RADIATION DOSE 



transfers between the ionizing particle and orbital electrons give rise to the 

 production of free radicals and to new stal^lc molecular configurations. A 

 proportion of these may be able to difiuse away from the track to distances 

 determined by their lifetime and chemical reactivity. They can, in principle, 

 react selectively with certain types of biological molecule, thus affecting a 

 much larger proportion of these particular kinds of molecule than can be 

 directly ionized by the moving particle. It is known that such indirect 

 inactivations take place in dilute aqueous solutions of enzymes, desoxyribose 

 nucleic acid (DNA) and other molecules of biological importance. Wc have 

 only meagre evidence as to the extent in which such indirect inactivations 

 take place in the living cell. Hutchinson and his colleagues^-" have con- 

 cluded that in the living yeast cell the effective difTusion range of products 

 formed by ionizing particles is of the order of 30 A. Thus, a dehydrogenase 

 molecule which has a radius of 36 A is inactivated by energy deposited within 

 a region about twice its own volume, and Co-enzyme A, of radius 6 A, by 

 energy deposited within 60 times its own volume. Such allowances for 

 indirect inactivation do not significantly alter the statistical aspects of dose 

 for any structure larger than an enzyme molecule. 



Biological response may be influenced by dose rate as well as by dose. On 

 a macroscopic scale, a cell irradiated at constant dose rate is being contin- 

 uously exposed to injurious agents and a level of damage is reached which is 

 a balance between the rate of injury and the rate of recovery. There is, 

 however, a statistical aspect of dose rate as well as dose. In terms of particles, 

 a volume element of the cell is discontinuously afTected by events which are 

 randomly distributed in time as well as in space. A dose-rate dependence 

 may thus arise from interactions between successive particles which pass 

 through the same volume element. These interactions may be at the chem- 

 ical level, in which case the time constant which describes the dose-rate 

 dependence will be related to the lifetime of intermediate species, as discussed 

 by Lea', and exemplified by the experiments of Chapiro^ Ghormley*^, 

 Sutton and Rotblat^", and others. 



Alternatively, the time constant may be related to cell metabolism, as is 

 thought to be the case when aberrant chromosome configui'ations are pro- 

 duced by the union of two or more tracks produced by different ionizing 

 particles" i-'^'^. Clearly, in the case of any form of biological damage 

 which arises in a uniform population of cells from the action of a single 

 ionizing particle, biological response cannot be dose-rate dependent. Dose- 

 rate dependence may, however, be observed even when injuries are induced 

 by single particles if the population itself is heterogenous and changing with 

 time in such a way that the distribution in sensitivity among the individual 

 cells depends on the duration of exposure. 



One example of the influence of dose rate on biological response is given 

 in Figure 4 (a) which reproduces the experimentally observed growth inhibi- 

 tion in Vicia roots exposed to y radiation at different dose rates. Each mem- 

 ber of the family of curves corresponds to a constant exposure time. It is seen 

 that a given dose was most effective when delivered in 8 min. Longer 

 exposures were less effective, but prolongation of the duration of exposure 

 from 1 2 to 24 hours resulted in no further decrease in biological effectiveness. 

 It will also be seen that there is an interdependence between dose and dose 



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