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PubMed2005

Serotoninergic system blockage in the prepubertal rat inhibits spermatogenesis development.

The stimulatory and inhibitory role of serotonin in gonadotropin secretion and in the onset of puberty in the male rat has been previously described, but its role in the establishment of spermatogenesis is not known. The aim of this study was to investigate the effects of serotoninergic inhibition by p-chloroamphetamine (pCA) on the prepubertal-to-adult stage of the rat reproductive system. Hypothalamic serotonin, gonadotropins and sex steroid hormone concentrations were measured, and a histopathological analysis of seminiferous epithelium was carried out on animals treated with pCA from day 30 and killed at 45 or 65 days of age. The pCA treatment significantly reduced the hypothalamic levels of serotonin and its metabolite (5-hydroxyindole-3-acetic acid). This inhibition did not affect the sex steroid hormone or LH concentrations, but rather it induced an increase in FSH concentration in animals of both ages. Spermatogenesis was impaired by pCA treatment. Disruption of seminiferous epithelium and the death of numerous germ cells were observed. Sperm produced by pCA-treated animals was of poor quality and appeared in small quantities. Apparently, serotonin depletion did not affect communication between the hypothalamus and the pituitary, but the FSH increase could have been related to alterations in the seminiferous epithelium effects. The seminiferous epithelium cycle was altered in rats killed at both 45 and 65 days of age, because at each age of killing the distribution of spermatogenesis stages was different. Germ cell apoptosis did not appear to be related to changes in the FSH concentrations, but other factors produced during spermatogenesis could have been involved in this induction. This study showed that serotonin was necessary for the development of normal spermatogenesis in prepubertal rats.

Animals↗
PubMed1994

Can testosterone alone maintain the gonadotrophin-releasing hormone antagonist-induced suppression of spermatogenesis in the non-human primate?

The combination of gonadotrophin-releasing hormone (GnRH) antagonist and delayed testosterone substitution provides a promising approach towards male contraception. However, the GnRH antagonists used clinically so far cause side-effects and have to be administered continuously. We therefore used the non-human primate model to see whether the GnRH antagonist cetrorelix (which exhibits a favourable benefit-to-risk ratio in terms of anti-gonadotrophic action in normal men) induces complete and reversible suppression of spermatogenesis and whether GnRH antagonist-induced suppression of spermatogenesis can be maintained by testosterone alone. Four groups of adult cynomolgus monkeys (Macaca fascicularis; five per group) were injected daily with 450 micrograms cetrorelix/kg ([N-acetyl-D-2-naphthyl-Ala1, D-4-chloro-Phe2, D-pyridyl-Ala3, D-Cit6, D-Ala10]-GnRH). Group 1 received the GnRH antagonist for 7 weeks followed by vehicle administration for another 11 weeks; group 2 was treated with GnRH antagonist for the entire 18 weeks with each animal receiving a single testosterone implant during weeks 11-18 to restore the ejaculatory response to electrostimulation; group 3 received the GnRH antagonist for 18 weeks and testosterone buciclate (TB) was injected during week 6 of GnRH antagonist treatment; group 4 was subjected to GnRH antagonist administration for 7 weeks and received TB (200 mg/animal) during week 6. Under GnRH antagonist treatment alone serum concentrations of testosterone were suppressed. TB maintained testosterone levels two- to fourfold above baseline levels in groups 3 and 4 and prevented the recovery of LH secretion for about 20 weeks after GnRH antagonist withdrawal, whereas inhibin levels increased significantly from week 8 onwards. Group 2 animals were azoospermic during weeks 12-18 of GnRH antagonist administration. The TB-replaced groups developed azoospermia or became severely oligozoospermic. Quantitation of cell numbers by flow cytometry during weeks 6 and 18 revealed that TB (groups 3 and 4) had prevented a further decline of germ cell production compared with group 2 but had maintained the spermatogenic status present at week 6 (onset of TB substitution). All inhibitory effects of cetrorelix and/or TB were reversible after cessation of treatment. These findings demonstrate that cetrorelix reversibly inhibits spermatogenesis in a non-human primate model. Although TB maintained the GnRH antagonist-induced suppression of spermatogenesis, azoospermia was not achieved. This latter effect may reflect either a direct spermatogenesis-supporting effect of the high dose of TB or the partial recovery of inhibin secretion (indirectly reflecting FSH secretion) or a combination of both.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed2006

Appearance of hyaluronan binding protein 1 proprotein in pachytene spermatocytes and round spermatids correlates with spermatogenesis.

