EFFECTS OF LOW X-KAY DOSES 25 



is, however possible that the reticiilo-endothelial system could participate in 

 this increase in the number of marrow cells as Pape (1951) has pointed out. It 

 is curious that notwithstanding the higher erythropoietic activity after 1 r, the 

 reticulocyte count is enhanced by about the same amount in the 1 r and 0-1 r 

 groups. This last test could be a very sensitive one. 



Actually we know different causes for an enhancement of erythropoietic 

 activity (excluding radiation), pre- (Valentine and Pearce, 1952; Stohlman 

 et al., 1955) and post-irradiation bleeding, or post-irradiation administration 

 of ^-aminopropiophenone (Stohlman et al., 1955) but in all these experiments, 

 the increase of erythropoietic activity is a result of hypoxia induced by bleed- 

 ing or PAPP. After 1 r or 0*1 r, we cannot speak of hypoxia. 



It is also very curious to note that the increase in the number of marrow 

 cells follows a very great gradient of X-ray dose. We have already pointed out 

 that 50 r also significantly increases the number of marrow cells, at least 

 between 7 and 21 days after (Maisin, 1961). One hundred roentgen is too 

 much (Maisin, 1959). The fact that the increase in the number of cells is 

 already so substantial after no more than one roentgen could ex^^lain even 

 pathological modifications occurring much later in marrow and lymph nodes; 

 for example the absence of threshold or a very low one in post-irradiation 

 leukaemogenesis occurring after repeated low doses (Lorenz et al., 1955). A 

 similar mechanism occurring after small X-ray doses in other organs not even 

 radiosensitive (Knowlton and Hempelmann, 1949) could also explain the 

 appearance of cancer in those organs (Lorenz et al., 1955). 



Finally we can be assured that the increase in cell numbers which must be 

 a consequence of mitotic activity is not synonymous with radioresistance and 

 that in the rat, radioresistance is not a question of the size of the pre- 

 irradiation dose for we gave a very large gradient of dose without ever 

 obtaining radioresistance. 



EEFEEENCES 



Betz, H. (1950). C.R. Soc. Biol., Paris 144, 1439. 



Dacquisto, M. p. (1959). Radiation Res. 10, 118. 



Knowlton, N. P., and Hempelmann, L. H. (1949). J. cell. comp. Physiol. 33, 73. 



Lorenz, E., Hollcroft, J. W., Miller, E., Congdon, C. C, and Schweisthal, R. 



(1955). J. nat. Cancer Inst. 15, 1049. 

 Maisin, H. (1959). Syndrome medullaii-e apres irradiation, Arscia, Bruxelles. 

 Maisin, H. (1961). Congres Association Radiobiologistes de I'Euratom, RapaUo (in press). 

 Pape, R. (1951). Radiol. AiLstriaca 4, 35. 

 Pape, R., and Jellinke, N. (1950). Radiol. Austriaca 3, 43. 



Paterson, E., Gilbert, C. W., and Matthews, J. (1952). Brit. J. Radiol. 25, 427. 

 Stohlman, F., Jr., Cronkite, E. P., and Brecher, G. (1955). Proc. Soc. exp. Biol., N.Y. 



88, 402. 

 Valentine, W. N., and Pearce, M. L. (1952). Blood 7, 1. 



