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Radiation-induced DNA double-strand breaks (dsb) were studied in Ehrlich ascites tumour cells (EATC) by sedimentation in neutral sucrose gradients at low centrifuge speed. Dsb induction was found to be linear with dose with a frequency of: ndsbmr-1D-1 = (11.7 +/- 2) x 10(-12)Gy-1 for 140 kV X-rays and ndsbmr-1D-1 = (19.1 +/- 4) x 10(-12)Gy-1 for 3.4 MeV 241Am-alpha-particles. Postirradiation incubation of cells under non-growth conditions leads to repair of dsb, reaching a maximum after trep = 24 h. More than 97 per cent of dsb were repaired after an X-ray dose of 25 Gy. The number of residual dsb was found to be a linear-quadratic function of dose: nresmr-1 = (0.0161 +/- 0.0008) x 10(-12)Gy-2D2 for X-rays and nresmr-1 = (1.2 +/- 0.7) x 10(-12)Gy-1D + (0.105 +/- 0.017) x 10(-12)Gy-2D2 for alpha-particles. Thus, after cellular repair the RBE value of alpha-particles was increased from RBE = 1.6 +/- 0.4 (induction of dsb) to a dose-dependent value of RBE = 2.7 +/- 0.4 (at 100 Gy alpha-particles) to 3.8 +/- 1.2 (at 10 Gy alpha-particles) for residual dsb. From the data presented it is concluded that residual dsb are a major cause for loss of the reproductive capacity of EATC after irradiation with X-rays as well as alpha-particles.

A theory for DNA double-strand break (dsb) analysis by pulsed field electrophoresis is presented, based on the size distribution of DNA fragments, which converts an induction of dsb linear with dose into a nonlinear fraction of extractable DNA, in agreement with experimental observations.

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The induction and repair of DNA double strand breaks (dsb) in early stationary Ehrlich ascites tumour cells by X-rays was determined using an improved sedimentation technique in neutral sucrose gradients. The disappearance of dsb was followed during post-irradiation incubation of the cells and was interpreted as dsb repair. Kinetics were approximated by exponential functions with time constants of t37 = 3.0 +/- 0.7 hours ('conditioned' medium) and t37 = 2.0 +/- 0.5 hours (growth medium). Maximal repair was reached after 24 hours and the relationship of the remaining breaks with dose was interpreted on the basis of a recombination repair model. Using these dsb data and on the assumption of one dsb being a lethal event, cell survival curves were calculated for different repair times and compared with experimental curves. It was shown that cell survival curves can be interpreted on the basis of one unrepaired dsb being a lethal event, when dsb repair continues for about 11 hours after plating the cells on nutrient agar.