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PubMed1996

Castration of calves: a study of methods used by farmers in the United Kingdom.

A postal survey of farmers was conducted to determine the main methods used to castrate calves, and by whom and how they were applied. Among the 28 per cent of farmers who replied, those who did castrate calves used one or more of three methods: the Burdizzo was used by 43 per cent of farmers, surgery by 39 per cent, and rubber rings by 32 per cent, with 10 per cent using more than one method. Calves were castrated at all ages from less than one week to over six months, with one third of them being castrated at an age that legally requires the operation to be done under local anaesthesia by a veterinary surgeon. Rubber rings were never used by veterinary surgeons, but they carried out 43 per cent of surgical castrations, which was the method of choice in older calves. Local anaesthetic was used on 15 per cent of farms, mainly for surgical castrations. Sixty-seven per cent of farmers using the Burdizzo applied it twice, with the majority correctly applying the second crush below the first, and 90 per cent used precautions to control infection after surgical castration.

Anesthesia, Local↗
PubMed1982

Photoperiodicity and circannual levels of LH, FSH, and testosterone in normal and castrated male, white-tailed deer.

To establish the relation between photoperiodicity and the levels of LH, FSH, and testosterone (T) in plasma, three intact and three castrated adult male white-tailed deer were sampled once a month for 2-3 years. The rang of average LH levels in controls varied between 0.8 and 2.0 ng/mL; the levels in castrates were considerably higher, 3.4 to 8.9 ng/mL. Average levels of FSH varied in controls between 25 and 112 ng/mL and in castrates between 141 and 240 ng/mL. A significant correlation between the seasonal time course of LH and FSH was found in castrated, but not in intact bucks. In castrates both gonadotropins exhibit two major elevations coinciding with spring and fall equinoxes in March and September. The seasonal time course of FSH in castrates correlates highly with seasonal levels of FSH in controls. However, the time course of the LH curve in controls is substantially different from the curve in castrates, presumably owing to feedback mechanisms. A possible role of testicular estradiol in this feedback is discussed. In controls, peak T levels are reached in December, i.e., 3 months after maximum levels of FSH and 5 months after peak levels of LH were detected. It appears that male deer undergo two periods of reproductive stimulation (one in the spring, the other in the fall). However, the organism responds with the full range of gonadal and behavioral mechanisms leading to the initiation of the rut only during the fall.

Animals↗
PubMed1998

A randomised comparison of 'Casodex' (bicalutamide) 150 mg monotherapy versus castration in the treatment of metastatic and locally advanced prostate cancer.

OBJECTIVES: To evaluate the efficacy and tolerability of 'Casodex' monotherapy (150 mg daily) for metastatic and locally advanced prostate cancer. METHODS: A total of 1,453 patients with either confirmed metastatic disease (M1), or T3/T4 non-metastatic disease with elevated prostate-specific antigen (M0) were recruited into one of two identical, multicentre, randomised studies to compare 'Casodex' 150 mg/day with castration. The protocols allowed for combined analysis. RESULTS: At a median follow-up period of approximately 100 weeks for both studies, 'Casodex' 150 mg was found to be less effective than castration in patients with metastatic disease (M1) at entry (hazard ratio of 1.30 for time to death) with a difference in median survival of 6 weeks. In symptomatic M1 patients, 'Casodex' was associated with a statistically significant improvement in subjective response (70%) compared with castration (58%). Analysis of a validated quality-of-life questionnaire proved an advantage for 'Casodex' in sexual interest and physical capacity. 'Casodex' had a substantially lower incidence of hot flushes compared to castration (6-13% compared with 39-44%) and the most commonly reported adverse events were those expected for a potent antiandrogen. However, in patients with M0 disease at entry, the data are still immature with only 13% of M0 patients having died. An initial analysis of this immature data has suggested that the results in these patients may be different to those obtained in patients with M1 disease. A further survival analysis in patients with M0 disease is therefore planned when the data are more mature. CONCLUSIONS: 'Casodex' 150 mg is less effective than castration in patients with M1 disease. However, 'Casodex' has shown a benefit in terms of quality of life and subjective response when compared to castration and has an acceptable tolerability profile. Thus 'Casodex' 150 mg monotherapy is an option for patients with M1 prostate cancer for whom surgical or medical castration is not indicated or is not acceptable.

