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PubMed1975

Changes in fine structure accompanying estrogen-induced tumorigenesis of Leydig cells in the mouse testis.

The development of estrogen-induced Leydig cell tumors in cryptorchid BALB/c mice was studied with the electron microscope. Changes in Leydig cell fine structure are apparent by 10 days after the s.c. implantation of a pellet of diethylstibestrol (DES). The smooth endoplasmic reticulum is diminished, and there is an increase in lipid droplets and free polysomes as compared with untreated cryptochid controls. These alterations persist as the Leydig cells proliferate to form focal areas of hyperplasia in the interstitial tissue. During this period of proliferation, activated macrophages containing large residual bodies appear among the Leydig cells. If DES treatment is continued for several months, malignant Leydig cell tumors, result. They are characterized by a nuclear and cytoplasmic pleomorphism of the Leydig cells and a decreased macrophage population. Virus-like particles are rarely seen within the cell during the period of tumorigenesis. Along with the reduction in smooth endoplasmic reticulum in the Leydig cells after DES treatment, evidence from the literature suggests that there is also a decrease in testosterone biosynthesis. However, it is not clear whether these two effect are correlated, since the level of the microsomal enzymes of steroid biosynthesis may vary independently of either the amount of smooth endoplasmic reticulum or the level of androgen secretion. The increase in lipid droplets seen in Leydig cells after DES treatment suggest the accumulation of precursors from the steroid biosynthetic pathway. The macrophages are though to represent scavenger cells, rather than a primary tumor cell population. The paucity of virus-like particles within altered Leydig cells implies that formed virus is not a prerequisite for tumorigenesis.

Animals↗

PubMed1976

[Endocrine and sperminogenic testicular function. 8. Relationships between testicular and plasma testosterone concentrations as well as between the number of Leydig cells in testicular tissue and their cell nucleus volume in boars of different ages].

Testicular tissue and blood samples (V. spermatica interna) were taken from 32 boars during castration. The animals were different age groups. Against this background, studies were conducted into the correlations between testicular and plasma testosterone, on the one hand, and the amount of interstitial cells of Leydig in testicular tissue as well as the latters' cell nuclei volumes, on the other. The results seemed to support the conclusion that any age-dependent increase of testicular and plasma testosterone concentrations was caused unambigously by an absolute increase in volume of androgenic testicular tissue, in concomitance with testicular growth, in other words, by rise in the total number of interstitial cells of Leydig.

Age Factors↗

PubMed1979

Evidence for the involvement of lutropin-independent RNA synthesis in Leydig cell steroidogenesis.

The effect of incubating purified Leydig cells in Eagle's medium and the subsequent effect of the RNA synthesis inhibitors, actinomycin D and cordycepin, on lutropin-stimulated testosterone synthesis have been investigated. The inhibiting effect was found to be inversely related to the time of preincubation; with cells preincubated for 0, 1, 2 and 3 h with Eagle's medium only, followed by 2-h incubation with lutropin with and without actinomycin D, testosterone synthesis was inhibited by 37 +/- 4, 31 +/- 3, 18 +/- 4 and 14 +/- 3% respectively (means +/- s.e.m., n = 5). In cells that had been preincubated for 3 h there was no significant effect of actinomycin D on testosterone synthesis during the first hour of incubation with lutropin. Thereafter the inhibition increased with time reaching a maximum of 30% after 5 h. The effects of preincubation were not due to endogenous lutropin in the Leydig cells because cells isolated from hypophysectomized rats gave similar results. The inhibition of [3H]uridine incorporation into the Leydig cell RNA was 80 +/- 1% with 8 microgram/ml actinomycin D. Increasing the concentration of this inhibitor to 80 microgram/ml did not significantly increase the inhibition of [3H]uridine incorporation or lutropin-stimulated steroidogenesis in preincubated and non-preincubated cells. With cordycepin the inhibition of both RNA synthesis and lutropin-stimulated testosterone synthesis in non-preincubated cells were the same; with 25.1--251 microgram/ml approx. 30--70% resp. With preincubated cells (3 h), 0--50% inhibition of testosterone synthesis was obtained respectively. The inhibitory effect of actinomycin D oimilar to that obtained with lutropin. These observations suggest that during preincubation and independently of lutropin, synthesis of intermediates, including RNAs required for stimulation of steroidogenesis, takes place and that subsequent stimulation of steroidogenesis by lutropin occurs without further de novo RNA synthesis. These results provide evidence for a permissive role of specific RNA and protein synthesis in the action of lutropin on testosterone synthesis in the Leydig cell.

