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¹ Prince Henry’s Institute of Medical Research, Level 4, 43-51 Kanooka Grove, Clayton, Victoria, 3168 Australia
² Institute of Reproductive Medicine, University of Münster, Münster, Germany
³ University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania, USA

(Requests for offprints should be addressed to S J Meachem; Email: sarah.meachem{at}princehenrys.org)

The roles of testosterone (T) and its metabolites on hamster spermatogenesis are poorly defined. This study assessed the effects of T, dihydrotestosterone (DHT) and oestradiol (E) on the re-initiation of spermatogenesis in the adult Djungarian hamster. Hamsters raised under long photoperiods (LD, 16 h light:8 h darkness) were exposed to short photoperiods (SD, 8 h light:16 h darkness) for 11 weeks to suppress gonadotrophins. Groups of eight animals then received T, DHT and E for 5 weeks. Cell numbers were determined using the optical disector (sic). The number of Sertoli cells was suppressed in SD controls to 48% (P < 0.001) of LD control and restored either fully or partially by exogenous DHTand E (2.6- and 1.8-fold above SD levels) respectively, corresponding with a twofold elevation of serum FSH. The number of germ cells in SD animals was reduced (all P < 0.001) to levels reported. The number of type A spermatogonia increased in line with the rise in Sertoli cell number, by 2.6-fold (P < 0.01) and 1.8-fold (NS) above SD controls after DHT and E treatments respectively. DHT increased the number of type B spermatogonia/preleptotene spermatocytes, leptotene/zygotene and pachytene spermatocytes by 3.5-, 5.7- and 21-fold above SD (all P < 0.01) respectively, compared with a 2.2-fold (P < 0.01), 2.4-fold (not significant, NS) and 6-fold (NS) in E-treated animals respectively. Exogenous T had little effect on cell numbers or serum FSH compared with SD controls. Spermatids were rarely observed after steroid treatment. We believe this study suggests that steroids can regulate the re-initiation of early spermatogenic cells via a mechanism which includes FSH.