[en] Full text: The contribution of genetic factors to the initiation of radiation-induced genomic instability remains poorly understood. Studies with high LET α-particles and very high doses of low LET radiation have described several common mouse strains that differ in their sensitivity to the induction of genomic instability and apoptosis. The aim here was to investigate whether low doses of low LET radiation would elucidate a similar genetic predisposition. To assess the influence of genetic factors on the initiation of genomic instability by low doses of low LET radiation, we irradiated stem cells from two mouse strains known to differ in susceptibility to radiation-induced delayed chromosomal instability. The frequency of delayed chromosomal aberrations was measured in bone marrow cells from CBA/H and C57BL/6 mice after exposure to 0.1 - 2 Gy of 250 kV X-rays. The yield of both chromosomal and chromatid-type aberrations were assessed 13-15 cell divisions post-irradiation in the clonal descendents of surviving stem cells. The apoptotic index of these surviving clones was scored as morphological changes by electron microscopy. At low doses, the frequency of cells with aberrations increased significantly in both strains, contrary to the strain differences observed with high LET α-particles in earlier studies (Watson et al. 1997). The percentage of apoptotic cells was similar between the strains at low doses, with both showing comparable levels of cells with aberrations and apoptotic cells. However, at higher doses, strain differences became evident: CBA/H cells had a substantially higher fraction of cells with aberrations to apoptotic cells, while the converse was true for C57/Bl/6. This data indicates that low doses may be insufficient to initiate the apoptotic pathway, while still resulting in significant induction of delayed chromosomal instability. Overall, these observations have important implications for low dose low LET radiation risk assessment and human health