Animals↗

PubMed1978

DNA synthesis and DNA polymerase activity in Leydig cells of diethylstilbestrol-stimulated mouse testes.

Using a modification of the collagenase dispersion method of Dufau et al., we examined changes in DNA synthesis produced by estrogens in the interstitial cells of mice that develop malignant Leydig cell tumors after prolonged estrogen administration. Previous work in cryptorchid mice indicated that during continuous estrogen administration [3H]thymidine incorporation into DNA rises to a maximum in 3 to 4 days and then falls to approximately base levels within 2 to 3 weeks. This was confirmed both in Leydig cell concentrates of estrogen-treated mice after either injection with [3H]thymidine or incubation with [3H]thymidine in vitro. This DNA synthesis was blocked by hydroxyurea. DNA synthesis in cells of estrogen-treated BALB/c mice of the Huseby substrain, which have a high incidence of Leydig cell tumors, was 5 to 11 times that in untreated controls. Cells from estrogen-treated C3H/Bi mice, which have a low incidence of Leydig cell tumors, showed only a 2- to 3-fold increase. In the Huseby substrain the rise of DNA synthesis is a peak and subsequent recession were paralleled by a rise and fall in DNA polymerase alpha activity. DNA polymerase beta did not show this variation. In C3H/Bi mice, neither polymerase showed significant change. The evidence suggests that the early estrogen-stimulated DNA synthesis is probably replicative and is associated with increased DNA polymerase alpha activity.

Animals↗

PubMed1975

Investigations on pituitary and Leydig cell function in chronic hemodialysis and after renal transplantation.

The hypothalamus-pituitary-Leydig cell axis was investigated in 20 male patients undergoing intermittent hemodialysis and in 21 male patients following renal transplantation compared to normal controls. Plasma testosterone as well as luteinizing hormone and follicle stimulating hormone were determined by radioimmunoassay under basal conditions and after stimulation with choriongonadotropic hormone and hypothalamus releasing hormone respectively. Suppressed Leydig cell function has been demonstrated in dialysed patients as well as in patients after renal transplantation. The Leydig cell insufficiency is more pronounced in the hemodialysed patients. None of these showed testosterone levels in the normal range. They are different in various dialysis schedules. In contrast Leydig cell function is much better in patients after renal transplantation compared to those undergoing intermittent hemodialysis. But even after renal transplantation a diminished Leydig cell function takes place. The degree of Leydig cell insufficiency however varies individually. In a few cases Leydig cell function is restored completely after transplantation. It remains uncertain whether the duration of the posttransplantation period or the function of the graft effects Leydig cell function. Anterior lobe insufficiency has been excluded since plasma concentrations of gonadotropins were slightly elevated before and after LH-RH stimulation as compared to normals.

Adult↗

PubMed1979

Leydig cell tumor of testis.

In adult patients with Leydig cell tumor of the testis, endocrinologic signs occur in 30 per cent of the cases and often precede the onset of a palpable testicular mass. Gynecomastia is the most common endocrinologic manifestation and probably is due to increased estrogen secretion by the Leydig cells. In the patient with adrenogenital syndrome and testicular enlargement it is difficult to distinguish Leydig cell tumor from adrenal rest hypertrophy. Four patients with Leydig cell tumor and endocrinologic manifestations are discussed; three are adults who presented with gynecomastia and the fourth is a patient with congenital adrenogenital syndrome. In the adult patient inguinal orchiectomy is the treatment of choice, while in the patient with adrenogenital syndrome initial management by high-dose steroid suppression should be attempted prior to testicular exploration.

Adrenal Cortex Neoplasms↗

PubMedDate not supplied

[Ultrastructure of human heterotopic Leydig cells].

It was demonstrated by light and electron microscopical methods that Leydig cells also exist outside of the testis. In the spermatic cord and near the intraabdominal testicular vessels cells were observed with the characteristics of intratubular Leydig cells. Such characteristics were intranuclear precrystalline inclusions, mitochondria with tubular interior structures and lipid droplets, and a well developed smooth and rough endoplasmatic reticulum. The last two items can be regarded as signs of hormonal activity. The extratesticular Leydig cells in the spermatic cord are located within nerves that contain myelinated axons forming monoaxonal Schwann cell units. Possible they are sensory nerves originating in the receptors of the tunica albuginea. Synapses between axons and heterotopic Leydig cells were not found. The degree of the cytological differentiation leads to the conclusion that these cells may serve, for instance after orchidectomy, as substitutes for the Leydig cells inside the testis.

