone levels, was ineffective to depress the post-castration rises of LH and FSH levels.

Age Factors↗
PubMed1996

Effects of castration on luteinizing hormone secretion and response to gonadotrophin-releasing hormone in sheep infected with Trypanosoma congolense.

The effects of trypanosomiasis on the endocrine function of the hypothalamo-pituitary-gonadal axis were investigated before and after castration of Scottish Blackface rams infected with Trypanosoma congolense and uninfected controls. Blood samples were collected at 15-min intervals for 6 h before and at 10, 20, 40, 60, 80, 100 and 120 min after injection of synthetic gonadotrophin-releasing hormone (GnRH, 20 micrograms iv) 2 days before infection and 26 and 54 days after infection, with castration being performed 28 days after infection. Mean luteinizing hormone (LH) pulse amplitude was higher (3.3 +/- 0.2 vs 2.6 +/- 0.3 ng/ml) and mean plasma testosterone concentration was lower (4.1 +/- 0.6 vs 7.6 +/- 1.2 nmol/l) in infected vs control rams 26 days after infection (p < 0.05). Mean plasma LH concentration and pulse amplitude increased in both groups after castration but both were significantly lower in infected compared to control rams (6.6 +/- 1.5 and 13.0 +/- 2.2 ng/ml, p < 0.01; 7.7 +/- 0.9 and 11.6 +/- 0.9 ng/ml, p < 0.001), respectively. However, LH responses to exogenous GnRH were similar in infected and control rams at each stage of the experiment, suggesting that the smaller increase in plasma LH after castration in infected rams was not caused by reduced responsiveness of the pituitary to GnRH but by alterations in GnRH secretion by the hypothalamus or its transport to the adenohypophysis. These results also demonstrate that impairment of testosterone secretion within 4 weeks of T. congolense infection in sheep may be due to testicular rather than pituitary effects.

Animals↗
PubMed1985

Effect of castration on prostaglandin-mediated changes in membrane potential and prostaglandin synthesis in guinea-pig seminal vesicle tissue.

Arachidonic acid stimulated an increase in transmural electrical potential difference (p.d.) in guinea-pig seminal vesicle tissue in vitro. Pretreatment with indomethacin abolished this response. Indomethacin pretreatment did not prevent the p.d. from increasing in response to theophylline. Changes in p.d. in response to arachidonic acid were greatly attenuated, and the response to theophylline was abolished in seminal vesicle tissue taken from castrated guinea-pigs. Seminal vesicles, aorta and ileum taken from castrated guinea-pigs synthesized and released more prostaglandins than did those from control animals. It is concluded that the effects of arachidonic acid on p.d. are mediated by its metabolism to prostaglandins; the inability of seminal vesicles from castrated animals to respond to arachidonic acid is not a result of a decrease in prostaglandin production, but is more likely a result of other degenerative changes attendant upon castration; and androgens appear to have some regulatory function on prostaglandin synthesis in a variety of tissues.

Animals↗
PubMed1991

Effect of castration on plasma concentrations of luteinizing hormone and follicle-stimulating hormone in adult Merino rams which were homozygous carriers or non-carriers of the Booroola fecundity gene.

Before castration, the mean plasma concentrations of luteinizing hormone (LH) and follicle-stimulating hormone (FSH) did not differ between FF and ++ Booroola rams. After castration, mean LH and FSH concentrations increased after 8 h, and for the next 14 days the rate of increase in FSH, but not LH, secretion was significantly faster in FF than in ++ rams (P less than 0.05). Mean FSH concentrations over this period were significantly higher in FF than in ++ rams (P less than 0.05). In both genotypes, the ranked FSH values did not significantly change their order over time, i.e. a significant within-ram effect was noted (P less than 0.05). Repeated-measures analysis of variance indicated a significant effect of genotype on mean FSH secretion (P less than 0.05) and a significant effect of sire in the FF (P less than 0.05), but not the ++ (P = 0.76), genotype. From Day 28 to Day 58 after castration, FSH and LH concentrations were variable and no overall increases in concentrations were observed. The mean concentrations of both hormones over this period were not related to genotype. There were no gene-specific differences in pulsatile LH secretion 14 weeks after castration. However, the mean LH, but not FSH, response to a bolus injection of 25 micrograms of gonadotrophin-releasing hormone (GnRH) was significantly higher in FF than in ++ rams (P less than 0.05) and this was not significantly affected by sire. These studies support the hypothesis that the F gene is expressed in adult rams, in terms of pituitary responsiveness to an injection of GnRH and to the removal of the testes, but it is not clear from this study whether the influence of sire is related to or independent of the apparent gene-specific differences.

