730 ADVENTURES IN RADIOISOTOPE RESEARCH 



As first shown by Howard and Pelc (1953) irradiation can stop cell division 

 even in that part of the interphase in which the DNA synthesis, preceding mitosis, 

 is already terminated. Cell division being blocked, DNA synthesis is bound to 

 stop after the lapse of hours the length of which depends on the system investi- 

 gated. We meet here a second indirect way of interference with DNA formation. 

 The third way is a direct interference with DNA synthesis. This is due, as made 

 very probable by Orden and Stock and others, to a disturbance of the template, 

 to a macromolecular lesion as denoted by Mitchell, and also to a change produced 

 in the phosphorylating enzymes. According to te results obtained by Lajtha et al. 

 (1958) investigating i*C incorporation into bone marrow cells, doses below 300 r 

 produce in cells which are in the presynthctic period at the time of radiation a 

 40—50 per cent depression of the number of cells entering the subsequent synthe- 

 tic period in a given time, without affecting the rate of subsequent DNA synthesis. 

 As to the 50 per cent depression of DNA formation due to exposure to radiation 

 Lajtha et al. put forward two alternative suggestions, (a) There are two cell 

 populations in the presynthctic phase, one sensitive and one resistant to small 

 doses of radiations. The sensitive cells can be prevented from entering the synthe- 

 tic period; the resistant ones will enter into and proceed in it undisturbed, (h) All 

 presynthctic cells are sensitive, and the maximum damage results in slowing down 

 the rate of entry into the synthetic period about half. This occurs not in a form 

 of accumulation of presynthetic stage cells just before the beginning of the synthe- 

 tic period, but more likely by slowing down the "progress through the presynthetic 

 period". Thus an unambiguous explanation of the 50 per cent depression of DNA 

 synthesis due to exposure to irradiation is still outstanding. 



References 



H. EuLER and G. Hevesy (1944) Ark. Kemi. A 17, No. 30. 



B. E. Holmes (1947) Brit. J. Radiol. 20, 450. 



B. E. Holmes (1949) Brit. J. Radiol. 22, 260. 



A. Howard and S. R. Pelc (1951) J. Exp. Cell Res. 2, 178. 



S. R. Pelc and A. Howard (1955) Radiation Research 3, 135. 



A. Howard and S. R. Pelc (1953) Heredity Suppl. 6, 261. 



L. G. Lajtha, R. Oliver, T. Kumatori and F. Ellis (1958) Rad. Res. 8, 1. 



