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1.
The effect of uni- and bilateral cryptorchidism on testicular inhibin and testosterone secretion and their relationships to gonadotropins were studied in rats. Mature Wistar male rats weighing approximately 300 g were made either uni- or bilaterally cryptorchid. Testicular inhibin and testosterone content and plasma levels of LH and FSH were examined 2 weeks later. A similar remarkable decrease in testicular inhibin content was found in uni- and bilaterally cryptorchid testes. On the other hand, the testicular testosterone content was significantly decreased only in unilaterally cryptorchid testis with an inverse increase in the contralateral testis. Plasma testosterone levels were normal and plasma LH and FSH increased significantly in both of the cryptorchid groups. These results showed that cryptorchidism impairs both Sertoli and Leydig cell functions. While testosterone production was compensated by increased LH for 2 weeks, neither inhibin secretion nor storage changed in cryptorchid or contralateral testes during the same period.  相似文献   

2.
The study was an examination of the effects of spinal cord injury (SCI) on spermatogenesis and Sertoli cell functions in adult rats with Sertoli cell-enriched (SCE) testes. The effects of SCI on the seminiferous epithelium were characterized by abnormalities in the remaining spermatogenic cells during the first month after SCI. Three days after SCI, serum testosterone levels were 80% lower, while serum FSH and LH levels were 25% and 50% higher, respectively, than those of sham control SCE rats. At this time, the levels of mRNA for androgen receptor (AR), FSH receptor (FSH-R), and androgen-binding protein (ABP) were normal whereas those for transferrin (Trf) had decreased by 40%. Thereafter, serum testosterone levels increased, but they remained lower than those of the sham control rats 28 days after SCI; and serum FSH and LH levels returned to normal. The levels of mRNA for AR, ABP, and Trf exhibited a biphasic increase 7 days after SCI and remained elevated 28 days after SCI. FSH-R mRNA levels were also elevated 90 days after SCI. Unexpectedly, active spermatogenesis, including qualitatively complete spermatogenesis, persisted in > 40% of the tubules 90 days after SCI. These results suggest that the stem cells and/or undifferentiated spermatogonia in SCE testes are less susceptible to the deleterious effects of SCI than the normal testes and that they were able to proliferate and differentiate after SCI. The presence of elevated levels of mRNA for Sertoli cell FSH-R and AR, as well as of that for the Sertoli cell proteins, in the SCE testes during the chronic stage of SCI suggests a modification of Sertoli cell physiology. Such changes in Sertoli cell functions may provide a beneficial environment for the proliferation of the stem cells and differentiation of postmeiotic cells, thus resulting in the persistence of spermatogenesis in these testes.  相似文献   

3.
Treatment of adult male rats with oestradiol benzoate (OB) for 21 days significantly decreased the body, testicular and accessory sex organ weights but increased anterior pituitary weight. OB treatment also significantly suppressed circulating FSH and LH levels as well as plasma and testicular concentrations of testosterone. The seminiferous tubules and interstitial cells were partly atrophied, and there was some effect on spermatogenesis, with step 14 to 19 spermatids being fewer than normal. Rats treated with OB for 21 days were then treated daily with LH-RH analogue ((D-Leu6, des-Gly-NH2(10))-LH-RH-ethylamide), to see if testicular function could be recovered. Circulating gonadotrophins were significantly elevated, testicular histology was normal and testicular and plasma testosterone concentrations and the accessory sex organ weights remained suppressed. These results suggest possible extra-pituitary effects of the LH-RH analogue, including a direct action on the testes and/or accessory sex organs.  相似文献   

