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A biophysical analysis is made of the results of recent experiments which used accelerated heavy ions of 20 to 470 keV micron-1 to induce inactivation and mutation (resistance to 6-thioguanine) in cultured V79 Chinese hamster cells and HF19 human diploid fibroblasts. It is shown that the discrete nature of the primary ions must be explicity taken into account before the numbers of induced lethal and mutagenic lesions can be deduced from the observed radiosensitivities. The measured numbers of lesions produced by the radiations of different LET are compared with the relative numbers predicted by various models of radiation action. The observations can be explained on the hypothesis that each lethal lesion is produced by a deposition of small energy (small number of ionizations) in a distance of about 3 nm. Two different lesions appear to be involved, one of which requires greater than or equal to 100 eV and is dominant with low-LET radiations, and the other requires greater than or equal to 300 eV and is dominant at high-LET. Similar conclusions may apply to mutagenic lesions except that the mechanism which dominates at high-LET requires significantly more than 300 eV. More precise assessments of the hypothesis and these numerical values must await detailed track structure calculations of the radiation on the nanometre scale. Alternative models which invoke 'accumulation of sublethal damage' or 'interaction between sublesions', over distances of the order of microns, do not provide a consistent explanation of the observations. This suggests that the frequently observed curvature of low-LET dose-responses is not due to interaction between sublesions but rather to some other mechanism such as a dose-dependent repair process. It is also shown that low velocity, high-LET ions produce an average of appreciably less than one lethal lesion in traversing the nucleus of the above mammalian cells; 90 keV micron-1 helium ions produce about 0.03-0.06 lethal lesions micron-1 of track through the nucleus of the cells of thickness about 7 microns. Some estimates are also made of the size of the nuclear region which is sensitive to the induction of mutation to 6-thioguanine-resistance; it is concluded that this region extends beyond the DNA of the structural gene itself.

SUMMARYThe lengths of organisms of Escherichia coli B/r grown in continuous culture in a glucose salts medium were measured over a wide range of population densities at 22' and 37'. In some cases the cultures were exposed to continuous gamma radiation at dose rates of 600 r./hr. at 22" and of 1000 r./hr. a t 37". The average length of the forms and the distribution with respect to length depended upon the temperature, population density and radiation dose rate. The growth rate was almost independent of population density over the range in which the average length of organism showed such a marked dependence. No significant differences in growth rate were observed as between unirradiated and irradiated cultures. Changes in average length of organisms are regarded as phenotypic responses to changes in growth conditions, some conditions favouring division and others inhibiting division amongst short organisms.

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