DISCUSSION TO PAPERS BY GEREBTZOFF AND BACQ, BETZ, 

 NEUKOMM, PEGUIRON AND HERVE, AND MAISIN AND FIEVEZ 



Z. M. Bacq : To my mind, the facts gathered by Jacobson and Cole, by Lamerton, 

 Loutit and Maisin, and by those who worked as chemists or cytologists with radiopro- 

 tectors, are just parts of one general story. We must put all these facts together and 

 try to formulate some kind of temporary logical idea which might be useful for 

 further work in these fields. This is what I have attempted in a book with Alex- 

 ander, which is now in press. ^ 



We think that the permeability of the nuclear membrane in haematopoietic tissues 

 of mammals is much increased by ionizing radiations. The nuclear factor (Cole) 

 escapes in large quantities in the cytoplasm, the activity of which is first very much 

 increased (Altman, Richmond and Salomon ; Nizet, Herve and Bacq) ; this factor 

 might escape in the blood ; it is rapidly destroyed and not resynthetized because 

 the nuclei are heavily damaged, if the whole body has received a sufficient dose of 

 radiation. 



If part of the haematopoietic system (bone marrow or spleen) has been shielded 

 or if a chemical protector has been injected, the primary damage to the haemato- 

 poietic system is decreased ; a substantial proportion of nuclei escape destruction ; 

 in these nuclei, the growth factor is synthetized in larger quantities, and the regenera- 

 tion of the haematopoietic system (about which everybody agrees) is activated. 



In my mind, chemical protectors are comparable to an imperfect physical screen 

 which decreases the primary radiation damage. During the first years after the 

 discovery of the phenomenon of chemical protection, many papers, even by our- 

 selves, were published showing that the behaviour of rodents protected by cysteine, 

 glutathione or cysteamine was exactly the same as that of the irradiated controls 

 during the first 2 to 4 days after irradiation. A closer analysis shows that this 

 idea is wrong ; Gerebtzoff and myself have just given evidence that the primary 

 cellular damage (at 6 hours) is less in the spleen of mice irradiated under protection 

 of cysteamine ; Devik, who is here (I hope that he will give us first-hand evidence), 

 has observed that very soon ( 1 hour) after irradiation, the number of mitotic abnor- 

 malities after X-irradiation is significantly reduced if cysteine or cysteamine has 

 been injected before irradiation ; when looking with Gray through some of my 

 published data^, I agreed that small differences which I had considered to be within 

 the limit of error, might show a significant lesser damage in cysteamine injected 

 animals. 



Thus our general idea seems to be consistent with the available observations. 



We would also like to suggest that the factor responsible for the polycythemia in 

 chronic anoxia is identical with the factor which, according to Jacobson and Cole is 

 active on haematopoietic tissues when injected after irradiation^ 



The behaviour of the adrenals is apparently complicated. We» have confirmed 

 previous evidence published by Patt. There is a very rapid drop (already marked 

 1 hour after 800 r, maximal at the second hour) in cholesterol values of the supra- 

 renals of the rat ; the values are normal at 24 hours and drop again to a very low 

 level at 4 days {see Figure 1). The main interest of the figure is that during the first 

 24 hours, the behaviour of the adrenals of rats protected by cysteamine (10 mg/lOOg) 

 is the same as that of the controls. 



Here again it looks at first sight that cysteamine has not protected against the 

 primary action, but we think that further work may show that for a certain, lesser 

 dose of X-rays, there will be a difference between chemically protected and control 

 rats. 



But, as I said in the discussion following Court-Brown's paper, the first hours after 

 irradiation are not a favourable period to observe the action of chemical protectors. 



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