The proprotein form of hyaluronan binding protein 1 (HABP1) has been reported to be present in the pachytene spermatocytes and the round spermatids of the adult testis. To explore the role of HABP1 proprotein in spermatogenesis, its expression in the testes of adult rats was compared with that in the testes of developing rats and that in the testes of adult rats that received estriadiol to halt spermatogenesis. Immunoblotting revealed that the mature form of HABP1 was consistently present in the testis, but its precursor form was not found in the testis of animals aged 7, 14, 21, and 28 days. However, immunohistochemical analysis revealed the presence of the proprotein form in the pachytene spermatocytes and the round spermatids of testes from rats aged 21 and the 28 days, the appearance of which correlated well with the appearance of these cells during spermatogenesis. Reverse-transcriptase polymerase chain reaction revealed transcriptional upregulation of HABP1 in the testes of adult rats, compared with the testes of developing rats. Finally, loss of HABP1 proprotein expression from the pachytene spermatocytes and round spermatids was observed in the testes from rats in which spermatogenesis was arrested. Collectively, these findings demonstrate the appearance of HABP1 proprotein in the pachytene spermatocytes and the round spermatids during the initial stages of postnatal testis development and suggest that this expression may be crucial for spermatogenesis.

Animals↗
PubMed2002

Seasonal changes in spermatogenesis of the Japanese lesser horseshoe bat, Rhinolophus cornutus from a morphological viewpoint.

Seasonal changes in spermatogenesis of Japanese lesser horseshoe bats, Rhinolophus cornutus, captured in Aomori Prefecture (Japan) were examined by light microscopy. In March, the seminiferous tubules revealed almost no lumen. The seminiferous epithelium consisted of Sertoli cells and spermatogonia. The interstitium occupied a relatively large area. In June, the seminiferous tubules gradually increased in diameter. Lumen was clearly seen at the center of seminiferous tubules. Mitotic figures of spermatogonia and spermatocytes were occasionally recognized. Interstitium occupation was still abundant. In August, the diameter of seminiferous tubules maximized. The interstitium occupied only a small area. Active spermatogenesis was obvious at this time. Released spermatozoa were frequently observed within the expanded lumen. In October, although spermatogenesis was still active, the diameter of seminiferous tubules tended to decrease in size. In December, active spermatogenesis completely disappeared. The diameter of tubules greatly decreased. In most cases, the seminiferous epithelium contained only Sertoli cells and spermatogonia. Thus, spermatogenesis in Japanese lesser horseshoe bats occurs from the middle or late summer to the middle autumn in Aomori Prefecture. In epididymal tracts, aggregated spermatozoa were recognized throughout the year. The cytoplasm of all Leydig cells in the interstitium was positive for 3beta-hydroxysteroid dehydrogenase throughout the year.

3-Hydroxysteroid Dehydrogenases↗
PubMedDate not supplied

Testosterone-dependent restoration of spermatogenesis in adult rats is impaired by a 5alpha-reductase inhibitor.