Aged↗
PubMed1981

Pituitary gonadotropin-releasing hormone receptors. Effects of castration, steroid replacement, and the role of gonadotropin-releasing hormone in modulating receptors in the rat.

To study the role of gonadotropin-releasing hormone (GnRH) receptors in the regulation of gonadotropin secretion, we used D-125I-alanine6 des glycyl10 GnRH ethylamide (D-125I-Ala analog), a nondegradable, superagonist GnRH analog to assess GnRH receptors on rat pituitary membranes. Receptor affinity in intact adult rats was 5.0 X 10(9) M-1 and was unchanged after castration in both sexes. Castration of adult male and female rats produced a twofold increase in GnRH binding capacity by 7 d and binding capacity remained elevated for the subsequent 14 d. GnRH receptor number rose more rapidly after castration in males than females, and the time-course of receptor rise was similar to the increase in serum gonadotropin levels. The increase in GnRH binding capacity was prevented by gonadal steroid replacement at the time of castration in both sexes. Injections of the GnRH analog, D-Ser6 (TBu) des Gly10 GnRH ethylamide for 4 d produced a 70% increase in GnRH receptor number in intact male rats and testosterone-replaced castrates. The same regimen, however, failed to increase the elevated receptor numbers present after castration. Administration of rabbit anti-GnRH serum concomitant with castration inhibited the rise in both GnRH receptor number and luteinizing hormone. The changes in pituitary GnRH receptors parallel previously demonstrated changes in hypothalamic secretion of GnRH. Thus, GnRH probably regulates its own receptor in vivo and gonadal steroids may influence pituitary GnRH receptors by changing hypothalamic GnRH secretion.

Animals↗
PubMed1985

Sexual differentiation of positive feedback: effect of hour of castration at birth on estradiol-induced luteinizing hormone secretion in immature male rats.

In the male rat, a dramatic increase in hypothalamic testosterone and estradiol concentrations occurs during the first few hours of postnatal life. These experiments sought to determine whether such increases participate in the defeminization of positive estrogen feedback effects on LH secretion. Newborn male rats were castrated either in utero (0 h males), or 10 or 24 h after birth. Some males were castrated at 0 h in utero and injected at the time of surgery with 1,2.5, or 5 micrograms testosterone propionate. A group of females was ovariectomized at 0 h in utero (0 h females). The control group consisted of male and female rats sham gonadectomized at 0 h in utero which were either gonadectomized at 21 days of age or left intact. The experimental groups were challenged before puberty to determine if estrogen induced a release of LH using two different types of estrogen treatment. The first treatment consisted of an injection of 0.2 microgram estradiol benzoate (EB) on day 28 followed by a second 10 micrograms injection of EB on day 29. This treatment resulted on the afternoon of day 30 in a surge of LH in intact females. Normal males, 0 h males, or females castrated at 21 days did not have a significant LH surge. The second test consisted of the daily injection of 0.05 microgram EB on days 23-27; on day 28 the rats were injected with 2.5 micrograms EB. Zero hour male and female rats showed a large LH surge on the afternoon of day 29; sham castrated males never responded to this treatment. No sex difference was observed in the mean size of the LH surge providing the males were castrated at 0 h in utero. The effect of the hour of castration on the day of birth also was studied. Males castrated at 10 or 24 h after birth showed either no LH surge or the magnitude of the surge was greatly reduced compared to that obtained in the 0 h males (P less than 0.001). The fact that 0 h males injected with 1 microgram testosterone propionate never showed an LH surge after prepuberal treatment with estrogen suggests that 0 h is a time during which the newborn is sensitive to the defeminizing effect of androgens. These results are consistent with the idea that the testicular hyperactivity which occurs at the time of birth could influence the defeminization of the LH surge mechanisms.

