L. H. GRAY 



were irradiated in low concentrations in a vessel which permitted constant 

 equilibration throughout the irradiation by bubbling the suspension in a gas 

 of the required composition. I described in a previous lecture the manner in 

 which Dr. Deschner and I have investigated this relation for Ehrlich ascites 

 tumour cells — the only mammalian cells so far examined. 



The results which Dr. Deschner and I obtained^ with ascites tumour cells 

 conform well to the relation proposed by Howard-Flanders and Alper 

 (Figure 1), namely: 



S-S. 



^-={m-\) 





where a?? = 3 + • 2 and K = b ±2 [jlM/1. at room temperature. 



^-r^-ui^ 



a '>'2- 



■Smax 



m-K 



05-1 



K 20 60 100 150 



Oxygen concentration 



J I I I 1 I L 



'max 



20 40 60 80 

 Oxygen tension 



100 



/ 



1350 

 p, M/L 



760 

 mmHg 



Figure 1. Influence of oxygen on radio-sensitivity (Erhlich ascites 



tumour cells) 



Under conditions in which cellular respiration was poisoned by Cupferron 

 (ammonium N-nitrosophenylhydroxylamine), Kihlman^ evaluated m and A' 

 for chromosome structural damage induced in Vicia faba roots by X radia- 

 tion. The observed \alue of m was significantly higher than the value for m 

 of 3 found by Kihlman and others'''^'^ in the absence of Cupferron. The 

 value oi K, on the other hand, was, within the limits of experimental error, 

 the same as for bacteria, yeast, and tumour cells {see Table 2). 



The cells composing most tissues exist at a variety of oxygen tensions, 

 depending on their distance from the source of supply of oxygen and on the 

 cellular respiration rate ((^o.) of the intervening cells. This is most evidently 



155 



