Focal disruption of spermatogenesis in the testis of adult rats after a single administration of human chorionic gonadotrophin

1989 ◽  
Vol 257 (1) ◽  
Author(s):  
J.B. Kerr ◽  
R.M. Sharpe
1962 ◽  
Vol 41 (1) ◽  
pp. 31-34 ◽  
Author(s):  
F. E. Szontágh ◽  
S. Uhlarik ◽  
A. Jakobovits

ABSTRACT The weight of the hypophysis and the ratio of the PAS-positive to PAS-negative cells in the anterior lobe of intact and ovariectomized adult rats increased significantly following treatment with serum gonadotrophin (PMS). After the administration of human chorionic gonadotrophin (HCG) a slight decrease of the hypophyseal weight and a moderate increase of the number of PAS-positive cells was observed in both intact and spayed groups of animals. Both gonadotrophic substances failed to inhibit the appearance of castration cells in the hypophysis.


1971 ◽  
Vol 68 (1) ◽  
pp. 41-49 ◽  
Author(s):  
R. Welschen ◽  
M. Rutte

ABSTRACT Treatment of the adult rat with pregnant mare serum gonadotrophin (PMS) followed by human chorionic gonadotrophin (HCG) is the standard procedure for inducing superovulation. Experiments were performed on rats with a 5 day cycle to determine why treatment with PMS only does not produce superovulation. In untreated animals all follicles in a range of [2267] 55 × 106 μm3 take part in ovulation. Similarly, in precocious ovulation induced by HCG in otherwise untreated animals, all follicles in this size range produce ovulations. After the injection of 5 IU of PMS into rats during oestrus the number of follicles in the size range of [2267] 55 × 106 μm3 is doubled, but only half of them take part in spontaneous ovulation, which occurs one day earlier than in untreated animals. An additional ovulating stimulus by means of treatment with HCG causes no increase in the number of ovulations. Data from hypophysectomized animals receiving HCG indicate that the ovulatory release of luteinizing hormone (LH) is not subnormal following treatment with 5 IU of PMS. After the administration of 10–35 IU PMS in oestrus, spontaneous ovulation does not occur. Data on hypophysectomized animals receiving HCG indicate that at this dose level of PMS, the ovulatory release of LH is subnormal. Indirect evidence suggests that this is due to high oestrogen levels in the blood, blocking the ovulatory release of LH. After 50–80 IU of PMS spontaneous ovulation of a small number of ova occurs on day 3. The ovulatory release of LH, estimated as in the previous experiments, is not distinctly subnormal. Therefore at this dose level of PMS a diminished responsiveness of the ovaries is responsible for the subnormal number of ovulations.


1986 ◽  
Vol 109 (3) ◽  
pp. 419-425 ◽  
Author(s):  
A. Widmark ◽  
J. E. Damber ◽  
A. Bergh

ABSTRACT The relationship between testicular vascular permeability and testicular microcirculation as measured by laser Doppler flowmetry was studied in adult rats. In untreated control animals there was an oscillatory testicular blood-flow pattern with a frequency of 10·6 ± 0·8 pulses/min and the amount of testicular interstitial fluid (IF) collected was 61·5 ± 2·2 μl/g testis. Treatment of the rats with 25–200 i.u. human chorionic gonadotrophin (hCG) s.c. 8 h before the experiment resulted in a change in the testicular flow pattern from pulsatile to continuous and an increase in IF volume. Treatment with hCG (50 i.u., s.c.) changed the testicular blood-flow pattern from oscillatory to continuous 4, 8 and 16 h after treatment. The flow pattern returned to being pulsatile 32 h after treatment with hCG. The IF information was increased at those times when the blood-flow pattern was continuous. No effects on blood flow or IF formation were observed with 12·5 i.u. hCG s.c. The present study shows a dose- and time-dependent covariation between the increase in testicular IF volume and the disappearance of the pulsatile flow in testicular microcirculation. It appears that a continuous flow pattern favours the transport of fluid from blood vessels to the interstitium. J. Endocr. (1986) 109, 419–425


