Apoptotic cell death induced by low-dose radiation in male germ cells: hormesis and adaptation

Biological effects of low-dose radiation (LDR) in somatic cells have captured the interest of radiobiologists for the last two decades. Apoptosis of germ cells is required for normal spermatogenesis and often occurs through highly conserved events, including the transfer of vital cellular materials to the growing gametes following death of neighboring cells. Apoptosis of germ cells also functions in diverse processes, including removal of abnormal or superfluous cells at specific checkpoints, establishment of caste differentiation, and individualization of gametes. Moreover, germ cells are very sensitive to radiation-induced genomic and cytological effects. Therefore, induction of germ-cell apoptosis has been observed in the testis of animals exposed to both high-dose radiation (HDR) and LDR. Exposure of male germ cells to LDR induces a stimulating effect, while exposure to HDR causes an inhibitory effect on the metabolism, antioxidant capacity, and proliferation and maturation of cells, a phenomenon termed hormesis. Preexposure to LDR also protects cells from subsequently HDR-induced genomic and cytological effects, a phenomenon termed adaptive response. This review describes the features of male germ-cell apoptosis. It reviews the evidence that LDR induces the hormesis and adaptive responses in the male germ cells in terms of apoptosis. This review also discusses the possible effects of LDR-induced apoptotic hormesis and adaptive response on the modulation of inheritable genomic damage caused by subsequent radiation exposure to male germ cells.