ABSTRACT
The modifications of Leydig cell function after efferent duct ligation [EDL] are mainly due to local changes within the testes providing further evidence for an intratesticular control of Leydig cell function. The aim of the current study was to investigate the effect of disruption of spermatogenesis that follows bilateral EDL on the functions of the Leydig cells. Four groups of animals were studied at 3, 7, 14, and 28 days after treatment, each group consisting of 12 animals, six treated and six controls. Pairs of animals [one control and one treated] were anaesthetized after the lapse of each period; their serum was subjected to the determination of testosterone, follicle stimulating hormone [FSH] and luteinizing hormone [LH]. Both testes were removed and weighed to the nearest gram weight. Sham-operated animals were used as controls. Bilateral EDL resulted in an initial increase in weight of the testes 3 days following the treatment compared to the control group. Thereafter, the testicular weight decreased significantly from day 7, 14 and 28 following treatments compared to that of the respective controls. The decrease in testicular weights was markedly obvious approaching up to 50% of the control groups on the day 14 and 28. There were no differences between serum testosterone concentration in the peripheral circulation on days 3 and 7 following treatments. However, testosterone level started to rise slightly on days 14 and 28 but was not significantly different from that of the controls. The serum LH remained normal until day 3 after the operation, followed by a gradual rise from days 7, 14 and 28 after treatment compared with that of the control groups, whereas FSH showed a sustain rise from day 7 and 14 onward reaching a highly significant levels on day 28 post-treatment. The bilateral EDL resulted in severe spermatogenic damage accompanied by a Leydig cell dysfunction. It is not possible to determine whether disordered androgen production is a manifestation of bilateral EDL or results from disruption of local control mechanisms between the seminiferous tubules and Leydig cells. The nature of the signals that mediate between seminiferous tubules and Leydig cells still remain elusive, hence this possibility needs further investigation to be elucidated