Malfunction of spermatogenesis in experimental ischemic mice

An experimental ischemia (EI)-induced mouse model was used toanalyze pathological and biochemical alterations in testes. Initialmorphological changes were observed in Sertoli cells of EI testes atthe light microscopic level. Examination of the ultrastructure usingtransmission electron microscopy confirmed that Sertoli cells werepartially detached from the basement membrane of the seminiferousepithelium and that the cell membranes of adjacent Sertoli cells werenot joined. The functional integrity of the blood-testis barrier (BTB)was assessed using the lanthanum tracer technique. Lanthanum hadpenetrated into the spaces between adjacent Sertoli cells in theadluminal compartment up to the lumen of the seminiferous epitheliumin EI testes. Proteome analysis showed that the expression of heatshock protein (HSP) 70 was significantly upregulated in EI testes.Western blot analysis confirmed that the expression of HSP70 increasedin a time-dependent manner after the EI procedure. HSP70immunostaining was observed in spermatocytes and in round andelongated spermatids in EI testes. Our results suggest that a changein the junctions between adjacent Sertoli cells on the basalcompartment is involved in the BTB disruption in EI testes. Therefore,male infertility caused by the BTB disruption could be associated withheat stress induced by ischemia.