Background: Rising of cancer incidences in population of Ukraine is connected with the increasing of cancerogenic loading where ionizing radiation has been recognized as a strong cancer causing agent. Today variations in radiation sensitivity between individuals are shown to be genetically determined and connected with the effectiveness of cell signaling system function after exposure to damaging agents. Recent reports have suggested that elevated chromosome aberration yields observed following radiation exposure of peripheral lymphocytes in G2 phase of cell cycle caused by the impaired DNA repair and hereditary predisposition to cancer. The goal of the presented study was to evaluate chromosomal sensitivity of lymphocytes of healthy individuals on the basis of the modified G2‐test.

Materials and Methods: Test‐system of human peripheral blood lymphocytes (PBL) of 110 healthy donors with the next metaphase analysis of chromosomal aberrations (chromatid breaks) was used. Test ‐irradiation of cell cultures was carried out at 1,5 Gy in the late G2‐stage. Cells were analyzed in the first mitosis.

Results: The obtained cytogenetic data has revealed high interindividual variability in the levels of radiation induced chromatid breaks (CV = 24%). It was shown that distribution of the examined cytogenetic parameter in the group did not correspond to normal distribution and had bimodal character. Application of variation statistics' methods has revealed existence of two subgroups of donors ‐ with “normal” and “increased” (11,6 % of the group) radiation sensitivity of lymphocytes on chromosomal level.

Taking into account correlations of high radiation‐induced genome instability of human somatic cells with cancer predisposition it is competent to relate these individuals with the group of increased radiogenic cancer risk. Application of cytogenetic examinations on the basis of G2‐assay is recommended for the formation of groups with the increased radiogenic cancer risk and promotes the efficiency of primary cancer prevention in the cohorts of occupationally exposed individuals.

Citation Information: Cancer Prev Res 2010;3(1 Suppl):A8.