Animals↗
PubMed2005

[Effect of the hypothyroidism-castration association on bone and parathyroids from adult female rats].

The effect of hypothyroidism on bone metabolism and the parathyroids in states of deficiency or sufficiency of sex steroids was studied in 32 two-months-old female Wistar rats distributed in 4 groups of 8 animals each: intact euthyroid (IE), castrated euthyroid (CE), intact hypothyroid (IH) and castrated hypothyroid (CH). After 120 days of treatment, animals were sacrificed and plasma taken to assess free T4. Hyperplasia or hypertrophy of all parathyroids were evident only in IH and CE groups. Of all groups, IH rats presented the most extensive osteopenia, reaching lumbar vertebrae, dental alveolae (jaw and mandible) and long bones. In this group osteopenia resulted from the reduced bone growth, inhibition of bone apposition and return of bone resorption. Although osteopenia in the CH group was almost always more intense in relation to osteopenia presented by CE rats, its intensity was variable when compared to IH rats and dependent on the region studied. Even though it also caused necrosis of higher metabolism bones, the association hypothyroidism-castration did not potentialize the resultant osteopenia of the isolated action of hypothyroidism or castration until 120 days of treatment.

Animals↗
PubMed2005

[Bone effects of the association hyperthyroidism-castration of adult female rats].

The relationship between thyroid, gonads and bone morphology was investigated in 5 month-old Wistar rats, castrated and kept in hyperthyroid or euthyroid state for periods of 30, 60 and 90 days. A non-castrated control group was maintained in the same condition. At the end of each period, plasma concentrations of free T4, progesterone and estradiol were measured. The bones from each group were submitted to radiological and histological analysis. Hyperthyroidism in intact rats caused variation in bone morphology throughout the experiment, leading to loss of trabecular bone tissue at day 60, due to increased bone resorption. At day 90 there was no bone loss, because the increase in bone resorption was accompanied by higher bone apposition. In castrated euthyroid rats reduction in progesterone levels inhibited the bone apposition, causing a slight loss of trabecular bone tissue in vertebrae and alveolar bone at day 30, which was intensified at days 60 and 90, affecting cortical bone tissue. The administration of thyroxine to castrated rats reversed osteopenia at days 30 and 60, which did not occur at day 90 when bone loss was more extensive. In conclusion, hypoprogesteronism and hypoestrogenism alter bone metabolism and the bone response to hyperthyroidism depends on the plasma profile of sex steroids, time of exposure and bone tissue configuration.

Animals↗
PubMed1998

Kinetic analysis of prostatic volume and prostate specific antigen (PSA) in patients with advanced prostatic cancer treated by castration.

The clinical usefulness of the kinetic analysis of prostate specific antigen (PSA) in patients with advanced prostatic cancer treated by castration has not yet been evaluated. The reduction of both prostatic volume and PSA was monitored in 37 patients with Stage C and Stage D prostatic cancer. The change of prostatic volume was measured frequently by transrectal ultrasonography (TRS) after castration, as was the change of PSA. A kinetic analysis of both prostatic volume and PSA was made by comparing the reduction time tau(PSA) (speed of the reduction of PSA) and tau prostatic volume (PV). There was a statistically significant correlation between tau(PSA) and tau(PV) in patients with a tau(PV) of less than 30 days. However, no correlation was observed in patients with a tau(PV) of more than 30 days, because the tau(PSA) in this group fell into a relatively low range similar to the group with a tau(PV) of less than 30 days. It was assumed that the change of PSA after castration reflected mainly the response of the hormone dependent portion of the total cancer volume. However, all data of tau(PV) with a tau(PSA) less than 10 days were within 30 days. In conclusion, tau(PSA) might be promising as a prognostic factor after castration in patient with advanced prostatic cancer, although tau(PSA) was not a direct substitute for tau(PV).

Adenocarcinoma↗
PubMed2003

Ultrastructural changes in subepithelial capillaries and their surrounding stroma in rat prostate and seminal vesicle after castration.

