The increased level of non-clonal chromosomal aberrations in the progeny of irradiated cells is recognized as the manifestation of radiation induced chromosomal instability (CI). The shape of the CI dose-response is different from that in the first post-irradiation mitosis; however, the origin of this difference is not established at present experimentally. In the present work, CI dose-response for unstable chromosomal aberrations is studied on the basis of the biophysical model of CI, taking into account formation of delayed dicentrics at different times after irradiation. The model based on the CI data analysis for low-LET radiation allows us to assess the contribution of the proposed mechanisms of CI, such as replication dependent generation of persistent DNA breakage in the descendents of irradiated cells, chromosome breakage-fusion cycle, etc.