Animals↗
PubMed1985

Characterization of rat pituitary luteinizing hormone charge microheterogeneity in male and female rats using chromatofocusing: effects of castration.

Chromatofocusing was used to characterize the isohormones of rat (r) LH present in extracts of pituitaries of intact and castrate, male and female rats. In each case, at least seven rLH isohormones were observed: one in the void volume of the column [isohormone I, isoelectric point (pI) greater than 9.8], five in the pH range of 9.25-8.97 (isohormones II-VI), and one which was bound to the column but could be eluted with 1.0 M NaCl (isohormone VII, pI less than 7.0). The distribution of immunoreactive rLH among the isohormones was affected by castration in both sexes but was not significantly different in intact males vs. proestrous female rats. Compared to castrates of both sexes, intact male and female rats possessed a larger percentage of immunoreactive rLH as isohormone I. All seven isohormones possessed significant LH biological activity. The bioactivity-immunoactivity (B/I) ratios of rLH isohormones from castrate female rats were significantly greater than those of intact and castrate male rats. The Bio-Index (the amount of biologically active rLH) of isohormones II-VI was markedly increased as a result of castration in both sexes. Changes in B/I ratios and amounts of immunoreactive rLH were not due to the cross-reactivity of rFSH, rTSH, and rPRL in the rLH RIA. Thus, in addition to altering the amount of rLH in the pituitary, castration also alters the pattern of rLH isohormones in the pituitary, yielding a dramatic increase in the isohormones with pI values in the range of 9.06-9.25.

Animals↗
PubMed1975

The effect of castration and testosterone replacement on specific proteins and androgen levels of the rat epididymis.

The normal weight increase of the epididymis during sexual maturation and its maintenance through adulthood were found to be dependent on the provision of androgens. Binding of [3H]dihydrotestosterone (DHT) to the epididymal 8S cytoplasmic receptor gradually decreased after castration to become undetectable after 25 days. Binding to the androgen binding protein (ABP) was absent 4 days after castration and was not reinduced by 3 weeks of testosterone (T) administration. Unilateral castration for periods of up to 27 days showed the disappearance of ABP with preservation of the 8S receptor on the castrated side, indicating a testicular source for ABP and the epididymal origin of the 8S receptor. The tissue concentrations of T and DHT in the epididymis became undetectable 30 days after castration and were restored to normal values by administration of testosterone in large doses (1.5 mg/100 g BW). Similar results were obtained in rats castrated at 10 days of age and injected with testosterone until 60 days old. The ratio DHT/T was depressed in the castrate and increased with testosterone treatment. The protein content of the epididymis (mg of protein/g wet weight) was also found to be influenced by androgens. Our results show evidence of some mechanisms involved in the trophic effect of androgens upon the epididymis and suggest the possible androgenic control of epididymal 5alpha-reductase activity. They also indicate that a testicular factor is required for the maintenance of the 8S cytoplasmic androgen receptor. It is not known whether this factor is testosterone or some other testicular secretion.

Androgens↗
PubMed2003

Characterization of C4-2 prostate cancer bone metastases and their response to castration.

UNLABELLED: New well-characterized preclinical models of prostate cancer (CaP) bone metastases are needed to improve our understanding of the development of CaP-related bone disease in patients. Here we describe characterization of a model consisting of direct injection of C4-2 cells into tibias. INTRODUCTION: Prostate cancer (CaP) has a high proclivity to metastasize to bone. Development and characterization of preclinical models of CaP bone metastases are of high interest. The objective of this study was to characterize C4-2 bone metastases and their response to castration. MATERIALS AND METHODS: Cell suspensions of C4-2, a subline of LNCaP, were injected directly into the tibias of intact male mice. In groups A (n = 7) and B (n = 5), animals were killed 3 and 8 weeks after injection of C4-2 cells, respectively. In group C (n = 7), animals were castrated 3 weeks after injection and killed 5 weeks after castration. Serum prostate-specific antigen (PSA) levels and bone mineral density (BMD) were measured, and bone histomorphometric analysis was performed. RESULTS: C4-2 cells decreased BMD of the injected tibias by 36.1% and bone volume by 74.1% versus normal tibias. Castration caused a 32.3% drop in serum PSA (p = 0.0438), with a nadir at day 14, after which it began to rise again. Bone destruction in the tumorous tibias of castrated animals was decreased by 15.9% versus tumorous tibias of intact animals (p = 0.0392). However, BMD in the tumorous tibias of castrated mice was still lower than in normal tibias of intact animals. Castration also decreased BMD and bone volume in nontumorous tibias (p = 0.0406 and 0.0232, respectively). CONCLUSIONS: The C4-2 model of bone metastasis recapitulates the response to androgen deprivation observed in CaP patients with bone metastases and is suitable for study of interactions between tumor and bone cells and evaluation of new therapeutic modalities.

