904 RADIATION BIOLOGY 



been shown by Hicks (1950) and by Kosaka (1927, 1928b, c, d), who 

 describe its various histological manifestations in detail. Temporary 

 mitotic inhibition is harder to demonstrate but the work on other organ- 

 isms, reviewed in Chap. 10, makes it likely that it can occur in mammals 

 also. In this connection, it should be pointed out that arrests in whole 

 tissues or organs, which have been reported by Wilson and Karr (1951), 

 and which may later turn into abnormality, need not be due to mitotic 

 inhibition but may be caused by death of a certain proportion of cells at 

 a stage preceding observation. Abnormalities involving an apparent 

 increase rather than defect, e.g., Polydactyly, or the formation of an 

 extra thoracic rib, are quite reconcilable with the idea that the initial 

 change is death or retardation of cells rather than acceleration: thus the 

 selective elimination of a region may divide a primordium, and result in 

 "twinning." Radiation effects on viability (except during cleavage 

 stages, which form a special problem because of the apparently great 

 regulatory powers of blastomeres) may be thought of as resulting from 

 damage to various key tissues or organs (e.g., liver, as suggested by 

 Wilson and Karr, 1951). It is then obvious that incidence as well as 

 time of mortality would vary with the stage irradiated, i.e., with the 

 different critical periods existing at the time of treatment. 



The work of Russell, Russell, and Major (1951) has shown that hypoxia 

 protects markedly against radiation-induced abnormalities. By obtain- 

 ing results at a particular stage for a variety of dosages both in 5 per cent 

 oxygen (+ 95 per cent helium) and in air, it could be demonstrated that 

 the magnitude of protection is approximately similar for all of six charac- 

 ters so far tabulated (see Fig. 13-9). Since hypoxia has been shown to 

 protect against chromosome aberrations (Giles, Baker, and others) and 

 mitotic inhibition (Gaulden and Nix, and others), it may be suggested 

 that the protection against developmental abnormalities is on the level of 

 the intracellular damage, but the results do not provide evidence in favor 

 of any one kind of intracellular damage. The fact that various characters 

 are protected to an approximately equal degree makes it likely that 

 different sensitive primordia are affected in a similar manner by radia- 

 tion to yield abnormalities. It is also noteworthy from the point of view 

 of the discussion which follows that, both in incidence and degree of 

 change, reduction in oxygen is equivalent to treatment with a lower dose. 



C. DOSAGE RELATIONS; VARIABILITY 



The commonest results obtained on increasing the dose are: (1) 

 increase in incidence, (2) increase in degree, and (3) extension of the 

 period during which radiation will yield the given abnormality (Russell, 

 1950, 1949). Exceptions to these points will be discussed. If the prob- 

 ability of affecting a potentially sensitive cell in a given precursor of n 

 cells is p, then the proportions of animals with 0, 1, 2, 3, . . . ,n cells of 