1989 ◽  
Vol 121 (2) ◽  
pp. 311-316 ◽  
Author(s):  
S. Maddocks ◽  
B. P. Setchell

ABSTRACT We have used a push–pull cannula to collect interstitial fluid from the testes of anaesthetized rats at various times after a single injection of human chorionic gonadotrophin (hCG; 50 IU), and compared the levels of testosterone in this fluid with the levels in testicular and peripheral venous blood collected at the same times. Following hCG injection, significant increases in testosterone concentrations were observed in all fluids with notable peaks occurring in interstitial fluid at 2, 8 and 24 h, in testicular venous blood at 2, 8 and 30 h, and in peripheral venous blood at 2, 8, 24 and 72 h. The results demonstrate for the first time that changes in testosterone concentrations in interstitial fluid can be different from those in testicular venous blood. In addition, when testosterone levels in interstitial fluid were compared with levels in testicular venous blood at each time-point, the results suggested that the partitioning of testosterone between these two compartments can be regulated. Furthermore, the changes in both interstitial fluid and testicular venous blood levels of testosterone do not always parallel those in peripheral venous blood, suggesting that changes in testicular blood flow and peripheral clearance rates of testosterone may also be important in the control of circulating testosterone concentrations. Journal of Endocrinology (1989) 121, 311–316


1989 ◽  
Vol 122 (3) ◽  
pp. 689-NP ◽  
Author(s):  
K. J. Teerds ◽  
D. G. de Rooij ◽  
F. F. G. Rommerts ◽  
R. van den Hurk ◽  
C. J. G. Wensing

ABSTRACT The influence of LH levels on the proliferation and differentiation of possible Leydig cell precursors was investigated in adult rats, after the destruction of the existing Leydig cells with the cytotoxic drug ethane dimethyl sulphonate (EDS). In rats bearing a testosterone implant which prevented the rise in plasma LH levels and kept them within the normal range after the destruction of the Leydig cells, the proliferative activity of possible Leydig cell precursors still increased seven- to eightfold 2 days after EDS administration. Apparently, in this situation, locally produced factors, and not LH, may play a role in the stimulation of proliferation. The proliferative activity of the possible precursor cells could be further stimulated by treating rats with daily injections of human chorionic gonadotrophin (hCG) following EDS administration. It was concluded that the proliferative activity of possible Leydig cell precursors is probably regulated by both paracrine and endocrine factors. Almost no Leydig cells were formed in the rats bearing a testosterone implant during the first 4 weeks after EDS administration. When these rats were treated with hCG, starting 28 days after administration of EDS, a substantial number of Leydig cells was found after 2 days, and these cells also showed 3β-hydroxysteroid dehydrogenase (3β-HSD) and α-naphtyl esterase (α-NE) activity. When hCG treatment was started at 14 or 21 days after EDS administration, some cells with the nuclear characteristics of Leydig cells were present after 2 days, but no 3β-HSD or α-NE activity could be detected. Finally, when hCG treatment was started directly after EDS administration, a considerable number of Leydig cells was found 14 days after EDS, and some of these cells already showed 3β-HSD and α-NE activity. It is concluded that precursor cells are able to develop into advanced precursor cells at normal LH levels, and that the rate of development of new Leydig cells strongly depends upon LH/hCG levels. Journal of Endocrinology (1989) 122, 689–696


1995 ◽  
Vol 132 (2) ◽  
pp. 218-222 ◽  
Author(s):  
F Gaytan ◽  
C Bellido ◽  
E Aguilar ◽  
N van Rooijen

