Objectives: The aim of the study is to confirm that karyometric evaluations of the seminal tubule cells in men with azoospermia indicate stimulating influence of the Leydig cell and testosterone on the functions of Sertoli cells, whereas serum LH concentration may in fact lead to regressive changes in the wall of the seminal tubule. Material and methods: Material consists of 75 patients with azoospermia and hypospermatogenesis. In all patients surgical biopsy of the testes was done, prior to an assessment of serum LH and testosterone levels. In histopathology, sperminal epithelium, basal membrane, myoid cells of the tubular wall and interstitial cells have been examined. Karyometry in Sertoli cells, spermatogonia and myoid cells was performed. Also, the thickness of the tubular wall was assessed quantitatively. Results: The size of Sertoli cells nuclei was significantly bigger in hypospermatogenesis associated with hyperplasia of Leydig cells than in hypospermatogenesis alone (p=0,01). Regression analysis revealed positive correlations between serum testosterone and the size of Sertoli cells nuclei (p=0,02), between the size of Sertoli cell nuclei and of spermatogonia and between nuclear size of myoid cells and spermatogonia (p=0,0001). Serum LH correlated positively with the thickness of tubular wall (p=0,01). Conclusions: Leydig cell hyperplasia and testosterone stimulate the functions of Sertoli cells whereas Sertoli cells activate spermatogonia. The Sertoli cell function is positively interrelated with the function of myoid cells. There is a close interrelationship between LH and the thickness of tubular wall, which may suggest that hippersecretion of LH causes the enlarged thickness of tubular wall, observed in hipergonadotropizm.