Animals↗
PubMed1975

Relation between circulating levels of testosterone lh and fsh in intact and castrated, adult, male rats after testosterone administration.

Serum levels of LH, FSH and testosterone were measured by radioimmunoassay in intact and castrated, adult, male rats after testosterone was administered subcutaneously for seven days in doses ranging from 25 to 200 mug per 100 g body weight per day. Such treatment increased circulating testosterone both in intact and castrated rats, but its effects on serum gonadotrophins were different in these animal groups. All doses of testosterone suppressed serum LH and FSH in the normal rat. In the castrates, treatment with the lowest dose of testosterone resulted in serum LH levels significantly above the high castrate levels, while serum FSH tended to drop. Administration of the highest doses of testosterone did not depress serum LH and FSH in the castrates to those of intact, normal animals, though serum testosterone in these castrates was much higher than in normal, male rats. It is concluded, that the sensitivity of the hypothalamic-pituitary system for daily, subcutaneous testosterone administration during seven days is not the same in the intact and castrated, adult, male rat and that testicular factors different from testosterone may play a role in regulating production and/or secretion of gonadotrophins by the hypophysis in male animals.

Animals↗
PubMed1984

Hypothalamic control of the post-castration rise in serum LH concentration in rams.

Sexually mature rams were left intact, castrated (wethers), castrated and implanted with testosterone, or castrated, implanted with testosterone and pulse-infused every hour with LHRH. Serum concentrations of LH increased rapidly during the first week after castration and at 14 days had reached values of 13.1 +/- 2.2 ng/ml (mean +/- s.e.m.) and were characterized by a rhythmic, pulsatile pattern of secretion (1.6 +/- 0.1 pulses/h). Testosterone prevented the post-castration rise in serum LH in wethers (1.0 +/- 0.5 ng/ml; 0 pulses/h), but a castrate-type secretory pattern of LH was obtained when LHRH and testosterone were administered concurrently (10.7 +/- 0.8 ng/ml; 1.0 pulse/h). We conclude that the hypothalamus (rather than the pituitary) is a principal site for the negative feedback of androgen in rams and that an increased frequency of LHRH discharge into the hypothalamo-hypophysial portal system contributes significantly to the post-castration rise in serum LH.

Animals↗
PubMed1984

Suppression of LH secretion by oestradiol, dihydrotestosterone and trenbolone acetate in the acutely castrated bull.

Twenty acutely castrated bulls were used to investigate the role of androgenic and oestrogenic steroids in the feedback control of LH secretion. The effects of 5 alpha-dihydrotestosterone (DHT) or the growth stimulants trenbolone acetate (TBA) or oestradiol-17 beta (OE2) on serum LH secretory profiles were measured. In addition, pituitary LH responses to exogenous LH releasing hormone (LHRH) were determined to differentiate between hypothalamic and pituitary sites of steroid action. At the time of castration, two groups of animals were given implants of either 45 mg OE2 or 200 mg TBA. Another group received equivalent to 30 mg daily injections of DHT. Control steers showed an increase in LH from 2.4 +/- 0.5 (S.E.M.) micrograms/l to 7.0 +/- 0.5 micrograms/l during the week after castration. Treatment with DHT and TBA prevented the post-castration rise in serum LH. In contrast, steers given implants of OE2 showed a significantly greater increase in LH than controls 1 day after castration, but by day 5 LH declined in the OE2-treated group to precastration values. Five weeks after castration control steers secreted LH in pulses at intervals of 40-50 min and with an amplitude of 4.2 +/- 0.4 micrograms/l. Pulses were not detected in the LH profiles of the steroid-treated steers. Dihydrotestosterone and TBA significantly reduced pituitary LH responses to exogenous LHRH, whereas steers receiving OE2 showed LH responses to LHRH which were similar to those observed in castrated controls. These results support the hypothesis that androgenic and oestrogenic components participate separately in the feedback control of LH secretion in the bull.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1984

