Risk of simulated microgravity on testicular injury induced by high-LET carbon-ion beams in mice

This study investigated the impact of simulated microgravity on acute injury induced by low doses of carbon ions in male reproductive organs of mice,and determined alterations in spermatogenic function and expression levels of apoptotic factors in mice following exposure to acute irradiation after 7 days of simulated microgravity.The results demonstrated that significant reductions in spermatozoa,primary spermatocytes and spermatogonia,and increased globular cells in seminiferous tubule and pro-apoptotic proteins were observed in the group exposed to over0.4 Gy irradiation.Collectively,the data suggest that lesions inflicted by simulated microgravity are not markedly modified by lower doses of irradiation(0.2 Gy)in mouse testis compared to the control group.However,testicular impairments were markedly evident in the group exposed to higher doses of carbon ions plus simulated microgravity,which may be due at least in part to elevated apoptosis initiated by the mitochondrial apoptosis pathway in germ cells.

This study investigated the impact of simulated microgravity on acute injury induced by low doses of carbon ions in male reproductive organs of mice, and determined alterations in spermatogenic function and expression levels of apoptotic factors in mice following exposure to acute irradiation after 7 days of simulated microgravity. The results demonstrated that significant reductions in spermatozoa, primary spermatocytes and spermatogonia, and increased globular cells in seminiferous tubule and pro-apoptotie proteins were observed in the group exposed to over 0.4 Gy irradiation. Collectively, the data suggest that lesions inflicted by simulated microgravity are not markedly modified by lower doses of irradiation （0.2 Gy） in mouse testis compared to the control group. However, testicular impairments were markedly evident in the group exposed to higher doses of carbon ions plus simulated microgravity, which may be due at least in part to elevated apoptosis initiated by the mitochondrial apoptosis pathway in germ cells.