Germ cell development (spermiogenesis in particular) in the adult rat is known to be testosterone dependent. Recently we proposed a role for the 5alpha reduction of testosterone to dihydrotestosterone (DHT) in the short-term restoration of round spermatid maturation when testicular testosterone levels are experimentally lowered. The current study aimed to further characterize the involvement of 5alpha-reductase in the restoration of spermatogenesis by investigating the short- and long-term restoration of specific germ cell populations by testosterone in the presence or absence of a 5alpha-reductase inhibitor (L685,273). Spermatogenesis in adult rats was suppressed for 8 weeks using 3-cm testosterone and 0.4-cm estradiol silastic implants (testosterone-estradiol [TE] treatment); spermatogenesis was then restored by administration of increasing doses of testosterone with or without a competitive 5alpha-reductase inhibitor or with the androgen receptor antagonist flutamide. Animals were then killed after either 4 days or 6 weeks of treatment so that we could study the short- and long-term restorations of spermatogenesis. Stereological analysis showed that germ cell development between late pachytene spermatocytes to round spermatids in stage VII during either short- or long-term restoration was not affected by 5alpha-reductase inhibition, but it was affected by flutamide. The conversion of round spermatids between stages VII and VIII was restored by testosterone treatment, but this restoration was prevented by flutamide. Both the short- and long-term restorations of this midspermiogenic event were significantly decreased when 5alpha-reductase was inhibited. After long-term restoration of spermatogenesis, elongated spermatids were restored to 42% of control but were significantly suppressed to 20% of control by coadministration of the 5alpha-reductase inhibitor because of a reduction in the number of round spermatids progressing between stages VII and VIII. The results demonstrate that the 5alpha-reduction of testosterone is particularly important for progression through midspermiogenesis, because this phase of germ cell development is more sensitive to withdrawal of androgens. We suggest that testicular 5alpha-reductase activity is important for the restoration or maintenance of low levels of sperm production in a hormonally based contraceptive setting.

5-alpha Reductase Inhibitors↗
PubMed1999

Hormonal treatment after cytotoxic therapy stimulates recovery of spermatogenesis.

Previous studies have shown that treatment of rats with gonadotropin-releasing hormone (GnRH) analogues or steroids either before exposure to procarbazine or radiation or after irradiation enhances subsequent levels of spermatogenesis. We demonstrate here that giving a GnRH agonist after procarbazine injection also enhances spermatogenesis and fertility. We also demonstrate that GnRH agonist stimulated recovery of spermatogenesis and fertility not only when the hormone was administered immediately after irradiation, but also at 20 weeks after irradiation, after the decline in spermatogenesis had occurred. These results suggest that GnRH agonist treatment given to azoospermic men after cytotoxic therapy for cancer may stimulate the recovery of spermatogenesis and fertility.

Animals↗
PubMed1999

Spermatogenesis and spermatogenic control: a state of the art.

In this short overview we summarize recent progress made in some areas of fundamental research related to spermatogenesis and its control. After a brief reminder of the main characteristics of the spermatogenic process we focus on the determinants of sperm output. Particular attention is paid to factors controlling the number of Sertoli cells, to the role of germ cell apoptosis, and to factors rendering human spermatogenesis relatively inefficient. Thereafter, we summarize recent insights on the relative role of testosterone and FSH in the endocrine control of human spermatogenesis. The potential contribution of testosterone metabolites such as 5alpha-dihydrotestosterone and 17beta-estradiol is discussed in the light of novel experimental paradigms. The contribution of cell-cell interactions to spermatogenic control is illustrated on the hand of the kit-ligand-c-kit-receptor system and the scientific and potential therapeutic potential of germ cell transplantation techniques underlined. Finally we focus on clinical and fundamental approaches which contribute to our understanding of specific genes involved in spermatogenesis. It is concluded that research in the field of spermatogenesis is rapidly expanding and that several recent findings will lead to diagnostic and therapeutic applications in the near future.

Animals↗
PubMedDate not supplied

Suppression of spermatogenesis with desogestrel and testosterone pellets is not enhanced by addition of finasteride.

Conversion of testosterone to dihydrotestosterone (DHT) by the action of 5alpha-reductase can amplify androgen action. This may be of particular importance in the presence of low testosterone concentrations and may contribute to maintenance of spermatogenesis in a proportion of men receiving male contraceptive regimens. We therefore investigated whether the addition of finasteride, a 5alpha-reductase inhibitor, to a prototype male hormonal contraceptive regimen consisting of desogestrel (150 microg orally daily) and repeated administration of testosterone pellets (2 x 200 mg per 12 weeks) would enhance suppression of spermatogenesis. Sixteen normal men were randomized to receive either the standard androgen/progestogen treatment alone (control group) or with finasteride (5 mg orally daily-FIN group) for 24 weeks. Both groups showed profound suppression of spermatogenesis with azoospermia being obtained in 6 of 8 subjects in the control group and in 5 of 7 in the FIN group. There were no significant differences between the groups with respect to sperm concentrations. Significant suppression of luteinizing hormone and follicle-stimulating hormone was achieved within 2 weeks of treatment in both groups, while testosterone concentrations were maintained in the normal physiological range. DHT concentrations fell in both groups but were significantly lower in the FIN group. Gonadotropin and testosterone concentrations were similar for both regimens throughout the study. This study demonstrates the potential for long-term suppression of spermatogenesis using a combination of an oral progestogen with repeated administration of a depot preparation of testosterone. However, these data do not support the involvement of 5alpha-reductase in maintaining residual spermatogenesis during gonadotropin suppression for hormonal male contraception.

