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J. B. Kerr

Summary. The occurrence of degenerating germ cells in the cycle of the seminiferous epithelium was measured in testicular tissues from eight normal adult rats. Testes were perfusion fixed, embedded in epoxy resin and, after sectioning a total of 180 randomly selected blocks at 1 μm, stained sections were examined by light microscopy; all cross-sectioned seminiferous tubules were categorized into one of 14 stages of the spermatogenic cycle. The number of degenerating cells per tubule was recorded in 2103 tubules. Degenerating germ cells were not detected at stages II–VI, and only rarely at stage VII (n = 366 tubules) in which one primary spermatocyte and one step 19 spermatid degenerated. All other stages exhibited a greater incidence of degenerative germ cells, particularly at stage XIV where, on average, the frequency of degenerating cells per round seminiferous tubule was about 40 times greater than at stage VII. The results indicated that, in the normal adult rat testis, the germ cells are least at risk of degeneration as they pass through stage VII.

Keywords: testis; spermatogenesis; germ cells; cell degeneration; rat

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The formation, distribution and fate of lipid inclusions within the seminiferous tubules of the rat has been studied throughout the spermatogenic cycle. The occurrence of lipid inclusions within the Sertoli cell exhibited cyclic variation with the stages of the rat seminiferous cycle. At stage 9 of the cycle, residual bodies of maturing spermatids were phagocytosed by the Sertoli cell and released numerous lipid droplets which appeared to coalesce into large inclusions at the base of the Sertoli cell at stage 10. The Sertoli cell lipid inclusions persisted throughout the completion of meiosis (stages 11 to 14) and the formation of young spermatids (stages 1 to 2) and their numbers appeared to reach a peak at stages 12 to 13 of the cycle. The inclusions decreased markedly within the Sertoli cell cytoplasm during stage 2 and remained low until stage 9 when lipid from the residual bodies again became available to the cell. This cyclic variation of lipid inclusions within the Sertoli cell does not support previously held views that there is a gradual decline in Sertoli cell lipid during stages 10 to 14 of the spermatogenic cycle. A hitherto unnoticed finding was the presence of large lipid inclusions in the cytoplasm of late pachytene to diakinetic spermatocytes, and some observations suggest a transfer of these lipid inclusions from the Sertoli cells to primary spermatocytes.

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J. B. Kerr and R. M. Sharpe

Summary. 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 μg 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 μg 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.

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R. M. Sharpe, J. B. Kerr, C. McKinnell, and M. Millar

This study assessed whether changes in production of seminiferous tubule fluid underlie the previously described androgen-dependent changes in protein secretion by seminiferous tubules at stages VI–VIII of the spermatogenic cycle. Testosterone withdrawal was induced in adult rats by administration of ethane dimethane sulfonate (EDS) and temporal changes in lumen area, the volume of seminiferous tubule fluid and testicular interstitial fluid were assessed and compared with the changes in secretion of [35S]methionine-labelled proteins in vitro by isolated seminiferous tubules at stages VI–VIII. Testicular interstitial fluid was reduced by about 50% by day 4 and later after EDS treatment when compared with controls. In contrast, the volume of seminiferous tubule fluid was unaffected at days 3 and 4 but was reduced by about 50% at days 6 and 8 after EDS treatment. In perfusion-fixed control testes, the lumen area of seminiferous tubules at stages VII–VIII was significantly greater than at stages I–VI and IX–XIV. This difference was also evident at 4 days after EDS treatment, but was abolished at 6 and 8 days after treatment. The volume of testicular interstitial fluid was reduced significantly at 3 and 4 days after EDS treatment, but was further reduced (about 50%) at 6 and 8 days. Administration of 25 mg testosterone esters every 3 days to EDS-treated rats prevented all of the changes described above. As the decrease in protein secretion by seminiferous tubules at stages VI–VIII following androgen withdrawal precedes the changes in lumen area and volume of seminiferous tubule fluid, it is concluded that there is differential control of these two androgen-dependent processes. The present data add to the evidence showing that testosterone plays a central role in regulating the production and movement of fluids (and therefore of nutrients) to and within the testis.

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D. C. Irby, J. B. Kerr, G. P. Risbridger, and D. M. de Kretser

Summary. Serum concentrations of LH, FSH and testosterone were measured monthly throughout the year in male bush rats. Testicular size and ultrastructure, LH/hCG, FSH and oestradiol receptors and the response of the pituitary to LHRH were also recorded.

LH and FSH rose in parallel with an increase in testicular size after the winter solstice with peak gonadotrophin levels in the spring (September). The subsequent fall in LH and FSH levels was associated with a rise in serum testosterone which reached peak levels during summer (December and January). In February serum testosterone levels and testicular size declined in parallel, while the pituitary response to an LHRH injection was maximal during late summer. The number of LH/hCG, FSH and oestradiol receptors per testis were all greatly reduced in the regressed testes when compared to active testes.