A histometrical study of immunohistochemically identified mitotic adenohypophysial cells in immature and mature castrated rats.

Two weeks after operation the effects of castration on all types of mitotic adenohypophysial cells in 30-day-old (immature) and 75-day-old (mature) male rats were studied immunohistochemically by light microscopy. The total number of mitotic cells in gland specimens increased 1.4 times in immature rats, but remained unchanged in mature animals; mitotic activity (mitotic cell number/mm2) was not affected in either age group. The population of mitotic gonadotrophs increased five to six times in comparison with intact controls. In addition, the percentage of mitotic gonadotrophs and their mitotic activity were raised in both age groups. Castration affected the mitosis of prolactin cells. The percentage of mitotic prolactin cells was reduced by one-third in castrated immature rats, but the total number and percentage of mitotic prolactin cells, as well as their mitotic activity, was reduced by about two-thirds in mature castrated rats. No significant changes in mitotic ACTH, TSH, GH and immunonegative cells were found after castration in either group of animals. Mitotic cells were more numerous in the anterior than in the posterior region of the gland in normal (uncastrated) immature rats, but were uniformly scattered in both regions in normal mature rats. On the other hand, castration induced a high population of mitotic cells in the anterior region regardless of age. This high population was the result of the enhanced mitosis of gonadotrophs. It is concluded that 2 weeks after castration the increment of mitotic divisions of all types of pituitary cells is age-dependent, and that mitosis takes place frequently in gonadotrophs and less frequently in prolactin cells.

Adrenocorticotropic Hormone↗
PubMed1985

Effects of hyperprolactinaemia and testosterone on the release of LH-releasing hormone and the gonadotrophins in intact and castrated rats.

We have investigated the effect of hyperprolactinaemia on the secretion of LH-releasing hormone (LHRH), LH and FSH in male rats of the PVG strain which were left intact, castrated or castrated and then implanted with either a 10 or 30 mm silicone elastomer capsule containing testosterone (T10 and T30 respectively). Hyperprolactinaemia was produced by pituitary grafts under the kidney capsule. Pituitary stalk blood, for LHRH estimation, and peripheral blood, for LH, FSH and prolactin, were collected under alphaxalone anaesthesia. Pituitary stalk blood was collected during three consecutive periods of 30 min each before, during and after the application of an electrical stimulus to the median eminence (ME). Hyperprolactinaemia significantly reduced the plasma concentrations of FSH in intact rats and the post-castration increase in the plasma concentrations of both LH and FSH. Neither hyperprolactinaemia nor castration had any significant effect on the spontaneous output of LHRH, but castration alone or castration plus implantation of a T30 capsule did significantly reduce the increment in LHRH output produced by ME stimulation, an effect not seen in rats bearing pituitary grafts. The T30, but not the T10 capsules suppressed the post-castration increase in the gonadotrophins, and the inhibitory effect of testosterone was not significantly affected by hyperprolactinaemia. An incidental but important finding was that the presence of pituitary grafts under the kidney capsule reduced the anaesthetic dose of alphaxalone by 63%.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1992

Age-related discrepancies between serum and pituitary gonadotrophin, and pituitary gonadotrophin subunit mRNA responses to castration and testosterone replacement in male rats.

