Abstract
Our present knowledge on interrelation between morphology/ultrastructure of mitochondria of the Leydig cell and its steroidogenic function is far from satisfactory and needs additional studies. Here, we analyzed the effects of blockade of androgen receptor, triggered by exposure to flutamide, on the expression of steroidogenic proteins (1) and ultrastructure of Leydig cells’ constituents (2). We demonstrated that increase in the expression level of steroidogenic (StAR, CYP11A1, 3β-HSD, and CYP19A1) proteins (and respective mRNAs) in rat testicular tissue as well as elevation of intratesticular sex steroid hormone (testosterone and estradiol) levels observed in treated animals correspond well to morphological alterations of the Leydig cell ultrastructure. Most importantly, up-regulation of steroidogenic proteins’ expression apparently correlates with considerable multiplication of Leydig cell mitochondria and subsequent formation of local mitochondrial networks. Interestingly, we showed also that the above-mentioned processes were associated with elevated transcription of Drp1 and Mfn2 genes, encoding proteins implicated in mitochondrial dynamics. Collectively, our studies emphasize the importance of mitochondrial homeostasis to the steroidogenic function of Leydig cells.
Highlights
Our present knowledge on interrelation between morphology/ultrastructure of mitochondria of the Leydig cell and its steroidogenic function is far from satisfactory and needs additional studies
Positive immunostainings for steroidogenic acute regulatory protein (StAR), CYP11A1, 3β-hydroxysteroid dehydrogenase (3β-HSD), and CYP19A1 were confined to Leydig cells of both control and flutamide-treated rats
The most apparent increase in the staining intensity was observed for StAR protein, what was confirmed by quantitative densitometric image analysis (P < 0.001) (Fig. 1a′)
Summary
Our present knowledge on interrelation between morphology/ultrastructure of mitochondria of the Leydig cell and its steroidogenic function is far from satisfactory and needs additional studies. In vitro experiments on Leydig cells isolated from Brown Norway rats and incubated with mitochondrial toxin myxothiazol (a blocker of electron-transport chain) evidenced an important role of mitochondria in basal and luteinizing hormone (LH)-stimulated testosterone p roduction[10]. Mitochondria contain their own genome (mitochondrial DNA, mtDNA) and protein synthesis machinery. Mitochondria supply cells with energy (in the form of ATP), regulate calcium signaling, and contribute to reactive oxygen species (ROS) p roduction[11,12] The latter process leads to a loss of metabolic functions, decline in mitochondrial membrane potential and, most.
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