In a controlled environment of decreased lighting (shortened photoperiod), temperature and food quality, the testes of sexually active adult males regressed at any time of the year, the resultant testicular morphology and endocrine status being identical to that of wild rats in the non-breeding season. Full testicular regression was achieved only when the photoperiod, temperature and food quality were changed: experiments in which only one or two of these factors were altered failed to produce complete sexual regression.

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G. P. Risbridger, J. B. Kerr, R. Peake, K. A. Rich, and D. M. de Kretser

Summary. 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.

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R John Aitken, Jock K Findlay, Karla J Hutt, and Jeff B Kerr

Apoptosis is a critical process for regulating both the size and the quality of the male and female germ lines. In this review, we examine the importance of this process during embryonic development in establishing the pool of spermatogonial stem cells and primordial follicles that will ultimately define male and female fertility. We also consider the importance of apoptosis in controlling the number and quality of germ cells that eventually determine reproductive success. The biochemical details of the apoptotic process as it affects germ cells in the mature gonad still await resolution, as do the stimuli that persuade these cells to commit to a pathway that leads to cell death. Our ability to understand and ultimately control the reproductive potential of male and female mammals depends upon a deeper understanding of these fundamental processes.

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G. P. Risbridger, A. E. Drummond, J. B. Kerr, and D. M. de Kretser

Summary. There was a significant (P < 0·05) and consistent increase in the potency of steroidogenic stimulatory activity (testosterone production by purified Leydig cells in vitro) in testicular interstitial fluid of the cryptorchid compared to the scrotal testis from 1 to 4 weeks after the induction of unilateral cryptorchidism. In contrast, the level of mitogenic activity ([3H]thymidine incorporation into 3T3 cells) was not significantly different between interstitial fluid from cryptorchid and scrotal testes for up to 4 weeks after surgery. These results indicate that the steroidogenic activity and the mitogenic activity are due to different, as yet unidentified, factors in testicular interstitial fluid.

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M Myers, K L Britt, N G M Wreford, F J P Ebling, and J B Kerr

Accurate estimation of the number of ovarian follicles at various stages of development is an important indicator of the process of folliculogenesis in relation to the endocrine signals and paracrine/autocrine mechanisms that control the growth and maturation of the oocytes and their supporting follicular cells. There are 10-fold or greater differences in follicular numbers per ovary at similar ages and/or strains reported in earlier studies using various methods, leading to difficulties with interpretation of ovarian function in control vs experimental conditions. This study describes unbiased, assumption-free stereological methods for quantification of early and growing follicular numbers in the mouse ovary. A fractionator approach was used to sample a defined fraction of histological sections of adult wild-type ovaries. Primordial and primary follicles were counted independently with the optical and physical disector methods. The fractionator/disector methods, which are independent of follicular size or shape, gave estimations of 1930 ± 286 (S.E.M.) and 2227 ± 101 primordial follicles, and 137 ± 25 and 265 ± 32 primary follicles per ovary at 70 and 100 days of age respectively. From exact counts on serial sections, secondary and later follicular numbers at 100 days of age were estimated at 135 per ovary. Remnants of zona pellucidae (a marker of previous follicular atresia) were estimated using a fractionator/physical disector approach and were approximately 500 per ovary. The application of the quantitative methods described will facilitate an improved understanding of follicular dynamics and the factors that mediate their growth and maturation and allow for a better comparison between different studies.

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J B Kerr, R Duckett, M Myers, K L Britt, T Mladenovska, and J K Findlay

Proliferation and partial meiotic maturation of germ cells in fetal ovaries is believed to establish a finite, non-renewable pool of primordial follicles at birth. The supply of primordial follicles in postnatal life should be depleted during folliculogenesis, either undergoing atresia or surviving to ovulation. Recent studies of mouse ovaries propose that intra- and extraovarian germline stem cells replenish oocytes and form new primordial follicles. We quantified all healthy follicles in C57BL/6 mouse ovaries from day 1 to 200 using unbiased stereological methods, immunolabelling of oocyte meiosis (germ cell nuclear antigen (GCNA)) and ovarian cell proliferation (proliferating cell nuclear antigen (PCNA)) and electronmicroscopy. Day 1 ovaries contained 7924±1564 (s.e.m.) oocytes or primordial follicles, declining on day 7 to 1987±203, with 200–800 oocytes ejected from individual ovaries on that day and day 12. Discarded oocytes and those subjacent to the surface epithelium were GCNA-positive indicating their incomplete meiotic maturation. From day 7 to 100 mean numbers of primordial follicles per ovary were not significantly depleted but declined at 200 days to 254±71. Mean numbers of all healthy follicles per ovary were not significantly different from day 7 to 100 (range 2332±349–3007±322). Primordial follicle oocytes were PCNA-negative. Occasional unidentified cells were PCNA-positive with mitotic figures observed in the cortex of day 1 and 12 ovaries. Although we found no evidence for ovarian germline stem cells, our data support the hypothesis of postnatal follicle renewal in postnatal and adult ovaries of C57BL/6 mice.