Testosterone Withdrawal Promotes Stage-Specific Detachment of Round Spermatids from the Rat Seminiferous Epithelium1

Abstract

Testosterone (T) has been shown to be essential for the completion of spermiogenesis. Our previous studies showed that when intratesticular T was suppressed for 11 wk, the conversion of round spermatids between stages VII and VIII of the spermatogenic cycle was markedly suppressed and that elongated spermatids were undetectable. The fate of the round spermatids that did not proceed through this conversion was unclear. The current study aimed to investigate this T-dependent loss of round spermatids during stages VII and VIII. Adult male Sprague-Dawley rats received 24-cm T implants for 1 wk to suppress LH while maintaining spermatogenesis. The T24 implants were removed and replaced with 3-cm T plus 0.4-cm estradiol (TE treatment) to suppress intratesticular T and spermatogenesis, and animals were killed at 0 and 4 days and 1, 2, 3, 4, and 6 wk later. The number of homogenization-resistant elongated spermatids in the testis was counted, and round spermatid populations in stages VII and VIII were quantified using stereological techniques. The hourly production rates (HPR) were calculated, and a ratio was made between the HPR of round spermatids in stages VII and VIII to assess the efficiency of their conversion through these stages. Testicular T levels were suppressed to 2-4% of control values by TE treatment. After 2 wk of TE treatment, the number of homogenization-resistant elongated spermatids was significantly suppressed, falling to < 0.5% of the control value by 6 wk. The HPR of round spermatids in stages VII and VIII was not affected by up to 2 wk of TE treatment, nor was the conversion between these stages interrupted. After 3 wk of TE treatment, the HPR of round spermatids in stages VII and VIII was significantly suppressed, as was the conversion between these stages, the ratio falling to 27% of the control value by 6 wk. In rats treated with TE, histological examination of the cauda epididymidis showed occasional round spermatids after 3 wk of treatment, and large numbers after 6 wk. We conclude that the failure of round spermatids to complete spermiogenesis following T withdrawal is due to stage-specific detachment of round spermatids between stages VII and VIII.

Blood–testis barrier dynamics are regulated by an engagement/disengagement mechanism between tight and adherens junctions via peripheral adaptors

“…In this report, an in vivo model using Adjudin was used to induce AJ restructuring in the testis without damaging the BTB (12). It is unlikely that the changes reported here are the result of a drug toxicity effect of Adjudin toward junctions, because many of the biochemical changes in the seminiferous epithelium, such as an induction of protein and lipid kinases, phosphatases, adaptors, and AJ-integral membrane proteins, that are associated with the event of germ cell depletion from the epithelium have been reproduced and validated (14,23,28) by using an intratesticular testosterone suppression model (29,30). Furthermore, a more recent study has illustrated that an AJ restructuring event in the testis can indeed be limited to the apical ES without compromising the BTB (14), consistent with data obtained from the Adjudin model (12).…”

Fertility of male adult rats submitted to forced swimming stress

“…The normal fertility exhibited by stressed males may be explained by the fact that forced swimming lasted 15 days, a period shorter than the 48-to 53-day duration of one cycle of the seminiferous epithelium. Previous studies have shown that long-term testosterone suppression led to reduced spermatogonial and spermatocyte production, and that losses during these earlier stages of germ cell development led to reduction in the spermatid population (18). When intratesticular testosterone was suppressed for 11 weeks, the conversion of round spermatids from stage VII to stage VIII was markedly suppressed and elongated spermatids were not detected.…”

EFEK EKSTRAK DAUN PEGAGAN (Centella asiatica (L.) Urban) TERHADAP PERKEMBANGAN SEL SPERMATID TIKUS (Rattus norvegicus)

“…Terganggunya fungsi sel Sertoli menyebabkan sekresi androgen binding protein (ABP), suplai nutrien, growth factors, laktat, dan transferin juga terganggu, sehingga mengakibatkan proses spermatogenesis akan terganggu, karena zat tersebut sangat dibutuhkan dalam proses spermatogenesis (Lohiya et al, 2002). Selain itu, hilangnya fungsi sel Leydig menyebabkan sekresi hormon testosteron menjadi rendah, sehingga proses spermiogenesis menjadi terganggu (Donnel et al, 1996). Senyawa aktif tanin diduga berperanan dalam menurunkan jumlah sel spermatid.…”