1 64 BIO-CHEMICAL JOURNAL 



have been discovered, which are in accord with the theory of 

 metabolism just propounded. 



The cases of deficiency of oxygen have been investigated 

 by Frankel and Geppert 4 and v. Terray 5 . The latter has shown that 

 there is not only an increased nitrogenous output, but also an 

 elimination of acids, such as lactic acid, in the urine. The cause of 

 the increased nitrogenous output is here clear. Owing to lack of 

 oxygeiij the oxidation of carbohydrate does not proceed to the 

 formation of the final product, carbonic acid, which is rapidly 

 eliminated by the lungs ; intermediary bodies, such as lactic acid, 

 are formed, in the presence of which, the autolytic enzyme is brought 

 into play, and so tissue degradation takes place. It is of interest to 

 note, that increased nitrogenous output does not take place directly 

 after a deficiency of oxygen ; it generally follows in the succeeding 

 days. This delay corresponds to the latent period of autolysis, and 

 there is sufficient ammonia present to neutralize the lactic acid when 

 first formed. 



A similar explanation can be applied to the case of phosphorus 

 poisoning, for Bauer 6 has shown that administration of phosphorus 

 causes a diminished output of carbonic acid and a decreased oxygen 

 consumption ; it acts as a toxin to the oxydases. 



We see from the above researches that the autolytic enzyme 

 functions, by setting up tissue degradation when the food supply is 

 insufficient for the energy needs of the organism ; in this case, these 

 needs are supplied by the utilization of degradation products of the 

 tissue. In this case autolysis is a strictly physiological process. 



There are, however, cases in which the process is pathological, as 

 for example, in atrophy of the liver, in phosphorus poisoning, etc. 

 Such conditions can result, as the above researches indicate, from a 

 variety of causes, such, for example, as insufficient respiration, local 

 stasis, etc. The difference between physiological and pathological 

 autolysis is probably quantitative rather than qualitative ; in the former 

 case, it always proceeds at such a rate, that the tissue, by the mechanism 

 already demonstrated, never becomes strongly acid ; in the latter 

 case, it is possible that the acid is produced at such a rate, that 



