[en] Enhanced cellular DNA repair efficiency and suppression of genomic instability have been proposed as mechanisms underlying the reduction of spontaneous and radiation-induced carcinogenesis in laboratory mice following low-dose radiation exposures. Our previous studies revealed that low-dose irradiation does not generate radio-adaptation by lowering radiation-induced DNA double-strand breaks, as indicated by the number of micronuclei in mouse spleen lymphocytes. These results were extended here by measuring dose and time dependent cytogenetic damage and proliferation changes in bone marrow erythrocyte populations of C57BL/6 and BALB/c mice. In C57BL/6 mice, the induction of micro-nucleated polychromatic erythrocytes (MN-PCE) was observed at doses of 100 mGy and greater, and suppression of erythroblast maturation occurred at doses of 500 mGy and higher. A linear dose response relationship for bone marrow MN-PCE frequencies 24 to 28 hours post-irradiation in C57BL/6 mice was established for doses between 100 mGy and 1 Gy, with departure from linearity at doses ≥ 1Gy. BALB/c mice exhibited increased MN-PCE frequencies following a 20 mGy radiation exposure but did not exhibit radio-sensitivity for MN-PCE frequencies following 2 Gy exposure. Radio-adaptation of bone marrow erythrocytes was not observed in either strain of mice exposed to low-dose priming irradiation (20, 100 mGy or 20 mGy x 4) administered at various times prior to acute 2 Gy irradiation, confirming the lack of radio-adaptive response for induction of cytogenetic damage or suppression or erythrocyte proliferation/maturation in bone marrow of these mouse strains. (author)