Humans↗

PubMed1976

Postnatal differentiation of Leydig cells in the rabbit testis.

After the gradual disappearance of fetal Leydig cells in the first week after birth, the interstitial tissue of the rabbit testis is composed principally of undifferentiated mesenchymal cells between one and five weeks of age. Also present during this time are scattered partially differentiated cells with oval-shaped nuclei, prominent nucleoli and abundant cytoplasm. These cells exhibit some of the cytoplasmic features of steroid-secreting cells, but extensive development of smooth endoplasmic reticulum and the grouped perivascular arrangement of characteristic of fully differentiated Leydig cells are not present. The latter features appear at five weeks of age, indicating the formation of mature Leydig cells at that time. By seven weeks, the bulk of the interstitial tissue consists of Leydig cell aggregates, typical of the appearance in adult testis. Since spermatogonial mitoses first appear at seven to eight weeks of age, the findings indicate that Leydig cell differentiation precedes the onset of spermatogenesis.

Animals↗

PubMedDate not supplied

Ectopic Leydig cells in a seminiferous tubules of an infertile human male with a chromosomal aberration.

A case of a human male infertility with chromosomal aberration is reported. The patient showed neither mental retardation nor physical abnormalities except that the testes were somewhat small and soft. Plasma follicle stimulating hormone and luteinizing hormone were 49.0 and 19.0 mIU/ml. Plasma testosterone was 2.6 ng/ml. Karyotype was considered to be 46 XY q-, long arms of the Y chromosome being deleted. Histological features of the testis were peculiar. Seminiferous tubules were small and devoid of spermatogenic cells, consisting only of Sertoli cells. Peritubular boundary layer of the tubules showed a marked increase in width due to the increase of collagen fibers. The base of some Sertoli cells was seen to protrude into the thickened peritubular boundary layer or, though rare, into the interstitial space. Unusual cells which had a round vesicular nucleus and abundant, dense cytoplasms also occurred in the boundary layer of most tubules. These cells were identified as Leydig cells because of an extensively developed smooth endoplasmic reticulum in their cytoplasm, although they lacked Reinke's crystals. These ectopic Leydig cells sometimes lay in direct contact with Sertoli cells in the seminiferous tubule.

Adult↗

PubMed1979

Ultrastructural and biochemical characteristics of Leydig cells from newborn androgen-insensitive rats.

Leydig cells of testis of newborn pseudohermaphrodite (tfm) rats have an ultrastructure similar to that of the normal, containing well developed organelles and inclusions. The cytoplasm is filled with smooth endoplasmic reticulum forming a network of interconnected tubules. Lipid droplets are surrounded by cisternae of smooth endoplasmic reticulum and are in close association with pleomorphic mitochondria. Many of the latter are cup-shaped and have tubular cristae and intramitochondrial dense bodies. Essentially, these are characteristics of normal Leydig cells. Accordingly, the production of testosterone by testes from newborn tfm rats is the same as that by testes from normal newborns and adults. However, it is significantly higher than that by testes of tfm adults. Also, the plasma testosterone levels of newborn tfm rats are the same as in the normal newborn, but lower than in normal adults and much lower than in adult tfm animals. Thus, since in the tfm rat the morphology of Leydig cells, androgen production, and maintenance of plasma levels of testosterone are normal in the newborn, but become abnormal with advancing age, it appears that defective androgen action rather than insufficient androgen production is the cause of male pseudohermaphroditism.

Androgens↗

PubMed1978

[Effect of ACTH administration on liberation of testosterone by the Leydig cell (author's transl)].

