[en] Full text: L5178Y (LY) sublines, LY-R and LY-S, differ in response to combined treatment with poly(ADP-ribose) polymerase inhibitor, benzamide (Bz) and ionising radiation: 2mM Bz sensitises LY-S but not LY-R cells [Acta Radiol. Oncol. 24, 451]. The high radiation sensitivity of LY-S cells is reasonably explained by the deficiency in DNA DSB repair [Radiat. Res., 112, 146]. Since, the rejoining of DNA breaks in LY-S cells is not sensitive to DNA-PK inhibitors [Mutat. Res., 409, 31], the deficiency in DSB repair is likely due to the impaired function of the enzyme. To investigate the role of polyADP-ribosylation in DNA-PK-mediated pathway of DNA repair, we compared the rates of DSB rejoining in LY sublines and a pair of CHO lines: wild type (WT) and mutant xrs6 cells. Cells were incubated with 2mM Bz at 37 deg C for 2 h, X-irradiated with 10 Gy and allowed to repair DNA breaks for 15, 60 and 120 min). The remaining DNA DSBs were estimated by the neutral comet assay. As expected, xrs6 cells repaired DSBs more slowly than CHO WT cells and the residual DNA damage after 60 min and 120 min of repair was higher in the mutant cell line. However, no effect of Bz treatment on the repair kinetic was observed either in xrs6 or WT cells. Interestingly, Bz inhibited the repair of DSBs in LY-S line but not its parental LY-R line, in agreement with previously observed sensitisation of LY-S cells to X-ray by Bz. An analysis of the repair kinetics of LY cells divided into cell cycle phases confirmed our findings. In conclusion, although the defect in repair of DNA breaks in LY-S is linked with the DNA-PK pathway, apparently, is not connected with impaired DNA-PK function in the NHEJ repair system

[en] Irradiation of human lymphocytes with small doses of X-rays (1 cGy, 37 C). Evoked a 30 % decrease in the frequency of micronuclei upon subsequent X-irradiation (1.5 Gy, 37 C). The DNA damage and its repair rate were determined by the single gel electrophoresis assay (comet assay). The adaptive response, seen as reduced micronuclei frequency, is not accompanied by an increase rate in DNA repair. (author). 11 refs, 6 figs, 1 tab

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[en] Human peripheral blood lymphocytes stimulated in vitro with phytohemagglutinin were exposed to an adaptive dose of 0.01 or 0.064 Gy of X-rays at 32 h of culture and to a challenge dose of 1.5 or 1.07 Gy, respectively, at 48 h. The lymphocytes were fixed at 54 h. In another set of experiments the cell cultures were irradiated only once with one of adaptive doses or one of the challenge doses at 32^nd or 48^th hour respectively. The frequency of chromatid breaks was lower than expected on the basis of additivity of the single treatments by 40% for the doses of 0.064 and 1.07 Gy and by 55% for the doses of 0.01 and 1.5 Gy. It is concluded that the low doses of X-rays render the lymphocytes less susceptible to the clastogenic action of a subsequent large dose of this radiation. 9 refs., 1 tab. (author)