5-alpha Reductase Inhibitors↗
PubMed2002

[Effect of MPA and MPA + TU on the rat spermatogenesis and sexual hormones].

OBJECTIVES: To investigate the effect of administration of MPA with/without TU on serum sexual hormones and spermatogenesis of male rats. METHODS: Twenty rats had been classified into four groups. Each group received injection of saline(group A) or MPA(37.5 or 75 mg/kg) (group B or group C, respectively) or MPA (75 mg/kg) + TU (25 mg/kg) (group D) every month during three months. Data from serum sexual hormones (FSH, LH, T), sperm counting and motility had been collected and analysed. RESULTS: Spermatogenesis of rats undergoing administration of MPA with or without TU had been suppressed. Serum FSH and LH of group B, C, D declined, and so did serum T of group D. Testis of rats of group D atrophied and sperm counting of group D decreased remarkably compared with group B and C. But there was no statistics difference of the sexual hormone level among group B, C and D. CONCLUSIONS: Administration of MPA alone could suppress the levels of FSH and LH and block the spermatogenesis of male rats. MPA combined with TU could offer stronger suppression on spermatogenesis. Mechanism of the suppression on spermatogenesis of MPA + TU is not only limited in the feed-back of gonadotropin, but there maybe exist a direct suppression on testis.

Animals↗
PubMed2002

[A serum marker of spermatogenesis--inhibin B].

Inhibin B is a glycoprotein secreted by testis, consisting of two disulfide-linked subunits, an alpha-subunit and a beta B-subunit. Serum inhibin B levels are significantly negatively correlated with the serum FSH levels in males, exerting a negative feedback on FSH secretion. In males the circulating levels of inhibin B increase shortly after birth and peak at 4-12 months of age, then decrease to low levels from 3-9 year. From the onset of puberty, the levels of inhibin B gradually increase. By pubertal stage II, the adult levels of inhibin B have been reached. At stage III of puberty, a negative correlation between inhibin B and FSH levels is present and persists from stage III of puberty onward. At 20-30 year of age, the levels of inhibin B reach another peak, then gradually decline with increasing age. The men with hypospermatogenesis and spermatogenesis arrest have significantly lower levels of inhibin B than those with normal spermatogenesis. The men with Sertoli-cell-only syndrome (SCO) have extremely low levels of inhibin B. There is a closely correlation between the presence of SCO and the level of serum inhibin B. A significantly positive correlation is also observed between testis volume and inhibin B level, as well as between sperm count and inhibin B level. The inhibin B is a direct product of the seminiferous tubules, reflecting the total testicular tissue. The measurable inhibin B production in adult requires the presence of germ cells. Inhibin B is regarded as a serum marker of spermatogenesis. The determination of serum inhibin B in males can be used to assess the spermatogenesis of infertile men, to diagnose the cryptorchidism and precocious puberty, to predict the outcome of testicular sperm extraction in men with non-obstructive azoospermia, and to evaluate the damage to spermatogenesis in men after radiotherapy or chemiotherapy.

Biomarkers↗
PubMed2004

[Effects of reproductive hormones on spermatogenesis].

Spermatogenesis, a continuous course of cell proliferation and differentiation, depends on reproductive hormones. FSH and LH-induced T are the main hormones regulating spermatogensis. Intratesticular T is one of the key factors in maintaining spermatogenesis, while FSH is just as important for origination and maintenance of normal spermatogenesis. Sertoli cells are the pivot of hormonal regulation. Interestingly, these reproductive hormones also regulate sperm cell apoptosis spermatogenesis. Further studies on the hormonal regulation of spermatogenesis provide a base for the development of safe and recoverable contraceptives for males.