4.
The testosterone responses to a single injection of hCG (100 i.u.) in hypophysectomized (hypox.), cryptorchid or sham-operated rats were followed over a 5-day period. In sham-operated rats, hCG induced a biphasic rise in serum testosterone, peaks being observed at 2 and 72 h. Reduced testis weights, elevated FSH and LH levels and reduced serum testosterone levels were found after 4 weeks of cryptorchidism, but hCG stimulation resulted in a normal 2 h peak in serum testosterone. However, the secondary rise at 72 h in cryptorchid rats was significantly lower than sham-operated rats. Reduced testis weight and undetectable serum FSH and LH levels together with decreased testosterone levels were found 4 weeks after hypophysectomy. Serum testosterone levels rose 2 h after hCG in comparison to hypox. controls but this peak was significantly reduced compared with sham-operated rats. The second rise in serum testosterone began on day 2, peaking on day 4 at levels comparable to that seen in sham-operated rats after hCG. The in vitro basal and hCG stimulated secretion of testosterone by cryptorchid testes was greater than that secreted by normal rat testes (518.0 +/- 45.9 and 3337.6 +/- 304.1 pmol per testis per 4 h compared with 223.6 +/- 24.9 and 1312.9 +/- 141.4 pmol per testis per 4 h for normal rat testes). In cryptorchid animals a single injection of 100 i.u. hCG resulted in a pattern of in vitro refractoriness similar to normal rats, lasting from 12 h to 2 days, during which testosterone secretion was reduced to near basal levels. The in vitro basal and hCG-stimulated secretion of testosterone by hypox. rat testes was severely diminished compared with normal rat testes. The temporal pattern of in vitro secretion of testosterone from hypox. rat testes mimicked the in vivo serum testosterone pattern seen in these animals. This study demonstrates important differences in the in vivo and in vitro testosterone response to hCG after testicular damage.  相似文献   

5.
Cryptorchidism surgically induced in 14-day-old rats, was allowed to persist until 35 days when one group was killed to assess testicular function. In a second group the cryptorchid testis was returned to the scrotum surgically (orchidopexy) and subsequently killed at 130 days. A third group remained persistently cryptorchid to 130 days, while in a fourth group two sham operations were performed at 14 and 35 days. At 35 days, cryptorchidism resulted in a significant decline in testis weight due to suppressed spermatogenesis. Sertoli cell function as measured by seminiferous tubule fluid (TF) production after unilateral efferent duct ligation and androgen-binding protein (ABP) production was significantly depressed in the cryptorchid group. Serum follicle-stimulating hormone (FSH) and luteinizing hormone (LH) levels were significantly elevated with cryptorchidism but serum testosterone levels were unchanged. Although morphometric measurements showed no change in Leydig cells cross-sectioned area, in vitro human chorionic gonadotropin (hCG)-stimulated testosterone production was significantly increased in the cryptorchid group at higher hCG doses. Similar changes were found in cryptorchid testes at 130 days except that Leydig cell cross-sectional area was now significantly increased. Orchidopexy at 35 days restored spermatogenesis and fertility during test mating was not impaired. TF production, ABP accumulation and serum FSH levels returned to normal following orchidopexy.(ABSTRACT TRUNCATED AT 250 WORDS)  相似文献   

6.
Reports from this and other laboratories have concluded that unilateral disruption of spermatogenesis induces a predominantly ipsilateral increase in the responsiveness of Leydig cells to stimulation with luteinizing hormone (LH) and have suggested that if such effects were mediated by locally produced hormones then such "factors" should be detectable in testicular interstitial fluid. We sought to demonstrate such factors in testicular fluid from gonads subjected to a variety of treatments that disrupt gametogenesis. Fluid (TF) was drained from testes of adult rats that had been sham treated, irradiated, or treated with busulfan in utero, made unilaterally or bilaterally cryptorchid, or were unilaterally or bilaterally efferent-duct-ligated. Leydig cells obtained from normal rats basally produced 8 +/- 1 ng androgen/10(6) Leydig cells/2 h and, when maximally stimulated with LH, produced 66 +/- 3 ng. The addition of the various TFs to the incubations significantly increased both basal and LH-stimulated androgen production. TF from lesioned testes was more effective in increasing androgen production than TF from control rats. Unilateral lesions caused an increase in the ability of TF from the disrupted testes to increase the androgen production by normal Leydig cells, as compared to TF from contralateral testes. Thus, locally produced "factor(s)" do appear to modify Leydig cell function. Additional studies using TF from control and bilaterally cryptorchid animals suggest that the "factor' in TF is heat-labile; has a molecular size between bovine serum albumin and ovalbumin; exerts a portion of its action independently of cAMP formation; and does not appear to be LH, follicle-stimulating hormone, prolactin, or gonadotropin-releasing hormone.  相似文献   

