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A phenotypical girl aged 16 years with primary amenorrhoea had an XY-karyotype and reacted positively to serologically demonstrable H-Y antigen. The left gonad was an immature testis while the right was a streak gonad with a gonadoblastoma. The value of H-Y antigen determinations in the diagnosis and choice of treatment is discussed.
We have studied the specific effects of highly purified pituitary hormones on testicular cell multiplication and differentiation in the immature hypophysectomized rat. LH exhibits multiplicative effects on Leydig cells and, curiously, regressive effects on germ cells. Seminiferous tubules are the main site of action of FSH which induces direct differentiation of Sertoli cells and paracrine effects on germ cells resulting in their multiplication to the pachytene stage (in the absence of androgen). Through interstitium-directed paracrine effects, FSH promotes the differentiation of Leydig cells. Prolactin and lactogenic growth hormones are capable of exerting both differentiative and multiplicative effects on Leydig cells. The purity of the hormone preparations permit to define their specific and direct effects and those mediated by paracrine or autocrine factors synthetized locally under their control. Among these potential factors, we have demonstrated the pituitary-dependent expression of IGF-I, c-myc, c-fos proteins. The purity of the preparations used in this work permits to distinguish clearly the specific and direct effect of each pituitary hormone from those mediated by paracrine or autocrine factors.
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BACKGROUND: In previous work, RNA transcripts for placental (P)-cadherin, a calcium-dependent cell adhesion molecule, were identified in the rat testis during the first 4 weeks of postnatal development. However, the cells in the testis responsible for P-cadherin expression have not yet been identified. METHODS: We used conventional epifluorescence microscopy to examine P-cadherin immunoreactivity in cryostat sections of mouse testis and scanning laser confocal microscopy to localize P-cadherin and beta-catenin in wholemount preparations of mouse seminiferous tubules. We used fluorescent phalloidin to identify actin filaments. RESULTS: Sertoli cells expressed P-cadherin on postnatal days 1, 3, and 8, but not on any day thereafter. In contrast, peritubular cells did not express P-cadherin on postnatal day 8 and continued expression in adulthood. beta-Catenin was localized near contact areas between peritubular cells on postnatal days 12 and 15. A mature pattern of actin filament organization in peritubular cells appeared on day 15 and coincided with the uniform appearance of P-cadherin and beta-catenin near areas of contact between adjacent peritubular cells. CONCLUSIONS: During postnatal development of the testis, the earlier expression of P-cadherin by Sertoli cells is replaced by the subsequent expression of P-cadherin by peritubular cells. The expression of P-cadherin in peritubular cells is correlated temporally with the expression of beta-catenin and the development of a mature network of actin filaments and is consistent with a role in intercellular adhesion and junction formation.
In this paper the localization of transforming growth factor alpha (TGF-alpha) is described in the rat testis at various stages throughout development, e.g. neonatal, prepubertal, and adult, in order to examine somatic cells and germinal cells at different stages of differentiation. This was done by immunoperoxidase staining using a monoclonal antibody that does not cross-react with epidermal growth factor (EGF). In sections of testes from neonatal rats, intense staining was present in Leydig cells. In the cells of the seminiferous tubules the staining was faint or undetectable. At the time when many mesenchymal cells differentiate into Leydig cells in the 21-day-old rat, TGF-alpha was visualized in most but not all of the identifiable Leydig cells. In interstitial cell cultures derived from 21-day-old rats, the majority of the Leydig cells contained TGF-alpha, but in a proportion of the Leydig cells TGF-alpha was undetectable. No staining was apparent in Sertoli cells and germ cells in seminiferous tubules or in Sertoli cell cultures derived from 21-day-old rats. Under these in vitro conditions it was found that peritubular-myoid cells also possessed TGF-alpha immunoreactivity. In the adult testis all Leydig cells stained positively for TFG-alpha, whereas no staining was found in the cells of the seminiferous tubules. Treatment of adult rats with ethylene-1,2-dimethane-sulfonate (EDS) resulted in the destruction of Leydig cells and the loss of all positively stained for TGF-alpha.(ABSTRACT TRUNCATED AT 250 WORDS)
The development of metastases from germ cell tumours of the testis is studied in terms of its histopathological, ontogenetic, anatomical and evolutive aspects. The treatment of non-seminomatous germ cell tumours and pure seminomas is analysed separately. The prognostic factors defined by the risk of failure of treatment are described and the medical and surgical strategies or combinations of both modalities are proposed for each stage of these cancers. The major points and novelties include: the usual histological polymorphism of these tumours. The markers include alpha-foetoprotein and HCG. Combination chemotherapy, essentially the EBP sequence, is the treatment for non-seminomatous germ cell tumours. In the case of failure, toxic sequences can be used followed by autologous bone marrow transplantation. In the case of persistent lesions (lung, mediastinum, liver, retroperitoneum), salvage surgery may be useful. Metastatic seminomas are treated by radiotherapy and/or chemotherapy, depending on their stage.
