EFFECTS OF RADIATION ON BACTERIA 419 



present A further difficulty arises in accounting for the first-order kinet- 

 ics frequently observed. If there are many molecules of a given enzyme 

 nresent in the cell, it is difficult to visualize that destruction of a single 

 such molecule would be lethal to the cell. Mcllwain (194G) has suggested 

 that only one or a very few molecules of certain enzymes may be present 

 in the cell If this is the case, the first-order kinetics can be explained. 

 If the extreme possibility, suggested by Mcllwain (1947), that the one or 

 few units of enzyme present in the cell are actually the units of inheri- 

 tance is correct, the lethal-mutation and enzyme-destruction hypotheses 

 of the ultimate damage responsible for the bactericidal effects merge. 



There is increasing evidence to indicate that attempts to explain the 

 bactericidal effects of irradiation on the basis of one mechanism are not 

 realistic Luria (1939), on the basis of microscopic examination ot 

 incubated irradiated cells, suggested that more than one mechanism of 

 killing existed and that an attempt to explain the bactericidal effects of 

 irradiation on the basis of a single mechanism did not seem warranted. 

 For both X rays and ultraviolet, an indirect mechanism is known to pro- 

 duce a portion of bactericidal effects, whereas apparently quite different 

 mechanisms account for the residual effects, although the ultimate dam- 

 age may be the same in both cases. It is interesting to compare some of 

 the known facts concerning E. coU B and B/r from the standpoint of 

 multiple mechanisms. 



Apparently, these two strains differ by mutation of a single gene. 

 Even though closelv related, they show many differences m behavior fol- 

 lomng ultraviolet irradiation. Strain B is much more sensitive than the 

 usual E coli strain (Tables 10-2 and 4), and Witkin (1947) and Roberts 

 and Aldous (1949) have shown that a large part of the killing seems to 

 involve damage to the cell-division mechanism. E. coli B exhibits expo- 

 nential killing with ultraviolet, is one of the few bacterial strains found to 

 exhibit heat reactivation (Anderson, 1949, 1951a; Stein and Meutzner, 

 1950), recovers partially when held in hquid media (Roberts and Aldous, 

 1949)' and does not exhibit catalase reactivation (Latarjet and Caldas, 

 1952)' Strain B/r is much more resistant both to ultraviolet and X rays 

 than strain B, exhibits a sigmoidal survival curve with ultraviolet, shows 

 only a small degree of heat reactivation, does not recover from ultraviolet 

 irradiation in liquid suspension (Roberts and Aldous, 1949), and exhibits 

 a small but definite amount of catalase restoration. Both strains exhibit 

 photoreactivation, and Demerec and Latarjet (1946) have shown that, for 

 equal doses of ultraviolet, the rate of phage resistance-mutation induction 

 is the same in each strain. 



At least two different mechanisms must be postulated to explain these 

 differences in behavior of the two strains following ultraviolet irradiation 

 and the catalase restoration may necessitate a third. Since both B and 

 B/r exhibit photoreactivation, it seems likely that the mitial photo- 