The possible rôle of the Leydig cells ithe changes of testosterone levels induced by ACTH administration is studied. 14 male Wistar rats weighing about 300 g were separated in two groups. One was treated with I mU.I./100 g/day of ACTH i.m. for 6 days and the other with saline solution as control Rats, testes and adrenal glands were weighed and plasma testosterone levels were measured. The Leydig cells dispersed collagenase was inbubated for 120 min at 37 degrees C in the presence and in the absence of 10 mU.I. of HCG. The weight of adrenal glands in the treated rats was greater than in the control group. Treated rats had lower plasma values than the controls. Testosterone secretion by the Leydig cells, in basal situation and after stimulation with HCG, was lower in the treated group. Leydig cells of untreated rats were incubated with 12.5, 6.2, 3.1, 1.5 mU.I. of ACTH and supplemented with 2.5 pU.I. of HCG. No difference in testosterone secretion in either groups was observed.

Adrenal Glands↗

PubMed1979

Histogenesis of human extraparenchymal Leydig cells.

From 64 consecutive autopsies of patients with neither testicular nor hormonal pathology, 26 showed extraparenchymal Leydig cells, located mainly in the epididymis and in the spermatic cord. The ultrastructural study of these specimens plus those obtained from 2 patients affected with functional testicular tumors leads to the following conclusions: (1) The origin of ectopic Leydig cells is not interstitial Leydig cells having infiltrated the testicular nerves and migrated along them towards ectopic locations. (2) The ectopic Leydig cells are considered to develop from undifferentiated precursor cells, located extraparenchymally, mainly inside and beside the testicular nerves. These precursor cells are similar to those observed in the testicular interstitium and have an ovoid shape and some cytoplasmic projections. The cytoplasm contains vesicles of smooth endoplasmic reticulum, lysosomes, lipid droplets and abundant microfilament bundles. The transformation from these cells into mature Leydig cells implies a progressive differentiation of the cytoplasmic components involved in steroid biosynthesis.

Adolescent↗

PubMed1978

Decreased Leydig cell responsiveness in the testicular feminized male rat.

The Stanley-Gumbreck pseudohermaphrodite or testicular feminized male (tfm) rat exhibits a decreased Leydig cell sensitivity to human CG (hCG) measured by androgen and cyclic-3',5',-adenosine monophosphate production in vitro. These changes were associated with an 80% reduction in the number of LH receptors in the tfm testis, when compared on the basis of equivalent amounts of testis particle protein or per 10(6) isolated Leydig cells. Androstenedione and not testosterone is the major androgen secreted by the tfm Leydig cell and androstenedione secretion is, therefore, a more appropriate end point than testosterone secretion for Leydig cell function in tfm animals. A dose of hCG (3 ng/2 ml) which elicited a near maximal response in androgen production from the decapsulated testes and Leydig cell suspensions of normals rats, did not significantly stimulate androgen production from Leydig cells of the tfm animals. A much higher dose of hCG (200 ng/2 ml) gave a response from the tfm Leydig cells which was comparable to that obtained with 3 ng from Leydig cells of normal littermates. This indicates that the small number of LH receptors on the tfm Leydig cell membrane are functional and that the reduction in receptor number results in a decrease in the sensitivity of response to LH rather than a reduction in the maximum steroid response.

Androgen-Insensitivity Syndrome↗

PubMed1975

[Adrenal-like Leydig cells (author's transl)].

Adrenal-like lipoid-rich Leydig cells, which could be found in a cryptorchid testis, were investigated by light and electronmicroscopy. There were nodular and diffuse proliferation of these adrenal-like cells in the interstitium of the testis. Electronmicroscopically these cells are fasciculated and characterized by large liposomes, many tubulovesicular mitochondria, and a large smooth endoplasmatic reticulum. But the presence of crystals of Reinke in these cells underlined their relationship to Leydig cells. The clinical history of this case is characterised by an extreme adipositas (167 kg) and high urinary estrogenexcretion. This excretion could be suppressed with dexamethasone and stimulated with HCG. After orchiectomy estrogen excretion decreased for 4 months and then increased again, after ACTH stimulation performed by reason of adrenal insufficiency. At this time there is no evidence of adrenal tumor; in the contralateral, scrotal testis, spermiogenesis and Leydig cells are without pathologic changes as revealed by biopsy.

Adrenocorticotropic Hormone↗

PubMed1977

Testicular involution following optic enucleation: the Leydig cell.

