212 A. V. LEBEDINSKY, V. M. MASTRYUKOVA AND A. D. STRZHIZHOVSKY 



within the range we are mostly interested in is tlie ])henomenon of 

 mitotic inhil)ition. Similar inhibition may ])e accompanied by subse- 

 quent restoration, whilst the duration of the inhibitory time interval 

 depends upon the number of ionizations occurring within the bio- 

 chemically efficient volume. The other form of mitotic inhibition may 

 be termed the genetic one. In its very essence it is of an irreversil)le 

 character; it develops very rapidly, leads to the appearance of patho- 

 logical mitoses and to destruction following a few subsequent genera- 

 tions. And lastly, the third form is also of a basic genetic nature, it is 

 also of an irreversible character and develops rapidly whereby the cells 

 are immediately destroyed. The inhibition of mitotic activity following 

 doses exceeding those of case 1 and case 2 leads as well to the destruction 

 of cells. 



The restoration processes mentioned above are included as obligatory 

 components of the tissue reaction to the radiation effect. When the 

 lesions occur in a limited biochemical volume, the restoration may be 

 of a complete and true character, i.e. it takes place at the expense of 

 cells that have experienced the damaging effect of radiation. In the 

 cases where genetic material is affected, the restoration is, practically 

 speaking, but a ])rocess of compensating for the defect at the cost of 

 cells having avoided damage. The very existence of a similar mechanism 

 under high dose radiation in the corneal epithelium of the mouse was 

 established by Strelin (1934, 1956). 



One of the final goals of investigation in the study of the effect of 

 radiation u]ion mitotic activity is the formation of equations to re])re- 

 sent the kinetics of the populations studied ; for the system composed 

 of an extensive series of constituents statistical analysis is most con- 

 venient. As the main effect is displayed in the retardation (delay) of 

 cell division, the aim of this kind of investigation is to determine the 

 probability K of division and the estimation of the perished cells //r })er 

 time unit in relation to time t and the radiation dose A. 



This type of statistical analysis is based upon a detailed elaboration 

 of a pattern of radiation injury introduced into cell division. In its turn 

 the pattern of the radiation injury caused to mitosis should be viewed 

 as a sequential event following from the pattern of normal mitotic 

 activity. For this purpose we have utilized the scheme of Watson and 

 Crick (1953). 



On the basis of this scheme the ideas dealing with radiation injury 

 to mitosis are as follows : 



It is known that the synthesis of biochemical materials used during 

 mitosis occurs during the interkinetic period and terminates at the l)e- 

 ginning of mitosis. The very fact that radiation inhibition of mitotic 