The undescended testis carries an increased risk of cancer; however, the exact individual risk of a cryptorchist during his life to develop cancer is unknown. The risk of developing cancer can be calculated from three important figures: (a) the number of cryptorchists in the population; (b) the number of malignant testicular tumors found in undescended testicles; and (c) the number of testicular tumors per annum. In the literature, a 48 times increased chance to develop testicular cancer is accepted; it is a high risk which is contrary to the fact that a malignant cryptorchid testis is a very rare disease. Based on the estimated risk for the cryptorchist in the Netherlands to develop testicular cancer, this article criticizes the value of the figures that are generally used to calculate the individual risk; it is concluded that even today the exact risk is unknown. In giving advice concerning the management of undescended testis, one must appreciate not only the supposed cancer risk, but also take into consideration morbidity and mortality after prophylactic orchidectomy and improved cure rates after electively treated testicular tumors.
The relationship between thyroid function and testicular development in the rat was investigated. Hypothyroidism was induced during fetal or post-natal life by adding methimazole (MMI) to the drinking water of pregnant or lactating mothers. A group of newborn rats was treated with MMI and i.p. injections of L-tri-iodothyronine (L-T3). Hypothyroidism was shown by the reduced serum levels of total T3 and of total thyroxine (T4) in pregnant mothers and in pubertal rats. Testes were studied using light microscopy at 18 and 21 days post coitum or during puberty (21, 35 and 50 days after birth); serum levels of gonadotrophins were also evaluated in pubertal rats. Hypothyroidism had no effect on testicular development during fetal life and when induced in newborn rats it was associated at puberty with reduced serum levels of FSH and LH and with delayed maturation of the testis compared with control rats. The delay in maturation consisted of a reduction in the diameter of seminiferous tubules, and a reduction in the number of germ cells per tubule; this was associated with increased degeneration and arrested maturation of germ cells. In addition, Sertoli cells demonstrated retarded development, as indicated by a delay in the appearance of cytoplasmic lipids and in the development of a tubule lumen. Hormonal and morphological abnormalities were absent in rats treated with MMI plus L-T3. In conclusion, hypothyroidism occurring soon after birth caused reduced levels of gonadotrophins in the serum and a delay in pubertal spermatogenesis, possibly due to retarded differentiation of the Sertoli cells.
Using immunohistochemistry, the expression of the D-type cyclin proteins was studied in the developing and adult mouse testis. Both during testicular development and in adult testis, cyclin D(1) is expressed only in proliferating gonocytes and spermatogonia, indicating a role for cyclin D(1) in spermatogonial proliferation, in particular during the G(1)/S phase transition. Cyclin D(2) is first expressed at the start of spermatogenesis when gonocytes produce A(1) spermatogonia. In the adult testis, cyclin D(2) is expressed in spermatogonia around stage VIII of the seminiferous epithelium when A(al) spermatogonia differentiate into A(1) spermatogonia and also in spermatocytes and spermatids. To further elucidate the role of cyclin D(2) during spermatogenesis, cyclin D(2) expression was studied in vitamin A-deficient testis. Cyclin D(2) was not expressed in the undifferentiated A spermatogonia in vitamin A-deficient testis but was strongly induced in these cells after the induction of differentiation of most of these cells into A(1) spermatogonia by administration of retinoic acid. Overall, cyclin D(2) seems to play a role at the crucial differentiation step of undifferentiated spermatogonia into A(1) spermatogonia. Cyclin D(3) is expressed in both proliferating and quiescent gonocytes during testis development. Cyclin D(3) expression was found in terminally differentiated Sertoli cells, in Leydig cells, and in spermatogonia in adult testis. Hence, although cyclin D(3) may control G(1)/S transition in spermatogonia, it probably has a different role in Sertoli and Leydig cells. In conclusion, the three D-type cyclins are differentially expressed during spermatogenesis. In spermatogonia, cyclins D(1) and D(3) seem to be involved in cell cycle regulation, whereas cyclin D(2) likely has a role in spermatogonial differentiation.