The testes of Syrian hamsters underwent pronounced involution within six weeks after blinding. The seminiferous tubules were devoid of all stages of spermatid development and mature spermatozoa were absent from the tubule lumina. The diameter of of the Leydig cells was 25% less than that of controls. Examination with the electron microscope revealed thick bundles of collagen fibrils interspersed between Leydig cells and surrounding Leydig cells in the blinded hamsters. The Leydig cell nuclei were shrunken and highly infolded. Lipid droplets that were often seen in normal Leydig cells were absent in the involuting Leydig cells. The size of the Golgi complex and the amount of smooth endoplasmic reticulum were reduced. Results of the present experiment confirm that inactivity of the Leydig cells is the reason for the decline in serum testosterone levels in blinded hamsters.

Animals↗

PubMed1978

Attrition of the human Leydig cell population with advancing age.

Existing evidence suggests that the aging human male experiences a gradual decline in testosterone production, a phenomenon that should be reflected in the Leydig cell population of the testis. It has been proposed that Leydig cells diminish in number with increasing age, but conflicting claims characterize reports of this topic. We have reinvestigated this possibility by histometric analysis of perfused testes from 25 men ranging from 18 to 87 years of age. Average single Leydig cell volume (2,943 +/- 623 micrometer 3, X +/- S.D.) did not change significantly with increasing age (r = 0.24, P greater than 0.2), suggesting that surviving cells remain active. Total testis weight (43.5 +/- 13.9 g) also did not change with age (r = 0.04, P greater than 0.5). However, both total Leydig cell volume and the absolute number of Leydig cells per individual decreased significantly as functions of age (r = -0.71, P less than 0.002, and r = -0.61, P less than 0.005, respectively). Analysis of relationship between these two parameters indicates that the total volume of Leydig cell cytoplasm contained within the human testis is determined by the number of cells present. Our results show that a pair of young adult testes endowed with more than 700 million Leydig cells at 20 years of age may be expected to undergo an attrition rate of approximately 80 million cells per subsequent decade of life. Thus, Leydig cell attrition is an important correlate of declining androgen status in aging men.

Adolescent↗

PubMed1977

Effect of lutropin on phosphorylation of endogenous proteins in testis leydig cells. Correlation with testosterone production.

The effect of lutropin on phosphorylation of endogenous proteins in testis Leydig cells was investigated, by incubating purified Leydig cells with lutropin and [(32)P]P(i) followed by sodium dodecyl sulphate/polyacrylamide-slab gel electrophoresis of the [(32)P]phosphoproteins. The radioactivity of the proteins was quantified by densitometry of the radio-autograms obtained. The following results were obtained. 1. Lutropin increased the amount of (32)P incorporated into three proteins (A, B and C) with apparent mol.wts. of 14300, 57000 and 77600 respectively. 2. The increase in incorporation of (32)P into these proteins was detectable within 5min, reaching a maximum in approx. 20min. 3. The (32)P incorporated into protein B (but not proteins A and C) was significantly increased with 0.1 and 1.0ng of lutropin/ml. Incorporation of (32)P into all three proteins was significantly increased with 10ng of lutropin/ml, reaching a maximum with 100ng/ml. 4. Testosterone production was significantly increased with 1ng of lutropin/ml, and between 10 and 1000ng/ml the degree of stimulation of testosterone production and incorporation of (32)P into proteins A, B and C was similar. 5. Cyclic AMP production was significantly increased with 10ng of lutropin/ml and had not reached a maximum with 1000ng/ml. 6. In Leydig cells isolated from hypophysectomized rats 3h after injection of choriogonadotropin in vivo, phosphoproteins with the same molecular weights as proteins A, B and C were found. No further increases in incorporation of (32)P into these proteins were obtained when lutropin was added to the Leydig cells in vitro. 7. Dibutyryl cyclic AMP (but not follitropin or testosterone) also stimulated the incorporation of (32)P into proteins A, B and C in Leydig cells.

Animals↗

PubMed1979

Acute stimulation of aromatization in Leydig cells by human chorionic gonadotropin in vitro.

Aromatization of testosterone in Leydig cells purified from mature rat testes was assessed. Leydig cells incubated for 4 hr with increasing concentrations of [3H]testosterone. At saturating concentrations of testosterone, human chorionic gonadotropin (hCG) acutely stimulated aromatization. This stimulation was first observed at 1 hr, an 8-fold increase being found during a 4-hr incubation. The maximal amount of estradiol produced at saturating concentrations of testosterone and hCG was 1.8 ng per 10(6) cells. These results demonstrate that purified Leydig cells have a high capacity for aromatization and that hCG can acutely stimulate aromatization independently of stimulating testosterone synthesis in vitro.

Animals↗