Level of Cyclin D1 protein in peripheral blood lymphocytes of Chornobyl clean-up workers in remote period after radiation exposure

Abstract

Aim: to assess changes of products of Cyclin D1 protein in lymphocytes of peripheral blood of Chernobyl clean-up workers as remote results of the action of ionizing irradiation. Methods: there were examined 120 Chernobyl clean-up workers in the remote period after radiation exposure and 45 persons of the control group. For assessing mitogen-induced levels of Cyclin D1, the micro-method of cultivating erythrocytes of whole blood was used. The quantitative assessment of the spontaneous and mitogen-induced levels of Cyclin D1 in lymphocytes of peripheral blood (PB) was realized using the reagents FITC Mouse Anti-Human Cyclin D1 Antibody Set (BD, USA) by the method of flow cytometry.Research results: there was determined the dose-dependent increase of the spontaneous level of Cyclin D1 in PB lymphocytes of Chornobyl clean-up workers. High values of the parameter were established in the subgroup of Chornobyl clean-up workers, irradiated in the diapason of doses as 500-1000 mSv. Maximal values of Cyclin D1 level in PB lymphocytes were observed in Chornobyl clean-up workers at exacerbation of the bronchial-pulmonary pathology, bronchial asthma in anamnesis and in reconvalescents of acute radiation sickness with the radiation doses D ≥ 500 mSv. After mitogen stimulation of lymphocytes, there was noted the decrease of Cyclin D1 level in the group of Chornobyl clean-up workers and the increase in persons of the control group.Conclusions: the research revealed the differences in products of Cyclin D1 in PB lymphocytes of Chornobyl clean-up workers and persons of the control group. The revealed changes of the spontaneous and mitogen-induced levels of Cyclin D1 in PB lymphocytes of Chornobyl clean-up workers with the somatic pathology reflect disorders in regulation processes of proliferation and cellular cycle. The obtained data add ideas about mechanisms of the radiation-induced disorder of the cellular cycle that may be a manifestation of genome instability and become a trigger factor of carcinogenesis in the remote period after radiation exposure