Ultrastructure of leydig cell paracrystalline inclusions, possibly related to reinke crystals, in the normal human testis

1973 ◽  
Vol 142 (1) ◽  
pp. 13-26 ◽  
Author(s):  
Arthur R. Sohval ◽  
J. Lester Gabrilove ◽  
Jacob Churg
2018 ◽  
Vol 110 (4) ◽  
pp. e164-e165
Author(s):  
R. Hayden ◽  
A. Mielnik ◽  
A. Bolyakov ◽  
R. Flannigan ◽  
D. Paduch

1993 ◽  
Vol 271 (3) ◽  
pp. 429-439 ◽  
Author(s):  
M. S. Davidoff ◽  
W. Schulze ◽  
R. Middendorff ◽  
A. -F. Holstein

Author(s):  
S. L. Asa ◽  
T. A. Bayley ◽  
E. Horvath ◽  
K. Kovacs

Leydig cell clusters in the adult human testis are known to enlarge during chronic stimulation with excess LH as in Klinefelter's syndrome or following administration of exogenous human chorionic gonadotropin (hCG). However, the ultrastructural features of this hyperplasia, to our knowledge, have not been reported in association with testicular neoplasms producing hCG.We report the case of a 21-year-old man who sought medical attention because of gynecomastia. Laboratory investigation revealed a marked increase in serum hCG and elevated a-fetoprotein. A testicular mass was palpable on examination and the patient underwent orchiectomy.


1989 ◽  
Vol 157 (1) ◽  
pp. 11-14 ◽  
Author(s):  
Richard Herriot ◽  
Frederick Walker

2020 ◽  
Vol 21 (10) ◽  
pp. 3649 ◽  
Author(s):  
Michal Duliban ◽  
Ewelina Gorowska-Wojtowicz ◽  
Waclaw Tworzydlo ◽  
Agnieszka Rak ◽  
Malgorzata Brzoskwinia ◽  
...  

Although epidemiological studies from the last years report an increase in the incidences of Leydig cell tumors (previously thought to be a rare disease), the biochemical characteristics of that tumor important for understanding its etiology, diagnosis, and therapy still remains not completely characterized. Our prior studies reported G-protein coupled estrogen receptor signaling and estrogen level disturbances in Leydig cell tumors. In addition, we found that expressions of multi-level-acting lipid balance- and steroidogenesis–controlling proteins including peroxisome proliferator-activated receptor are altered in this tumor. In order to get deeper into the other molecular mechanisms that regulate lipid homeostasis in the Leydig cell tumor, here we investigate the presence and expression of newly-described hormones responsible for lipid homeostasis balancing (leptin and adiponectin), together with expression of estrogen synthase (aromatase). Samples of Leydig cell tumors (n = 20) were obtained from patients (31–45 years old) and used for light and transmission electron microscopic, western blotting, and immunohistochemical analyses. In addition, body mass index (BMI) was calculated. In tumor mass, abundant lipid accumulation in Leydig cells and various alterations of Leydig cell shape, as well as the presence of adipocyte-like cells, were observed. Marked lipid content and various lipid droplet size, especially in obese patients, may indicate alterations in lipid homeostasis, lipid processing, and steroidogenic organelle function in response to interstitial tissue pathological changes. We revealed significantly increased expression of leptin, adiponectin and their receptors, as well as aromatase in Leydig cell tumors in comparison to control. The majority of patients (n = 13) were overweight as indicated by their BMI. Moreover, a significant increase in expression of phospholipase C (PLC), and kinases Raf, ERK which are part of adipokine transductional pathways, was demonstrated. These data expand our previous findings suggesting that in human Leydig cell tumors, estrogen level and signaling, together with lipid status, are related to each other. Increased BMI may contribute to certain biochemical characteristics and function of the Leydig cell in infertile patients with a tumor. In addition, altered adipokine-estrogen microenvironment can have an effect on proliferation, growth, and metastasis of tumor cells. We report here various targets (receptors, enzymes, hormones) controlling lipid balance and estrogen action in Leydig cell tumors indicating their possible usefulness for diagnostics and therapy.


2004 ◽  
Vol 167 (5) ◽  
pp. 935-944 ◽  
Author(s):  
Michail S. Davidoff ◽  
Ralf Middendorff ◽  
Grigori Enikolopov ◽  
Dieter Riethmacher ◽  
Adolf F. Holstein ◽  
...  

The cells responsible for production of the male sex hormone testosterone, the Leydig cells of the testis, are post-mitotic cells with neuroendocrine characteristics. Their origin during ontogeny and regeneration processes is still a matter of debate. Here, we show that cells of testicular blood vessels, namely vascular smooth muscle cells and pericytes, are the progenitors of Leydig cells. Resembling stem cells of the nervous system, the Leydig cell progenitors are characterized by the expression of nestin. Using an in vivo model to induce and monitor the synchronized generation of a completely new Leydig cell population in adult rats, we demonstrate specific proliferation of vascular progenitors and their subsequent transdifferentiation into steroidogenic Leydig cells which, in addition, rapidly acquire neuronal and glial properties. These findings, shown to be representative also for ontogenetic Leydig cell formation and for the human testis, provide further evidence that cellular components of blood vessels can act as progenitor cells for organogenesis and repair.


1969 ◽  
Vol 43 (4) ◽  
pp. 499-NP ◽  
Author(s):  
A. FABBRINI ◽  
M. RE ◽  
C. CONTI

SUMMARY Histological and histochemical investigations were carried out on the testes of normal subjects in order to define the distribution of glycogen and some related enzymes. Intratubular glycogen is abundant in the prepubertal stage; it diminishes strikingly with the beginning of puberty, reappears during the period of complete sexual maturation, and the highest increase is found in the tubules in involution. Glycogen is abundant at some stages of spermatogenesis and almost completely absent in others. Glycogen is mainly, but not exclusively, localized in the Sertoli cells. 1–4 Amylophosphorylase and 1–4, 1–6 transglucosidase are present in the tubule as well as in some extratubular structures. It is not possible to demonstrate the presence of either UDPG-glycogen transferase or glucose-6-phosphatase.


Sign in / Sign up

Export Citation Format

Share Document