Immunohistological determination of oestrogen receptor, progesterone receptor, and intermediate filaments in Leydig cell tumours, Leydig cell hyperplasia, and normal Leydig cells of the human testis

1989 ◽  
Vol 157 (3) ◽  
pp. 225-234 ◽  
Author(s):  
Wolfgang Düe ◽  
Klaus-Peter Dieckmann ◽  
Volker Loy ◽  
Harald Stein
Keyword(s):  
Progesterone Receptor ◽  
Intermediate Filaments ◽  
Leydig Cell ◽  
Leydig Cells ◽  
Oestrogen Receptor ◽  
Human Testis ◽  
Cell Hyperplasia ◽  
Leydig Cell Hyperplasia ◽  
Leydig Cell Tumours

THE MECHANISMS INVOLVED IN TESTICULAR DEGENERATION IN MAN

1967 ◽  
Vol 56 (4_Suppl) ◽  
pp. S17-S40 ◽  
Author(s):  
Svend G. Johnsen
Keyword(s):  
Leydig Cell ◽  
Leydig Cells ◽  
Cell Function ◽  
Frequent Occurrence ◽  
Human Testis ◽  
Cell Hyperplasia ◽  
Number Of Factors ◽  
Leydig Cell Hyperplasia ◽  
Leydig Cell Function ◽  
Testicular Degeneration

ABSTRACT The study presents a correlation between the regulatory mechanisms of the human testis and a number of factors involved in the degenerative processes in idiopathic hypospermatogenesis. As a working hypothesis, it is assumed that temporary damage cannot result in permanent hypospermatogenesis unless this is maintained by a special mechanism, and the object of the study is to find such a mechanism. It is shown 1) that in man the full spermatogenetic cycle can take place in the absence of Leydig cells; 2) that decreased spermatogenesis leads to increased release of gonadotrophins and further to Leydig cell hyperplasia; 3) that spermatogenetic lesions do not per se induce deposition of hyaline material in the tubular wall, but that hyalinization damages the epithelium; 4) that a special feature of the structure of the testis in Klinefelter's syndrome strongly suggests that the hyalinization process is not a direct gonadotrophin effect but is related to Leydig cell function. The nature of Leydig cell function has been shown to depend upon the qualitative nature of gonadotrophin stimulation, and findings indicating a qualitative change in the secretion of hyperplastic Leydig cells in hypospermatogenesis are presented. From these relationships a theory of the pathogenesis of "idiopathic" hypospermatogenesis is advanced. Temporary damage to the germinal epithelium induces increased gonadotrophin release and changes in the FSH/LH ratio. These result in Leydig cell hyperplasia and in qualitative changes in Leydig cell function. This may start a hyalinization process which damages the epithelium, this damage in turn maintains the gonadotrophin rise, etc., etc., The existence of a pathogenetic vicious circle in the human testis affords an explanation for the frequent occurrence of testicular degeneration and permanent cryptogenetic, hypospermatogenesis in man. The aim of this presentation is to correlate the mechanisms involved in the regulation of testicular function in man with the processes of non-specific testicular degeneration. By a total consideration of a large number of factors an attempt will be made to arrive at an explanation of the frequent occurrence of testicular degeneration in man. Although testicular degeneration has frequently been dealt with in the literature (cf. below), no such attempt has apparently been published.

Effects of local testicular heat treatment on Leydig cell hyperplasia and testosterone biosynthesis in rat testes

2016 ◽  
Vol 28 (9) ◽  
pp. 1424 ◽  
Author(s):  
Zhonghai Li ◽  
Jianhai Tian ◽  
Genggang Cui ◽  
Meng Wang ◽  
Dapeng Yu
Keyword(s):  
Heat Treatment ◽  
Cell Cycle ◽  
Heat Stress ◽  
Western Blot ◽  
Leydig Cell ◽  
Proliferative Activity ◽  
Leydig Cells ◽  
Cell Hyperplasia ◽  
Testosterone Biosynthesis ◽  
Leydig Cell Hyperplasia

Cryptorchidism or local testicular heat treatment induces reversible oligospermia or azoospermia in rodents and humans via increased germ cell apoptosis. Research in this field has concentrated on the impact of heat on spermatogenesis, with rather little attention paid to the molecular effects of heat treatment on Leydig cell function. In the present study, we investigated the effects of exposure to heat stress on the proliferative activity and testosterone biosynthesis of Leydig cells. We subjected adult rats to a single local testicular heat treatment of water at 43°C for 30 min. The expression of Leydig cell-specific markers, such as cholesterol side-chain cleavage (P450SCC) and 3β-hydroxysteroid dehydrogenase, was evaluated by immunohistochemistry and western blot analysis. The proliferative activity of Leydig cells was detected by immunostaining with proliferation-associated markers, including Ki67, bromodeoxyuridine and phosphohistone-H3 (pHH3). The mRNA and protein levels of cell cycle proteins and testosterone synthesis-related enzymes were measured by real-time polymerase chain reaction and western blot analysis, respectively. The testes of heat-treated rats contained 50% more Leydig cells than those of control rats, indicating induction of Leydig cell hyperplasia by testicular heat treatment. Increased proliferative activity in Leydig cells, evidenced by enhanced expression of cell cycle proteins, was the main cause of Leydig cell hyperplasia. In addition, heat treatment reduced serum and testicular testosterone concentrations. Consistent with this finding, heat stress downregulated two enzymes required for testosterone biosynthesis, namely cytochrome P450, family 17 (CYP17) and steroidogenic acute regulatory protein, in Leydig cells. Together, the results suggest that testicular heat leads to Leydig cell hyperplasia and a reduction in testosterone biosynthesis in adult rat testes.

A review of drug-induced Leydig cell hyperplasia and neoplasia in the rat and some comparisons with man

1995 ◽  
Vol 14 (7) ◽  
pp. 562-572 ◽  
Author(s):  
DE Prentice ◽  
AW Meikle
Keyword(s):  
Leydig Cell ◽  
Leydig Cells ◽  
Safety Assessment ◽  
Hormonal Status ◽  
Control Mechanisms ◽  
Hormone Production ◽  
Drug Induced ◽  
Cell Hyperplasia ◽  
Etiological Factors ◽  
Func Tion

This paper describes control of normal Leydig cell func tion and testosterone production. The macroscopic and histopathological appearances of spontaneous Leydig cell hyperplasias and tumors (LCT) in the rat are reviewed together with their incidence and hormonal status. Drugs which induce LCTs in chronic studies are discussed and include busereline, carbamazepine, cimetidine, finas teride, flutamide, gemfibrozil, histrelin, hydralazine, indomethacin, isradipine, lactitol, leuprolide, metronida zole, mesulergine, nafarelin, norprolac and vidarabine. The known mechanisms of LCT induction in the rat are reviewed together with other possible etiological factors. The incidence, clinical picture and etiological factors of LCTs in man are also surveyed. Hormone production in Leydig cells and LCTs in rats and man are compared. Differences between the two species are considered, par ticularly with regard to Leydig cell control mechanisms. The paper concludes that drug-induced LCTs in rats are most probably not predictive for man and their occurrence has little relevance in human safety assessment.

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