Androgens↗
PubMed2006

Gene expression in mouse spermatogenesis during ontogenesis.

In this study, we evaluated the expression of genes probably involved in spermatogenesis in the mouse. We examined cytosolic chaperonin theta subunit (CCTtheta), Ngg1 interacting factor 3 like 1 binding protein 1 (NIF3L1 BP1) and apolipoprotein H (ApoH) expression during mouse onto-geny using RT-PCR. Testicular tissue was obtained from mice 3, 6, 8, 10, 12, 14, 18, 20 and 40 (adult) days after birth. For each mouse, one testis was used for histological examination, whereas RNA was extracted from the controlateral testis for expression analysis. RT-PCR analysis showed that CCTtheta gene expression was low until day 10, but increased drastically afterwards. At this age, spermatocytes started to be present in the mouse testis. Therefore, CCT protein could be involved in chromatin packaging and remodeling during spermiogenesis, as also suggested by other studies. NIF3L1 BP1 expression increased steadily during ontogenesis reaching maximum levels in the adult mouse when all germ cell stages are present. This finding suggests that NIF3L1 BP1 is a gene not expressed by a specific germ cell type. ApoH expression was very low or absent during prepuberal stages, whereas it was detectable in the adult testis when spermatogenesis was completed. This suggests that ApoH may be involved in clearing apoptotic bodies during spermatogenesis since apoptotic events increase during spermatogenesis. This study contributes to understanding the role played by genes important for spermatogenesis.

Animals↗
PubMed1991

The cycle of the seminiferous epithelium and stages in spermatogenesis in dd-mice.

For the basis to study the testicular functions using dd-mice, the cycle of the seminiferous epithelium and stages in spermatogenesis, classification of late spermatogenesis, and postnatal development of spermatogenesis were examined by light and electron microscopy in the testes from these animals at day of birth and 1, 2, 3, 4, 5, and 8 weeks of age. For light microscopy, paraffin sections of the testes were stained with periodic-acid and Schiff reagent (PAS) and hematoxylin. In spermiogenesis, 16 steps of spermatids were distinguished according to shapes of the nuclei and acrosomes. Step 15 and 16 spermatids, which have similar nuclei and acrosomes, were easily distinguishable by positions of nuclei and appearance of basophilic granules in the cytoplasm; steps 15 and 16 were thus subdivided into 3 and 2, respectively. The granules were accumulations of ribosome-like particles. Step 13 spermatids were present with step 1 spermatids, step 14 with steps 2 and 3, step 15 with steps 4-6, and step 16 with steps 7 and 8. Thus, the cycle of the seminiferous epithelium was divided into 12 stages (stages I-XII) in the order of steps 1 to 12. Type A spermatogonia were present in all stages, and intermediate and type B spermatogonia appeared from stages II and VI, respectively. In primary spermatocytes, the resting phase appeared from stage VII, leptotene from stage VIII, zygotene from stage X, pachytene from stage III, diplotene in stage XI, and diakinesis and secondary spermatocytes in stage XII. The seminiferous tubules were lined by Sertoli cells and contained gonocytes at day of birth, type A spermatogonia appeared at 1 week of age, spermatogenesis proceeded until pachytene spermatocytes at 2 weeks, until step 1 spermatids at 3 weeks, and all stages of the seminiferous epithelium were completed at 5 weeks. The findings indicate that combination of germ cells in each stage of the seminiferous epithelium in dd-mice does not correspond to generally accepted one, step 15 and 16 spermatids are accurately classified by referring the position of nuclei and appearance of granules in the cytoplasm, and spermatogenesis in immature mice proceeds faster than in adults.

Age Factors↗
PubMedDate not supplied

Quantitative maintenance of spermatogenesis in cyclosporine-treated rats by exogenous administration of testosterone propionate.

