Consequences of irradiation on adult spermatogenesis: Between infertility and hereditary risk.

Abstract

DNA damage response in adult spermatogenic cells should limit the propagation of mutations to the offspring, without being detrimental to fertility. In differentiating spermatogenic cells, the genomic instability is limited in time, whereas in spermatogonial stem cells it can be maintained all along life. Spermatogonial stem cells are long-lived cells that support normal germ cell differentiation and must be preserved throughout life. However after irradiation spermatogenesis recovery can be impaired as a consequence of the radiation-induced decline in spermatogonial stem cell. In this review, we summarize the differential sensitivities to DNA damage of spermatogenic cell populations, and the DNA repair mechanisms activated in these cells that paradoxically might favour the maintenance of cells with impaired genomic integrity. We describe how the testis tissue collapses in response to irradiation and we discuss the molecular pathways involved in the control of DNA damage response and homeostasis in spermatogonial stem cells.