The responses of gonadotrophin gene expression, pituitary content and serum levels to castration alone and castration plus testosterone replacement (silicone elastomer implants) were compared in male rats at 10, 30, 60 and 90 days of age. Sham-operated animals served as controls. In addition, 30-day-old castrated rats were treated with dihydrotestosterone (DHT) and diethylstilboestrol (DES). When killed 7 days after castration, the increases in serum LH (six- to eightfold; P < 0.01) and FSH (two- to fourfold; P < 0.01) were similar at all ages studied. Likewise, testosterone reversed the effects of castration in a largely similar fashion at all ages. In contrast, great age-related differences were observed in the responses of gonadotrophin subunit mRNAs to the treatments. Castration increased the common alpha subunit mRNA two- to fourfold on days 10 and 30 (P < 0.01), sixfold on day 60 (P < 0.01), but not at all on day 90. Testosterone reversed the increases at all ages, but the levels were below those of controls only at 90 days (P < 0.01). The highest increases (sixfold; P < 0.01) of LH-beta mRNA were seen on days 10 and 60, the others being two- to threefold higher (P < 0.05-0.01). Testosterone reversed this effect at 60 days and suppressed LH-beta mRNA to below the control levels at other ages (P < 0.01). Castration had no effect on FSH-beta subunit mRNA at 30 and 90 days but a four- to fivefold increase was seen on days 10 and 60 (P < 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Aging↗
PubMedDate not supplied

Changes in testosterone and dihydrotestosterone levels in male rat accessory sex organs, serum, and seminal fluid after castration: establishment of a new highly sensitive simultaneous androgen measurement method.

It is known that abnormal androgen dynamics in the tissues is a cause of androgen-dependent disorders. Investigation of tissue androgen levels could provide a clue to the elucidation of disorders. However, it is difficult to measure a trace amount of androgen in the tissues. We established a highly sensitive simultaneous quantification method of testosterone and dihydrotestosterone (DHT), which play the most important roles in the body among androgenic steroids in trace amounts, and investigated time course changes in testosterone and DHT levels in male accessory sex organs, serum, and seminal fluid after castration in rat models. In addition, changes in the testosterone/DHT ratio of male accessory sex organs and seminal fluid were observed. The simultaneous testosterone and DHT measurement method established by us was validated. Intra-assay variation and interassay precision and accuracy were all within +/-20%, and the quantification limits of testosterone and DHT were both 15.6 pg/g. With the use of this method, the testosterone and DHT levels in the prostate, seminal vesicles, and serum immediately after castration were similar to those previously reported. The testosterone and DHT levels were 350 pg/g and 605 pg/g, respectively; which showed dominance of DHT in seminal fluid, although it was not as marked as that in the male accessory sex organs. Androgens decreased with time after castration in the accessory sex organs, serum, and seminal fluid. In the prostate and seminal vesicles, testosterone and DHT decreased to about 50% and about 2% of the normal levels, respectively, 72 hours after castration. The serum levels were under the quantification limits 6 hours after castration and thereafter. In seminal fluid, the testosterone and DHT levels decreased to 49% and 35% of normal levels, respectively, 72 hours after castration. The testosterone/DHT ratio in the male accessory sex organs was lower in the prostate (0.06) than in the seminal vesicles (0.13) immediately after castration. In the seminal fluid, changes in the ratio were small compared with those in the accessory sex organs and serum. These results showed that our method was capable of measuring testosterone and DHT in very small amounts of samples such as prostate biopsy specimens, and it might provide a clue to the elucidation of the pathology of androgen-dependent disorders.

Animals↗
PubMed1989

Inhibitory effects of estrogen and castration on the early stage of pancreatic carcinogenesis in Fischer rats treated with azaserine.