The authors had previously shown that the subcutaneous administration of cyclosporine (CsA) resulted in an impairment of spermatogenesis. Testosterone levels declined and gonadotropin levels increased, suggesting that CsA primarily affects the synthesis and secretion of testosterone. In this study, the authors attempted to determine whether the exogenous administration of testosterone would maintain spermatogenesis in animals treated with a very high dose of CsA. Sexually mature, male Sprague-Dawley rats were treated subcutaneously with CsA (40 mg/kg per day) alone, or in combination with testosterone propionate (TP; 2 and 5 mg/d per rat), for 14 days. As expected, CsA reduced the body and reproductive organ weights and the levels of serum testosterone, while elevating the levels of follicles-stimulating hormone (FSH) and luteinizing hormone (LH). Quantitative analysis of spermatogenesis revealed a decline in all the different types of germ cells in tubules at stage VII of the cycle of the seminiferous epithelium. Administration of TP in 2 and 5 mg/d per rat doses restored the body and reproductive organ weights and the circulating levels of FSH. The serum levels of LH were below the assay's minimum level of detectability. Analysis of spermatogenesis revealed a dose-dependent increase in the germ cell counts after the administration of 2 and 5 mg of TP. The circulating levels of CsA were also significantly reduced after TP administration. These results revealed that CsA-induced alteration in spermatogenesis can be prevented by the exogenous administration of testosterone.

Animals↗
PubMed1986

Reflections on the evolution of the regulation of spermatogenesis.

We have developed the concept that mechanisms evolved very early for the modulation of spermatogenesis in response to changes in the external environment, and that these ancient control mechanisms were retained during subsequent evolution. In nearly all animals, the regulation of germinal cell development is postulated to be mediated through the control of gonadal somatic cell functions, associated with the creation and maintenance of an optimal milieu within the spermary of seminiferous tubule in which gametogenesis takes place. In primitive organisms, a small number of stages intervenes between environmental stimuli and subsequent alteration of gonadal somatic cell functions. In contrast, in more complex organisms, the number of intervening stages is greatly amplified and modulated via neuroendocrine mechanisms involving receptors, transducers, and various sorts of relays and messengers. The evolution of these neural and endocrine controls appears to have occurred in lock-step with the evolution of increasing layers of complexity of regulators of spermatogenesis. This is not unduly surprising, since the requirement to have functionally fertile male and female partners of the same species together at the same time and place would require considerable integration of behavioral and recognition mechanisms during courtship and mating. The nature of these neural mechanisms is likely to prove no less complex than that of mechanisms in the gonad required for successful gamatogenesis. The neuroendocrine regulation of spermatogenesis in starfish and in chordates is postulated to act in a manner completely homologous to the ways in which external environmental stimuli influence spermatogenesis in more primitive organisms. In both sets of cases, the gonadal somatic cells (nurse cells) are the ultimate targets which mediate the effective turning on or turning off of spermatogenesis. The hormone-responsive nurse cells are postulated to achieve this simply by creating a microenvironment in the vicinity of germinal cells which permits the expression of program required for development, or by failing to do so. In mammals, Sertoli cells and peritubular cells, only when optimally stimulated by hormones and paracine factors, are thought to form a functional unit which provides this necessary microenvironment. In less complex organisms, other nurse cell arrangements exist to nourish the syncytia of developing germ cells with the mixture of nutrients, salts, etc. required for a gametogenesis to take place in a protected milieu.

Animals↗
PubMed1983

[Effect of aromatic retinoid on spermatogenesis in rats. Light microscopy findings in the testes (including some other selected organs)].

In an experimental study we examined the influence of a toxic dose of aromatic retinoid (Ro 10-9359) on the spermatogenesis of 30 Wistar rats. Aside from testis tissue of both testes, liver, heart, lung, kidney, adrenal gland as well as the skin have been investigated histologically. The rats received retinoid at a daily rate of 25 mg/kg body weight in physiological salt solution by means of a gastric tube. Another 20 rats receiving only physiological salt solution served as control group. 8 weeks after application of retinoid resp. physiological salt solution, 15 animals with retinoid intoxication as well as 10 control animals were killed. The remaining 25 animals were killed after an application-free interval of 8 weeks. 8 weeks after retinoid intoxication, 6 rats revealed a reduced spermatogenesis, 2 of them with a complete spermatogenic arrest at the stage of spermatocytes I in all analyzed parts of the testes. The diameter of the seminiferous tubules turned out to be decreased by about 30% in comparison to the other 9 rats having received retinoid and to the control group. The spermatogenesis of these 9 rats was equally normal as that of the control group. 8 weeks after withdrawal of the drug there was no sign for reduced spermatogenesis with 14 animals, whereas the 15th rat did not show any cells of spermatogenesis but only Sertoli cells in the seminiferous tubules in all parts of its testes. In liver, heart and lung we observed minimal pathological findings which have to be regarded as an unspecific reaction caused by drug intoxication. All other investigated organs proved histologically no pathological findings.