Iron is essential for male fertility, and disruptions in iron balance lead to impairment of testicular function. The divalent metal transporter DMT1 is a key modulator of transferrin- and non-transferrin-bound iron homeostasis. As a first step in determining the role of DMT1 in the testis, we have characterized the pattern of DMT1 expression in the developing and adult rat testis. Northern blot analysis and RT-PCR of testis polyadenylated RNA revealed the presence of iron-responsive element (IRE) and non-IRE transcripts. Semiquantitative immunoblotting of immature and adult rat testis uncovered the expression of two distinct DMT1 protein species. Immunohistochemistry showed that DMT1 was widespread throughout each seminiferous tubule and was expressed in the intracellular compartment. In the adult rat testis, DMT1 was immunolocalized to both the Sertoli and germ cells. In contrast to the immature testis, expression was dependent on the stage of the spermatogenic cycle. DMT1 was not detected on any plasma membranes in either the developing or the adult testis, suggesting that DMT1 is not primarily responsible for translocating iron across this epithelium. Our data suggest an important role for DMT1 in intracellular iron handling during spermatogenesis and imply that germ cells have a need for a precisely targeted and timed supply of iron. We suggest that DMT1 may, as it does in other tissues, play a role in transporting iron between intracellular compartments and thus may play an important role in male fertility.
The final step in the biosynthesis of testosterone is the reduction of androstenedione to testosterone catalysed by the enzyme 17beta-hydroxysteroid dehydrogenase (17betaHSD). Five isoforms of the enzyme have been identified in the mouse and the type 3 isoform has been shown to be the predominant reductive form present in the adult human and mouse testis. In this study the regulation of 17betaHSD type 3 isoform mRNA levels and the cellular localisation of the enzyme mRNA have been studied in the mouse testis. To examine regulation of 17betaHSD type 3 mRNA expression in the testis, mRNA levels were measured during development in normal mice and in mice lacking circulating gonadotrophins (hpg) or functional androgen receptors (Tfm). In these mutants testicular descent does not occur at the normal time (25 days) and control animals were, therefore, rendered cryptorchid at 19 days. In neonatal mice, it has been shown a peak of type 3 expression occurs around day 5 and this was found to be normal in all groups in the current study. In normal animals there was a marked increase in type 3 isoform expression between 25 and 30 days and this continued into adulthood. In cryptorchid animals the increase in type 3 mRNA levels after 25 days was less marked than in untreated controls and by 90 days was about 15% of normal animals. In Tfm mice, levels of 17betaHSD type 3 mRNA failed to show any increase around puberty (25 days) and in adult Tfm mice, levels were less than 1% of cryptorchid controls. In hpg mice, levels of type 3 mRNA increased slowly after puberty and were about 30% of cryptorchid controls by 90 days. Studies using in situ hybridisation showed that the type 3 isoform was expressed only in the interstitial tissue of the adult normal mouse testis. No specific hybridisation could be determined in adult hpg or Tfm testes. Results show that 17betaHSD type 3 is an interstitial enzyme in the testis and is, probably, localised in the Leydig cells. During neonatal development expression of 17betaHSD type 3 is independent of gonadotrophin action while the increase in type 3 expression at puberty is primarily dependent upon androgen action although testicular descent and gonadotrophins are also required.
The boar testis was used as a model for examining the possible role of production of the insulin-like growth factors (IGF) in steroidogenesis and/or testicular growth as testicular development occurs in waves. Blood and testes were sampled from boars at different ages (100-102 days of gestation; 7, 19, and 30 days; and 10 and 25 wk), selected to occur during and between the last two waves of testicular development. Serum was analyzed for testosterone and RNA was extracted from the testes for Northern and dot-blot analysis of IGF mRNA. Testosterone concentrations declined (p = 0.01) from 7 days to 10 wk of age and rebounded at 25 wk, indicating completion of the second and third waves of testicular development. The quantity of testicular mRNA for IGF-I increased gradually with age, and that for IGF-II decreased. We therefore conclude that regulation of the expression of the mRNAs for IGF-I and -II in the pig testis is not a function of either the waves of testicular development or the level of steroidogenesis.