Gaytan F, Bellido C, Aguilar E, van Rooijen N. Pituitary–testicular axis in rats lacking testicular macrophages. Eur J Endocrinol 1995;132:218–22. ISSN 0804–4643 Testicular macrophages were depleted selectively in adult rats by intratesticular injections of liposome-entrapped dichloromethylene diphosphonate (Cl2MDP-lp), whereas control animals received intratesticular injections of phosphate-buffered saline-containing liposomes or 0.9% NaCl. The absence of macrophages in Cl2MDP-lp-injected rats was confirmed histologically. Rats lacking testicular macrophages showed significantly increased (twofold on average) serum concentrations of luteinizing hormone at 5 and 10 days after treatment. Serum luteinizing hormone concentrations drop to control values at 15 days after treatment. Serum testosterone concentrations were increased significantly (twofold on average) at 5, 10 and 15 days after treatment. No significant changes were found for follicle-stimulating hormone serum concentrations, or for the weights of the testes and sex accessory organs. Testicular histology was unchanged, except for the absence of testicular macrophages in Cl2MDP-lp-treated animals. Rats treated with NaCl or Cl2MDP-lp were injected with 100 IU of human chorionic gonadotrophin and sacrificed 2 h later. Serum testosterone concentrations increased 8.6-and 3.5-fold in NaCl and Cl2MDP-lp-treated rats, respectively, in response to acute human chorionic gonadotrophin treatment. These results point out the relevance of testicular macrophages for the regulation of the pituitary–testicular axis. F Gaytan, Department of Cell Biology, School of Medicine, 14071 Córdoba, Spain


1977 ◽  
Vol 75 (2) ◽  
pp. 271-276 ◽  
Author(s):  
J. W. SIEBERS ◽  
W. ENGEL

The binding of 125I-labelled human chorionic gonadotrophin (HCG) to ovarian tissue was studied in hypophysectomized immature and adult rats. The ability of the ovaries of adult rats to bind HCG was markedly reduced within 3 days of hypophysectomy and remained low for at least 20 days. The extent of the reduction depended on the stage of the oestrous cycle at which hypophysectomy was performed. The highest loss of HCG binding capacity was seen in rats hypophysectomized at dioestrus II, while rats hypophysectomized at the oestrous stage exhibited similar HCG binding to control rats at the same stage of the cycle. Scatchard analysis indicated that the reduction in the capacity of the ovary to bind HCG after hypophysectomy was caused by the loss of specific receptors and not by a decrease in binding affinity. In contrast to adult rats, in immature rats the HCG binding capacity of the ovaries did not change during the 3 days after hypophysectomy, but after this a slow decline took place. Twenty days after pituitary ablation, almost identical values for binding of HCG were found in immature and adult rats. Since hypophysectomy in adult rats causes a rapid regression of large follicles, our results indicate that the remaining HCG binding activity arises largely from small follicles which are known to be unaltered by the deprivation of hypophysial hormones. This assumption is supported by our observation that in the ovaries of 25-day-old immature rats, which lack large follicles, only a slow decrease in the ability of the ovaries to bind HCG occurs in the 20 days after the operation.


1993 ◽  
Vol 136 (3) ◽  
pp. 415-420 ◽  
Author(s):  
A. Bergh ◽  
J.-E. Damber ◽  
N. van Rooijen

ABSTRACT Liposome-entrapped dichloromethylene diphosphonate (Cl2MDP) was injected locally into the right testes of adult rats in order to deplete testicular macrophages. The number of testicular macrophages in the treated testes was reduced by at least 90% at 7 and 14 days after treatment. Unilaterally testicular macrophage-depleted animals were treated with 100 IU human chorionic gonadotrophin (hCG) subcutaneously and the inflammatory response was compared in the macrophage-depleted and intact contralateral testis. Four hours after hCG treatment, intratesticular testosterone was similarly increased in intact and macrophage-depleted testes. In macrophage-depleted testes there was a large increase in the number of leukocytes in testicular blood vessels and numerous leukocytes had migrated into the interstitial tissue. This response was greater than in the intact contralateral testis. It was concluded that testicular macrophages are probably not the origin of the inflammatory mediator secreted in the rat testis after hCG treatment. On the contrary, it appears that testicular macrophages may secrete factors inhibiting hCG-induced testicular inflammation. Journal of Endocrinology (1993) 136, 415–420


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