Adrenal Glands↗
PubMed1995

Onset of spermatogenesis in Corriedale ram lambs under extensive rearing conditions in Uruguay.

The present study was undertaken to estimate the time for the attainment of spermatogenesis in springborn Corriedale ram lambs under conditions of extensive grazing systems in Uruguay. Clinical (live weight, scrotal circumference, penile/preputial separation), morphological (light and electron microscopy) and endocrinological (testosterone levels) parameters were examined. Two experiments in 2 consecutive years were carried out. In Exp. I, 40 ram lambs were clinically examined, weighed, and blood-sampled at 2 week-intervals between 78 and 216 days of age. Sixteen were castrated in 3 selected periods: 132-162 (n:2), 145-175 (n:6) and 186-216 days (n:8). In Exp. II, 40 ram lambs appertaining to the next generation of the same flock were examined as above at 180-210 days of age, and castrated for morphological studies. The time for attainment of complete spermatogenesis correlated significantly with most corporal parameters (i.e. scrotal circumference (r = 0.52); testicular weight (r = 0.61), epididymal weight (r = 0.60), penile/preputial separation (r = 0.75). The age of castrated ram lambs correlated with the degree of spermatogenesis (r = 0.83), although no significant correlations were found with live weight or with levels of circulating testosterone. The histology showed major variations in the degree of development of the seminiferous epithelium. Cells undergoing degeneration were a common finding through the initial stages of spermatogenesis, coincident to the presence of sperm abnormalities and foreign cells in semen. By day 180 and onwards, both histology and seminal picture normalized. It is concluded that, under these rearing conditions, the onset of puberty (expressed as morphologically established spermatogenesis) in Corriedale ram lambs is attained at 180-216 days of age when they reach 23 cm of scrotal circumference and 191 g of testis weight. The finding of a high correlation between these parameters (r: 0.93) confirms the usefulness of the measurement of scrotal circumference during clinical examination of ram lambs in this breed.

Analysis of Variance↗
PubMedDate not supplied

Can spermatogenesis be maintained quantitatively in intact adult rats with exogenously administered dihydrotestosterone?

It is well established that testosterone (T) is required to maintain spermatogenesis in the mammalian testis, presumably acting through a receptor mechanism, as elsewhere. It is puzzling, however, that the T concentration that is required to maintain spermatogenesis quantitatively in intact adult rats (15-20 ng/ml) is well in excess of the concentration required to saturate testicular androgen receptors. If, indeed, T regulation of spermatogenesis is mediated through the androgen receptor, 5 alpha-dihydrotestosterone (DHT) would be expected to more effectively maintain spermatogenesis than T because of its greater affinity for, and slower rate of dissociation from, the androgen receptor. To test this hypothesis experimentally, the quantitative relationship between the intratesticular concentration of exogenously administered DHT and the maintenance of germ cell production was examined in intact rats in which endogenous T production was suppressed. To this end, rats received increasing doses of DHT via polydimethylsiloxane implants of 6-36 cm in length for 8 weeks. In each DHT-treated rat, serum luteinizing hormone (LH) concentration was reduced to below the limit of detectability by radioimmunoassay (RIA), and intratesticular T concentration was reduced by > 90%. Serum and intratesticular DHT concentrations increased with increasing implant size. The serum and intratesticular concentrations of 5 alpha-androstane-3 alpha, 17 beta-diol(3 alpha-Diol) were consistently higher than DHT concentrations because of conversion of DHT to 3 alpha-Diol. Spermatogenesis was maintained qualitatively in some rats that received implants of 6 cm, in most rats that received implants of 12 cm, and in all rats that received implants of 18 cm.(ABSTRACT TRUNCATED AT 250 WORDS)

Analysis of Variance↗