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I incorporated in DNA is known to be exceptionally toxic. Values of D range from about 40 to about 90 decays for survival of mammalian cells. The effectiveness ofI in DNA with respect to the induction of breaks of the DNA strands, however, appears to be comparatively low. The numbers of strand breaks per energy deposited in subnuclear cellular structures such as DNA is smaller for a disintegration ofI than for γ-rays. The difference in effectiveness diminishes with increasing mass of the considered sensitive volume. The apparent inefficiency ofI-decay may, on one hand, result from a waste of local energy deposition. On the other hand, it may be caused by a multitude of local strand breaks (clusters) induced byI-decay which are measured as one break only by the conventionally applied techniques of strand break measurement. The apparent inefficiency ofI may be evidence furthermore for the importance of considering not only the DNA as the sensitive target but with equal pertinence the gross sensitive volume, i.e. the whole cell nucleus [12]. Further, for drawing meaningful comparisons, it may be necessary to take into consideration the microdosimetric event size distributions for the critical targets [1]. [ABSTRACT FROM AUTHOR]

Human kidney cells in culture and cells of mouse sarcoma-180 were allowed to incorporate bromine into their DNA. Cultured cells with and without incorporated BUdR were irradiated with electromagnetic radiations ranging in energy from 12 keV X-rays to 60Co gamma-rays to find out whether or not there exists any energy dependence of the bromine dose enhancement ratio BER. Such a dependence should show in the immediate neighbourhood of the K-absorption edge of bromine (13.5 keV). Any influence of the Auger effect triggered in bromine by external irradiation should show by a significant increase of the BER for energies rising from slightly below to slightly above the bromine K-edge. Values of D37, D0 and the extrapolation numbers of the cell survival curves served as biological endpoints. Measured values of BER ranged from 1.12-2.00 without any significant dependence energy. A weakly pronounced peak was found for 50 kV X-rays of 26 keV mean energy. Sarcoma-180 were irradiated with 14 kEV X-rays and 60C gamma-rays. BUdR was administered i.v., i.p. and directly into the tumours in quantities of up to 1 ml of a 10(-3) M solution. Tumour regression caused by the irradiations served as a measure of the radiation effects with and without incorporated BUdR. No significant dose enhancement effect of bromine was observed in this case. Within error limits, the combination of BUdR with 14 keV X-rays proved more effective than BUdR combined with 60Co gamma-rays.

Biological effects of 125I incorporated into DNA exceed those to be expected from the absorbed radiation dose by a factor 3--30. The reason for this discrepancy suggests special mechanisms introduced by 125I transmutation, decays by K-capture leading to the emission of an average of 6 low energy electrons including Auger electrons and to a highly positively charged daughter nuclide. The effect of 125I decay on DNA strand breakage and subsequent repair was studied. Human kidney cells T in the deep frozen state (-196 degrees C) were exposed to incorporated 125I and 60Co gamma-rays. The number of DNA single strand breaks (ssb) was determined by DNA centrifugation in alkaline sucrose gradients. DNA repair was studied by incubating the cells after thawing at 37 degrees C. For 125I decay in frozen cells which were kept with or without dimethyl-sulfoxide, 4 and 6 ssb were measured per decay. The gamma-rays produced 1ssb per 26 eV absorbed energy. Most of this damage was repaired 30 to 40 min after onset of incubation. No repair of the damage caused by 125I was observed. The high efficiency of 125I decays for the production of unreparable ssb provides evidence for the high radiotoxicity of this isotope. The observed lack of repair may in part be due to the high numbers of at least 2,000 125I decays per cell nucleus necessary for the assay system. Damage from many 125I decays may interfere with enzymatic repair processes.