Death and Dissolution of the Organism 353 



life, since nothing indicates the destruction of the 

 hypothetical antidigestive enzymes through lack of 

 oxygen. The recent work of Bradley and Morse 1 

 and of Bradley 2 has thrown some light on the problem. 

 These authors found that proteins of the liver which 

 are indigestible can be made digestible by the liver 

 enzymes if an acid salt or a trace of acid is added to 

 the mixture. A m/2OO HC1 solution gives marked 

 acceleration of the autodigestion of the liver. This 

 would explain why autodigestion takes place after 

 oxidations cease. In many if not all the cells, acids 

 are constantly formed during lifetime, e. g., lactic acid, 

 which through oxidation are turned to CO 2 , and this 

 diffuses into the blood so that the H ion concentration 

 in the cells does not rise materially. If, however, the 

 oxidations cease, as is the case after death, the forma- 

 tion of lactic acid continues, but the acid is not oxidized 

 to CO 2 and thus removed, and as a consequence the 

 H ion concentration increases in the cells and the self- 

 digestion of proteins, which the digestive enzymes con- 

 tained in the cells themselves could not attack formerly, 

 becomes possible. Acid increases the digestibility 

 of a protein, probably by salt formation. Theoreti- 

 cally we should not be surprised that while in the liver 

 an increase in the CH favours autolysis in other tissues 



the same -result is produced by the reverse effect. We 



-:. . - ' v -.* -, 



1 Bradley H. C. t and Morse, M., Jour. Biol. Chem., 1915, xxi. f 209. 

 a Bradley, H. C., ibid., 1915, xxii., 113. 

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