7.
Male rats given 250 mug oestradiol benzoate by subcutaneous injection on Day 4 of postnatal life showed a marked delay in the onset of the pubertal increase in the weight of the testes and seminal vesicles and in spermatogenesis but not a complete failure of sexual development. The increase in plasma testosterone concentration at puberty was also delayed in oestrogen-treated males but the eventual increase in seminal vesicle weight was closely related in time to the delayed increase in plasma testosterone concentration. Both plasma LH and FSH concentrations were reduced for about 10 days after oestrogen administration as compared to control values. After 22 days of age, plasma LH concentration did not differ significantly from the control values. The plasma FSH concentration of the oestrogen-treated males showed a delayed rise to values equal to or higher than those of controls of the same age. The delayed rise in plasma FSH concentration in the oestrogen treated males preceded the delayed rise in plasma testosterone in these animals. The decrease in plasma FSH concentration from the high prepubertal values to the lower values in adults occurred at different ages in the control and in oestrogen-treated rats but in both groups the decrease occurred as plasma testosterone levels were increasing and the first wave of spermatogenesis was reaching completion. The increase in plasma FSH concentration after castration was reduced in oestrogen-treated males during the period throughout which FSH levels in the intact animals were subnormal but the levels in oestrogen-treated males castrated after the delayed rise in FSH had occurred did not differ from control values. It is suggested that the delayed sexual maturation of male rats treated with high doses of oestrogen in the neonatal period is related principally to abnormalities in the secretion of FSH.  相似文献   

8.
Pregnant rats were irradiated with 2.1 Gy gamma-ray of 60Co at day 20 of gestation. Seventy days after birth, the body weight of the fetally irradiated male pups was significantly lower than the control. The testes, ventral prostates and seminal vesicles were atrophied by irradiation, whereas no decreased weight of the adrenals was observed. Histological examination of the testes of the irradiated rats revealed a complete disappearance of germinal cells. Sertoli cells and Leydig cells appeared normal, and no apparent histological difference was observed in the adrenals between the control and the irradiated rats. Activities of microsomal delta 5-3 beta-hydroxysteroid dehydrogenase (HSD) + isomerase, 17 alpha-hydroxylase/C17,20-lyase, 17 beta-HSD and 7 alpha-hydroxylase per pair of testes were decreased in the irradiated rats (36-86% of the control). In contrast, no decreased activity of 20 alpha-HSD in the cytosol fraction was observed by irradiation. No decreased activity of adrenocortical enzymes, such as delta 5-3 beta-HSD + isomerase, 21-hydroxylase, 11 beta-/18-hydroxylase and 5 alpha-reductase, was also observed in the irradiated group. Concentrations of LH, FSH, TSH, prolactin, testosterone, progesterone and aldosterone in serum were measured by radioimmunoassay. Only the FSH concentration was significantly increased by the irradiation, while no difference was found in the concentration of other hormones. It was concluded that irreversible damage was induced in spermatogenesis and androgen production by the fetal irradiation, whereas corticoidogenesis was not affected.  相似文献   

9.
Serum LH and FSH concentrations were measured in adult male rats. Blockage of the ductuli efferentes by surgical ligation or treatment with the anti-fertility drug alpha-chlorohydrin did not produce any changes in serum LH or androgen-dependent organ weights. Serum FSH in both groups was significantly raised by 4 days after treatment and remained so throughout most of the experimental period (42 days) but did not attain the values obtained in castrates. The gonadotrophin changes were accompanied by an initial increase in the weight and turgidity of the testes which then became flaccid and atrophied. These changes were similar but not identical after both treatments. Androgen secretion was impaired in adult rats treated with ethylene dimethane sulphonate; serum LH values were similar to those of 14-day castrates, and serum FSH was also elevated but not to the level found in the castrates. Ligation of the ductuli efferentes did not produce any further changes in concentrations of either hormone in spite of the retention of the testicular products within the testes as reflected by an increase in weight. The results are consistent with the view that changes in serum FSH after blockage of the ductuli efferentes are related to disturbances in the production of inhibin from the seminiferous epithelium rather than retention of inhibin with the testicular tubules.  相似文献   