Effects of sex steroids on pancreatic carcinogenesis during the early stage were studied in azaserine-treated rats of both sexes. Fischer rats were given weekly i.p. injections of azaserine (30 mg/kg) [CAS:115-02; diazoacetate serine(ester)] at 2 and 3 weeks of age and were divided into six groups. Castration, ovariectomy, and s.c. implantations of either a 0.3-mg or a 1.0-mg 17 beta-estradiol (CAS:50-28.2; estradiol) pellet were performed at 7 weeks of age. The groups were as follows: group 1, intact male; group 2, castrated; group 3, castrated plus 0.3 mg estradiol; group 4, castrated plus 1.0 mg estradiol; group 5, ovariectomized; and group 6, intact female. Rats were killed 4 months after the last injection of azaserine. Azaserine treatment induced atypical acinar cell foci and nodules (AACN) in both sexes. The acidophilic AACN are considered preneoplastic lesions. An apparent sex difference was observed; the number of acidophilic AACN was greater in male rats than in female rats. Castration caused a significant decrease in both the serum testosterone levels and the number of acidophilic AACN, which were comparable to those in ovariectomized female rats. Furthermore, when estradiol treatment was administered to the castrated male rats, a linear decrease in the number of acidophilic AACN and an elevation in the serum estradiol levels were observed and were dose dependent. There were also positive relationships between estradiol treatments and the mean pituitary and pancreas weights. These results showed that estradiol treatment and the drop in testosterone levels caused by castration were highly effective in inhibiting the development and growth of preneoplastic lesions of the pancreas of the rats treated with azaserine. This estradiol effect was dose dependent. The present study, therefore, provides evidence that estrogen may act as an inhibitor and androgen as a promoter in the early stage of pancreatic carcinogenesis in rats.

Animals↗
PubMed1986

Androgen-mediated development of irradiation-induced thyroid tumors in rats: dependence on animal age during interval of androgen replacement in castrated males.

When male Long-Evans rats at age 8 weeks were radiation treated (40 microCi Na131I), thyroid follicular adenomas and carcinomas were observed at age 24 months with a high incidence of 94%. Castration of males prior to irradiation significantly reduced this tumor incidence to 60%. When testosterone (T) was replaced in castrated, irradiated male rats, differentially increased incidences of thyroid tumors occurred, depending on the time interval for hormone replacement. Immediate (age 2-6 mo) or early (age 6-12 mo) T replacement at approximate physiologic levels led to thyroid follicular tumor incidences of 100 and 82%, respectively, whereas intermediate (12-18 mo) or late (18-24 mo) T treatment led to only 70 and 73% incidences, respectively. Continuous T replacement (2-24 mo) in castrated irradiated male rats raised thyroid tumor incidence to 100%. Since elevated thyroid-stimulating hormone (TSH) is a reported requisite for development of radiation-associated thyroid tumors, the effects of T on serum TSH levels were examined. Mean serum TSH values in all irradiated animal groups were significantly elevated above age-matched nonirradiated animals at 6, 12, 18, and 24 months. Serum TSH levels were higher in continuous T-replaced irradiated castrates than in intact, irradiated males, whereas such intact male TSH levels were greater than those for irradiated castrates without T treatment. Interval T replacement in castrated male rats was generally associated with increased serum TSH levels during the treatment interval and with lowered TSH levels after discontinuation of T treatment, particularly in irradiated rats. However, when irradiated, castrated males received late T replacement (age 18-24 mo), there was no elevation of TSH at the end of the treatment interval. Thus an indirect effect of T via early stimulation of TSH may be at least partly responsible for the high incidence of irradiation-induced thyroid tumors in rats.

Age Factors↗
PubMed1981

Castration atrophy and pharmacological reactivity of the rat coagulating gland.

1. The reactivity and sensitivity of the rat coagulating gland to acetylcholine, adrenaline, serotonin and barium chloride was studied 7, 15 and 30 days after castration. 2. The wet and the dry weight of the coagulating gland progressively decreased with time after castration. 3. Spontaneous contractions were observed in the coagulating gland 15 and 30 days after castration. 4. The maximum force developed per gram tissue was significantly higher than control for serotonin and barium chloride on the 7th day, while for acetylcholine and adrenaline the increase was observed only on the 15th day after castration. 5. The pD2 values for adrenaline, barium chloride and serotonin increased significantly 15 days after castration, whereas the change in sensitivity to acetylcholine was detected only 30 days after castration. 6. These results suggest that changes in reactivity and sensitivity of the rat coagulating gland caused by castration are not related only to muscle atrophy, since the time course of the development of the effects is different for the four agonists studied.

Acetylcholine↗