80 TISSUE FERMENTS 



tically constant and virtually independent of diet ; neverthe- 

 less it varies with the state of functional activity of the 

 tissue. In fetal tissues it is at minimum, but the amount 

 of erepsin rapidly increases as development proceeds, reach- 

 ing the maximum soon after birth. It is asserted, too, that 

 the increased protein destruction which is brought about by 

 excessive thyroid substance entering the system is also mani- 

 fested by increase of post-mortem autolysis 10 ; although 

 these statements have been opposed. Addition of thyroid 

 material has not been found to directly increase autolysis 

 (consult Vol. I of this series, p. 450, Chemistry of the 

 Tissues ) . It has been found that autolysis is decidedly more 

 active in case of animals which have fasted before death 

 than in those that were well nourished. 11 It is possible to 

 interpret this as a continuation of the tissue destruction 

 which is going on in marked degree in fasting ; but one might 

 on the other hand be justified in assuming just the opposite, 

 namely, that the "functional activity " of the tissues is 

 lowered in states of fasting while their digestive ability is 

 increased, in line with the fall in quantity of erepsin in the 

 tissues of hibernating animals and persons reduced by 

 disease which Vernon very satisfactorily demonstrated. 12 

 A number of objections have been presented against 

 regarding autolysis as a physiological or vital process. - It is 

 said that autolysis cannot possibly be a direct continuation of 

 a vital process because it does not appear immediately when 

 death occurs, but after a period of latency of several hours. 13 

 Then, too, the predilection of the autolytic ferments for an 

 acid reaction has been made an objection 14 ; (although this 

 is answered by the fact that even with the natural reaction 



10 Cf. G. Bayer (M. Lowit's Lab., Innsbruck), Sitzungsbericht d. Wiener 

 Akad., 118'", 181, 1909. 



11 J. E. Lane-Claypon and S. B. Schryver, Journ. of PhysioL, 31, 169, 1904. 



M H. M. Vernon, Journ. of PhysioL, 38, 81, 1905. 



13 Lane-Claypon and Schryver, 1. c. 



14 H. Wiener (J. Pohl's Lab., Prague), Centralbl. f. PhysioL, 19, 349, 1905. 