10.
The effects of testosterone administration on testicular inhibin content and histology were studied in bilaterally cryptorchid rats, in which a marked decrease in testicular inhibin content had been observed. Mature male Wistar rats weighing approximately 300 g were made bilaterally cryptorchid by placing the testes in the abdominal cavity. Testosterone in oil, 0.1, 1.0 or 10 mg, was given i.m. each week. Testicular inhibin and testosterone content, histology and plasma LH, FSH and testosterone were studied 2 weeks later. Abnormally decreased testicular inhibin in cryptorchidism was restored toward normal by testosterone in a dose dependent manner in 2 weeks after surgery. Sertoli cell structure also recovered toward normal with increasing amount of testosterone. Decreased testicular testosterone content and Leydig cell atrophy were observed with suppressed plasma LH and FSH after testosterone. These results showed that the increased plasma concentration of testosterone had a stimulatory effect on the Sertoli cell function in cryptorchidism, in which compensated Leydig cell failure was demonstrated.  相似文献   

11.
Adult rats (16-18/group) received a single intratesticular injection of 25, 100 or 400 microliters glycerol solution (7:3 in distilled water, v/v). Half of the rats in each group were given implants of testosterone, a testosterone-filled Silastic capsule (1.5 cm length) to provide serum values of testosterone within the normal range. After 1 week all animals were killed by decapitation. Serum concentrations of gonadotrophins, testosterone and immunoactive inhibin as well as testicular concentrations of testosterone and bioactive inhibin were determined. Testicular histology was studied in Paraplast-embedded tissue stained with PAS and haematoxylin-eosin. Glycerol treatment caused a dose-dependent ablation of spermatogenesis in a distinct area around the site of injection. Serum concentrations of FSH increased proportionally with increasing spermatogenic damage while serum LH and testosterone remained unaltered except with the highest glycerol dose. The rise in serum FSH was significantly correlated with serum (r = -0.70, P less than 0.001) and testicular (r = -0.66, P less than 0.001) concentrations of inhibin. A less pronounced correlation was found between LH and serum inhibin (r = 0.48). No correlation was found between the concentrations of LH and testicular inhibin or between serum concentrations of FSH and serum testosterone in the 25 and 100 microliters groups. Maintenance of low to normal serum testosterone concentrations by means of Silastic implants blocked the elevation of FSH in glycerol-treated animals but failed to affect significantly serum FSH in untreated rats. In all testosterone treated rats testicular inhibin concentrations were markedly reduced in the presence of lowered concentrations (7-14%) of testicular testosterone and unaltered serum FSH concentrations.  相似文献   

12.
The effects of single or combined daily treatment with an LHRH agonist and low or high doses of LH upon the testes of adult hypophysectomized rats were studied for up to 2 weeks in which changes in testicular histology, particularly the interstitial tissue, were examined by morphometry and related to functional assessment of the Leydig cells in vivo and in vitro. Compared to saline-treated controls, LHRH agonist treatment did not alter testis volume or the composition of the seminiferous epithelium or any of the interstitial tissue components although serum testosterone and in-vitro testosterone production by isolated Leydig cells were significantly reduced. With 2 micrograms LH for treatment, testis volume was increased, spermatogenesis was qualitatively normal, total Leydig cell volume was increased, serum testosterone values were initially elevated but subsequently declined and in-vitro testosterone production was enhanced. Testis volume with 20 micrograms LH treatment was unchanged compared to saline treatment, the seminiferous epithelium exhibited severe disruption but total Leydig cell volume was greatly increased due to interstitial cell hyperplasia. This group showed elevated serum testosterone concentrations and major increases in testosterone production in vitro. Treatment with LHRH agonist with either dose of LH resulted in reduced testis volume, moderate to very severe focal spermatogenic disruption and increased total Leydig cell volume although serum testosterone values and in-vitro testosterone production were markedly reduced compared to control rats. It is concluded that, in the absence of the pituitary, LHRH agonist fails to disrupt spermatogenesis and the previously described antitesticular action of LHRH agonists in intact rats is therefore dependent upon the presence of LH, which alone or in combination with LHRH agonist, may focally disrupt spermatogenesis in hypophysectomized rats whereas the Leydig cells undergo hyperplasia. The findings show that impairment of spermatogenesis is accompanied by alterations of the interstitial tissue and suggest that communication between these two compartments is involved in the regulation of testicular function.  相似文献   

