210 CHARLES PACKARD 



there was a strength of radiation which produced no noticeable 

 affect, i.e., the initial acceleration was overcome by a subse- 

 quent retard. These similarities strengthen the view that in 

 living eggs the- changes in division rate are brought about by 

 changes in the rate of enzynie action. 



Assuming this hypothesis to be the correct explanation, it 

 remains to explain why an acceleration or retard of the enzyme 

 action can account for the differences in response under similar 

 exposures during different phases of mitosis. Mathews sug- 

 gests that while the nuclear wall is intact the enzymes are re- 

 stricted in their action, but that they are able to produce oxida- 

 tions as soon as the nuclear wall breaks down, that is, just 

 before the metaphase. Then a mild radiation, during the pro- 

 phase, although it activates the enzymes, results in little change 

 in the egg since they are unable to act to advantage. But when 

 the nuclear wall disappears and, under normal condition, active 

 oxidation takes place, a slight radiation activates them as 

 before, but because they are able to react with the protoplasm 

 more vigorously than before, their activation leads to a more 

 marked acceleration. If the radiation is more intense a retard 

 results, that is, the optimum radiation has been exceeded and 

 the enzymes are injured. These results are analogous to those 

 obtained by treating protoplasm with poisons. A small amount 

 of CO2 accelerates muscular action while a larger amount re- 

 tards it. 



This hypothesis throws light on the well recognized fact that 

 actively dividing cells are more susceptible than those which 

 are not undergoing mitosis. Slow growing tumors are not 

 susceptible (unless they are superficial and can be so intensely 

 radiated that the protoplasm is injured) while rapidly proliferat- 

 ing tumor cells are very susceptible. 