The purpose of this study was to clarify the androgen-ablation-induced morphological changes in the capillaries and stroma near the epithelial cells in prostate and seminal vesicles (SV) using transmission electron microscopy (TEM). In ventral prostate (VP) and SV of immature male rats, the luminal areas of subepithelial capillaries and the width of the stromal layers between endothelia and epithelia were measured quantitatively after castration using TEM and a computed image analyzer. The luminal areas of the capillaries were significantly reduced in VP and SV in the short-term after castration. In the stromal layer, the width of the collagen layer surrounding the capillary significantly increased in VP and SV in the long-term after castration. These data suggest that the reduction of the capillaries and the thickening of collagen surrounding them are related to the involution of glandular epithelial cells in VP and SV after castration.

Animals↗
PubMed1987

Failure of the synthetic androgen 17 beta-hydroxy-17 alpha-methyl-estra-4,9,11-triene-3-one (methyltrienolone, R1881) to duplicate the activational effect of testosterone on mating in castrated male rats.

Administration of the synthetic steroid, 17 beta-hydroxy-17 alpha-methyl-estra-4,9,11-triene-3-one (methyltrienolone, R1881), which is an androgen receptor agonist not metabolized in vivo, at doses of 400, 800 or 2400 micrograms/kg s.c. in propylene glycol stimulated mounting and ejaculation only slightly in sexually experienced castrated rats. A similar low level of mating was observed in a group of castrated rats given testosterone at doses of 400 followed by 800 micrograms/kg. However, when treated with a higher dose of testosterone (2400 micrograms/kg) these castrated rats displayed significantly higher levels of mounting and ejaculation than rats treated with any of the doses of R1881. Also, when this higher dosage of testosterone was substituted for each dose of R1881, significant increments in mounting and ejaculation occurred in all groups. These findings show that R1881 is only marginally effective in restoring sexual behaviour in castrated rats, suggesting that the activation of neural androgen receptors cannot by itself account for the activational effect of testosterone on mating behaviour in gonadally intact male rats.

Animals↗
PubMed1988

Differential effects of testosterone, 5 alpha-dihydrotestosterone and oestradiol-17 beta on plasma concentrations of LH in castrated ferrets.

The biological activity of testosterone often depends on the conversion of testosterone within the target cell to an androgenic or oestrogenic metabolite. The purpose of this study was to compare the relative ability of testosterone and two of its metabolites, dihydrotestosterone (DHT) and oestradiol, to suppress LH secretion in castrated male ferrets. Castrated ferrets were treated with five different doses of steroid by implanting various numbers of s.c. silicone elastomer capsules packed with either testosterone, DHT or oestradiol. The lowest dose of oestradiol (0.1 mm capsule length/100 g body weight, mean estimated total release rate of 25 ng/day) significantly suppressed plasma concentrations of LH in castrated ferrets. Higher amounts of DHT (2.5 mm capsule length/100 g body weight, mean estimated total release rate of 88 ng/day) were required for a significant reduction in plasma concentrations of LH. Concentrations of LH were also significantly lowered by testosterone when administered at a 2.5 mm capsule length/100 g body weight; however, estimated total release rate was 312 ng/day from these capsules. The fact that oestradiol was more effective than DHT, and that DHT was more effective than testosterone in inhibiting LH secretion in castrated ferrets, suggests that in gonadally intact ferrets, testosterone may be converted to DHT or oestradiol within target cells that mediate steroid negative feedback on LH secretion.

Animals↗
PubMed1989

Tissue-specific effects of castration and ovariectomy on murine epidermal growth factor and its mRNA.

The polypeptide mitogen, epidermal growth factor (EGF), was originally isolated from mouse submaxillary gland (SMG). In mice, these glands are sexually dimorphic; the SMG of male animals typically contains up to 400 pmol EGF/mg protein whereas EGF concentrations in the SMG of female mice are only 5-20 pmol/mg protein. When mice were castrated at 8 weeks of age, EGF mRNA levels in the SMG fell rapidly to the low levels observed in control female animals. Although the concentration of EGF in the SMG, measured by radioimmunoassay, also fell to very low levels (13.8 +/- 0.7 (S.E.M.) pmol/mg protein) in the castrated mice, the rate of decrease was considerably slower than that of the mRNA. In contrast to the loss of EGF and EGF mRNA from mice following castration, ovariectomy led to a rise in EGF mRNA levels in SMG, with a maximal increase (approximately 100-fold) 4-6 weeks after ovariectomy. Concentrations of EGF in the SMG also rose markedly in the ovariectomized animals, from a control value of 5.4 +/- 0.8 to 34.7 +/- 7.9 pmol/mg protein at 6 weeks. In mice, the kidney displays the second highest level of EGF gene expression. However, in contrast to the effects on SMG, kidney EGF mRNA was not affected by either castration or ovariectomy. These results provide further evidence for the tissue-specific control of EGF gene expression in response to steroid hormones.

