Exposure of neonatal mice to Sevoflurane may induce male germ cell apoptosis in testicular tissue after puberty

common use of sevoflurane in congenital defects during repeated surgeries may have detrimental effects on spermatogenesis after puberty.

This study investigated sevoflurane effects on spermatogenesis process in male mature mice after exposure in prepubertal time.

24 neonatal NMRI male mice were randomly classified in three groups. Experimental 1 and 2 groups (exposure to 1 minimum alveolar concentration (MAC) and 2 MAC sevoflurane, respectively in 2 lit/min oxygen (O2) for 7 days (30 min, daily) and control. All groups were sacrificed after 2 months. Histological assessment, immunohistochemistry and apoptosis process was done. Bax and Bcl2 expression was evaluated in the testicular tissue by real time Poly Chain Reaction.

Our results showed that the integrity of testicular tissue was preserved in both experimental groups. Count of spermatogonial cells had significant decrease in group 2 compared to others. The rate of apoptosis in spermatogonial cells was 15±3% and 9±2% in the group 2 and 1, respectively. Also, Bax/Bcl2 ratio was 0.2615, 1.0070 and 9.3657 in control, experimental group 1 and 2, respectively. This result was significant (p≤0.002) between groups 2 with other groups.

Continuous exposure of 2 MAC sevoflurane in 2 lit/min O2 simultaneous during prepubertal may create more testicular tissue damage in terms of cellular and molecular function compared to continuous exposure to lower level of sevoflurane by increase in ratio of Bax/Bcl2 and apoptosis in germ cells after puberty.