MECHANISM OF DEATH 367 



death (see next chapter), the theory of Traube seems 

 far too generalized to be accepted as such. It is already 

 partly disproved by the researches of Reichel and 

 Gegenbauer (p. 363). The same criticism applies to 

 a similar theory by Davis (1927). 



A different explanation of toxic action upon cells 

 was given by Rahn (1915) who believed that chemical 

 poisons are catalysts for certain destructive reactions 

 in the cell. He used the well-known parallelism between 

 heat effects and poison effects, (see p. 137) assuming 

 that the poison accelerates the constructive processes 

 as well as the destructive ones, but that the latter are 

 affected more strongly. 



However, it seems most probable that death i.e. 

 loss of power of reproduction by chemical poisoning is 

 caused by the reaction of at least one gene with the 

 poison. Fermentation and similar life processes might 

 still continue after the cell has lost the power to repro- 

 duce. This is the only cause of death likely to give a 

 logarithmic order of death. 



Possibly, some chemicals may not affect the chromo- 

 somes, but inactivate enzymes, destroy membranes or 

 produce other damage. In this case, many molecules 

 must have doubtless reacted before the cell is dead, and 

 this must result in a period of no deaths, a bulging sur- 

 vivor curve and an increasing death rate. 



Gaidukov (1910) defined death as a change from a 

 hydrosol to a hydrogel. He considered the dying of the 

 protoplasm to be a coagulation process. Twenty years 

 later, Bancroft and Richter (1931) came to the same 

 conclusion. They demonstrated the coagulation in the 

 dark field, but failed to prove that the cells showing 

 this symptom were dead. Probably, they had been 

 dead for a considerable time, and coagulation of the 