Animals↗
PubMed2000

Cyproterone acetate reduced antler growth in surgically castrated fallow deer.

We studied the role of androgens in antler growth. In particular, we investigated whether the onset of antler regrowth is triggered by a short-term pulse of testosterone and if low levels of androgens are required for antler growth. The study was conducted on 12 surgically castrated fallow deer bucks (Dama dama) aged approximately 27 months. Six animals (CA group) were given the antiandrogen, cyproterone acetate (CA, 1000 mg/treatment); the others were given vehicle solution only (control). Before each CA treatment, blood was sampled and analysed for testosterone, androstenedione, IGF-1, cortisol, FSH, and LH. CA treatment and blood sampling were performed 2 days before castration, on the day of castration and afterwards at 2-day intervals until day 22. Subsequently, CA treatment and blood sampling continued at weekly intervals until day 270. All animals cast their antlers, followed by antler regrowth in all control bucks, but in only four of the six CA-treated castrates. Plasma testosterone concentrations were low in all animals (between 0.01 and 0.20 ng/ml), but were significantly (P<0001) greater in the controls. In both groups, a temporary increase in testosterone values was recorded around the time of antler regrowth, the peak being significantly (P<0.01) higher in the controls. Androstenedione showed a similar pattern as testosterone. Plasma IGF-1 concentrations increased sharply during the antler growth spurt and did not differ significantly between the two groups throughout the study period. Cortisol concentrations were greater in controls than in the CA group. However, no link with the antler cycle was apparent. FSH and LH concentrations were higher in the controls for most of the study. Antlers produced by the control bucks were significantly larger than those in the CA group (P<0.03). For antler length, testosterone, androstenedione and IGF-1, areas under the curve (AUC) were calculated over the period of antler growth. For the pooled deer (n=12) significant correlations existed between AUCs of antler length and testosterone, but not for antler length and IGF-1. Also, a trend for a positive correlation between AUCs of antler length and androstenedione was noted. It is concluded that a plasma androgen concentration at least above a minimal threshold level is a necessary prerequisite for normal antler regrowth in fallow deer, and that this androgen effect is not mediated via circulating IGF-1. The biological role of low levels of androgens may be to sensitize antler cells to the stimulating effect of IGF.

Androgen Antagonists↗
PubMed2003

The effects of sex steroids on the formation of gap junctions between folliculo-stellate cells; a study in castrated male rats and ovariectomized female rats.

We investigated the relationship between gap junction formation and the sex steroids testosterone, progesterone and 17beta-estradiol in the anterior pituitary glands of castrated male rats and ovariectomized female rats. Male and female 30-day-old Wistar-Imamichi strain rats were castrated or ovariectomized, and 30 days later they were subcutaneously injected with the above sex steroids. They were divided into six groups according to the injected materials: sesame oil (control), testosterone, progesterone, 17beta-estradiol, testosterone with 17beta-estradiol, and progesterone with 17beta-estradiol. Five rats from each group were sacrificed 1, 2, 3, 4 and 5 days after the injections, and the anterior pituitary glands were prepared for observation by transmission electron microscopy. We quantified the number of follicles and gap junctions and calculated the rate of occurrence of gap junctions as the ratio of the number of gap junctions existing between folliculo-stellate cells per intersected follicle profile in electron photomicrographs. The administration of testosterone to castrated male rats increased the rate of gap junctions between folliculo-stellate cells; however, progesterone and 17beta-estradiol did not affect the formation of gap junctions. The administration of progesterone to ovariectomized female rats increased the rate of gap junctions between folliculo-stellate cells; this progesterone effect was prevented by the simultaneous administration of 17beta-estradiol, which by itself did not affect the rate of gap junctions between folliculo-stellate cells. These observations indicate that the formation of gap junctions within the anterior pituitary gland is regulated differently by sex steroids in castrated male and ovariectomized female rats.

Animals↗