Undifferentiated spermatogonia cell cycle arrest contribute to the impairment of spermatogenesis in the testis under chronic inflammation

SOBARZO CM; THEAS MS; FERREIRO E; JACOBO P.V.; MENDEZ CS; LUSTIG L

CABA

Congreso; Reunión conjunta de Sociedades Biomédicas; 2017

Testis inflammation and infections are frequent causes of male infertilityand are associated to spermatogenic arrest. We developed an experimental model of autoimmune orquitis (EAO) useful to understand the mechanisms underlying spermatogenesis disruption. EAO is characterized by an interstitial lymphomonocyte cell infiltrate, moderate in the focal phase and abundant in severe EAO, higher levels of nitric oxide (NO) and TNFα, apoptosis of post-meiotic germ cells (GC) and cell cycle arrest of pre-meiotic GC, spermatogonia (EP) and preleptotene spermatocytes. The aim of this study was analyze the cell cycle of undifferentiated EP (CD9+) and evaluate if NO and TNFα are able to regulate cell cycle progression of pre-meiotic GC. Flow cytometric analysis showed that in focal EAO the % of EPCD9+ in each phase of the cell cycle was similar to normal (N) rats (G1 N:73.52±1.24, EAO:72.42±0.97; S N:11.56±0.70, EAO:10.76±0.89; G2 N:14.88±0.79, EAO:16.79±0.58). In severe EAO the % of EPCD9+ significantly decreased in G1 and increased in G2 phase vs N rats (G1 N:72.45±1.78, EAO:32.06±6.69*; S N:11.17±1.83, EAO:10.68±3.15; G2 N:16.43±1.22, EAO:56.84±9.41*, *p