13.
U. Rai    S. Haider 《Journal of Zoology》1986,210(2):251-259
Effects of mammalian FSH, LH and testosterone on sexually regressed testes of Hemidactylus flaviviridis were investigated. Quantitative as well as histochemical studies revealed that only FSH could stimulate spermatogenesis and steroidogenesis. LH showed no effect either on the spermatogenesis or on steroidogenesis. Although testosterone did not induce any change at the initial stage, when given for a longer period the division of spermatogonia was completely checked.  相似文献   

14.
Experiments were conducted to test the hypothesis that acute TCDD toxicity is associated with pituitary hypofunction. Sexually mature male Sprague-Dawley rats were given graded doses of TCDD (0-100 micrograms/kg) and evaluated 7 days later. Despite pronounced hypophagia and body weight loss, plasma concentrations of growth hormone (GH), follicle-stimulating hormone (FSH), and luteinizing hormone (LH) were not significantly affected by any dose of TCDD. Only prolactin (PRL) concentrations were reduced, while, as previously reported, thyroid-stimulating hormone concentrations were elevated. Also, plasma LH, PRL, and adrenocorticotropic hormone (ACTH) concentrations were not significantly affected 1, 2, 3, 4, 5, or 7 days after a single dose of TCDD (50 micrograms/kg). We conclude that (1) pituitary hypofunction is not a major cause of the initial stages of acute TCDD toxicity, (2) growth retardation in TCDD-treated rats is not the result of a deficiency of GH, (3) alterations in plasma corticosterone concentrations are due to altered responsiveness of the adrenal to ACTH stimulation rather than to changes in plasma ACTH concentrations, and (4) that impaired spermatogenesis is not associated with a decrease in plasma FSH concentrations. In addition, the lack of a consistent effect on plasma PRL concentrations suggests that alterations in plasma PRL concentrations do not play a critical role in the toxicity of TCDD. Finally, because TCDD treatment causes a serious androgenic deficiency without increasing the rates at which androgens are catabolized or excreted, the fact that plasma LH concentrations were unaffected indicates that TCDD treatment must reduce the responsiveness of the testis to LH stimulation.(ABSTRACT TRUNCATED AT 250 WORDS)  相似文献   

15.
Male rats were passively immunized at Day 5 of age with LH-RH antiserum. Their response to LH-RH at 100 days of age was examined. Serum FSH and LH concentrations increased more than in control rats, although basal plasma levels were similar. The pituitary content of LH, but not FSH, was significantly increased, and hypothalamic content of LH-RH was similar in both groups. The testes and seminal vesicles were smaller in experimental animals than in controls. It is suggested that transient blockade of LH-RH secretion during the neonatal period produces abnormalities in pituitary-testicular functon in the adult rat.  相似文献   

16.
The testicular inhibin content showed an initial increase in the first 2-3 days after bilateral ligation of the efferent ducts of rats, followed by a subsequent decline to levels significantly below normal by 14 days, and reached 25% of control values at 42 days. Serum concentrations of FSH and LH were significantly increased at Day 6-7 after treatment and were still elevated after 42 days. The decline in testicular inhibin content at times associated with elevated FSH concentrations is consistent with the hypothesis of inhibin being involved in the feedback control of FSH secretion.  相似文献   

17.
Adult rats were made bilaterally cryptorchid and studied at intervals of 3, 7, 14 or 21 days to study temporal changes in Leydig cell function. Serum FSH and LH levels were measured and the cross-sectional area of the Leydig cells assessed by morphometry. The function of the Leydig cells was judged by the binding of 125I-labelled hCG to testicular tissue in vitro and the testosterone response of the testis to hCG stimulation in vitro. By 3 days after cryptorchidism, the binding of labelled hCG to testicular tissue was significantly decreased compared to that of controls, but the testes were able to respond to hCG stimulation in vitro. At 7, 14 and 21 days after cryptorchidism, an enhanced testosterone response was observed and the size of the Leydig cells was significantly greater than that of the controls, which indicated increased secretory activity by the cryptorchid testis. Although serum FSH levels were significantly elevated after 3 days of cryptorchidism, serum LH levels did not rise until 7 days, thereby suggesting that the loss of receptors is unlikely to result from down-regulation by LH. The reduced testosterone response of the cryptorchid testis in vivo to low doses of hCG and the enhanced response at high doses are probably related to the reduced blood flow to the cryptorchid testis and the decreased sensitivity of the Leydig cells induced by LH/hCG receptor loss.  相似文献   

