252 E. Y. GRAYEVSKY, et Cll. 



The death of cells remaining after early mass destruction is due to 

 chromosome unbalance and to inability to complete division because 

 of gross structural injuries to the chromosomes; the death of such 

 cells is observed in generations Fi to F3. 



The main factor limiting regeneration of tissues exposed to 700 to 

 3,000 r has been shown to be the small number of residual viable cells 

 since most cells have lethal chromosome aberrations. The number of 

 such injured cells reaches 90 per cent after exposure to a minimum 

 lethal dose (700 r of X-rays for mice). 



The data presented show that the realization of radiation damage 

 depends in some cases on environmental conditions. Delay of the 

 development of injury may in some cases contribute to recovery. 

 But even if the process of spontaneous repair does not play any signi- 

 ficant role, latent damage may be influenced experimentally. 



Reasons for the different radiosensitivity of haematopoietic and 

 digestive systems are still unexplained. From the viewpoint of cellular 

 radiobiology these differences may be due to: (1) a different number of 

 cells affected by the early mass destruction; (2) a different number of 

 cells with lethal chromosome damage ; (3) a different rate of cell multi- 

 plication ; (4) differences in the minimum number of cells necessary for 

 the preservation of the viability of the irradiated animal. The answers 

 to these questions w^ill clear up some peculiarities of "bone-marrow" 

 and "intestinal"' death. 



Thus, cellular changes underly the mammalian radiation syndrome. 

 Radioprotective agents exert their influence on the organism by attenu- 

 ating the action of radiation on the cells; the number of viable cells is 

 thus increased and the recovery of mitotic activity proceeds more 

 rapidly. As a result, the regeneration of damaged systems becomes 

 more intensive. 



A series of agents (hypothermia, neurotropic substances, substances 

 linking to haemoglol)in, dimercajDto-compounds) have been shown by 

 the direct measurements of 02-tension in tissues to protect by decreas- 

 ing 02-tension in the tissues. The protective effect ajDpears when 02- 

 tension falls to 50 per cent of the initial level. 



Protective action of the agents mentioned above is due to hypoxia 

 in the cells of radiosensitive organs by accumulation of substances in 

 cells, blocking up of Oo-transport, inhibition of respiratory centres, 

 spasm of vessels, etc. Among various forms of hypoxia only the histo- 

 toxic one exerts no protective action because it does not significantly 

 change the 02-tension in the tissues. The radiojirotective action of hypo- 

 thermia in homoiothermal animals is related to hypoxia arising, appa- 

 rently, as a result of the fact that tissue respiration is inhibited more 