18.
The role of endogenous opioids in the control of gonadotropin secretion in uremic male rats was investigated using the narcotic antagonist, naloxone. In order to eliminate the effect of weight loss due to uremia-induced anorexia as a cause of previously described altered gonadotropin secretion in uremia, we also studied a group of normal pair-fed control animals who exhibited a weight loss comparable to that of the uremic animals. Naloxone administration had no effect on the basal or LRH-stimulated peak concentrations of LH and FSH in the normal or the uremic rats. Basal and LRH-stimulated gonadotropin responses in the pair-fed rats were comparable to those seen in the normal rats. Similarly, opioid blockade produced no change in the basal or LRH-stimulated gonadotropin responses in the pair-fed animals. Testosterone concentrations were significantly lower in the uremic and pair-fed animals compared to the normal rats. The data suggest that experimental renal failure is not associated with altered opioidergic tone, as it relates to gonadotropin secretion, or to diminished sensitivity of the gonadotroph to LRH stimulation. The decreased testosterone concentration seen in the uremic and pair-fed rats may reflect abnormalities in gonadal hormone secretion due to primary pathology occurring at the level of the gonad. These abnormalities may be reflected as diminished Leydig cell sensitivity to LH. The inappropriately low concentrations of LH in the presence of low testosterone together with normal gonadotropin response to exogenous LRH also suggest an abnormal secretion of endogenous LRH. It is not clear whether this presumed abnormality in LRH secretion is a primary event or is related to decreased testosterone production by the testes in the uremic and pair-fed rats.  相似文献   

19.
The effect of experimentally-induced diabetes mellitus on reproductive organ weights, serum and pituitary gonadotropin levels and serum testosterone levels was studied in 3-month old rats. In experiment 1, intact rats were treated with alloxan monohydrate or streptozotocin. In experiments 2 and 3, intact and castrated rats were rendered diabetic with alloxan (experiment 2) or streptozotocin (experiment 3). The duration of each experiment was 3 weeks. In each experiment diabetes resulted in body weight losses or reduced body weight gain, elevated serum glucose concentrations and reduced assessory sex gland weights (intact rats). Serum levels of testosterone were depressed (P less than 0.05 or P less than 0.01) in diabetic rats. Serum levels of LH were significantly (P less than 0.05) lower in intact diabetics than in controls when pooled data from the three experiments were compared. Serum levels of FSH were not affected by diabetes. Pituitary concentrations of FSH were elevated (P less than 0.05) in diabetics in two of the three experiments, while LH concentrations were elevated (P less than 0.05 or P less than 0.01) in diabetics in all experiments. The hypersecretion of gonadotropins in castrated rats was not affected by diabetes.  相似文献   

20.
Summary The effects of FSH on the testicular interstitial tissue of immature hypophysectomized rats were studied by comparing morphological changes in Leydig cells with quantitative changes in interstitial tissue histology using morphometric analysis. Three groups of rats received subcutaneous injections of 0.5 ml saline vehicle or 10 g rFSH or 20 ng oLH (equivalent to the amount of LH known to contaminate the FSH), twice daily for 7 days. Administration of FSH significantly increased testis weight and stimulated more advanced spermatogenesis compared to saline or LH. Morphometric analysis of testes of LH-treated rats showed a small but significant increase in total interstitial cell volume compared to saline treatment. FSH caused much greater increases in the total volume of interstitial tissue and interstitial cells than either saline or LH and significantly increased the total volume of interstitial fluid by comparison with the other groups. FSH but not saline or LH treatment resulted in a striking hypertrophy of Leydig cells, to produce cells ultrastructurally identical to Leydig cells from adults. Since the target tissue of FSH is the seminiferous epithelium, the observed effects on Leydig cells by FSH treatment suggest that the secretion of factors by the seminiferous tubules may mediate the maturation of Leydig cells.  相似文献   

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