Again the question arises: Why do the tissues not undergo autolysis during lifetime and what protects them, and the answer is that self-digestion is a consequence of the lack of oxidations. The presence of antiferments must continue after death and cannot be the cause which prevents the self-digestion during life, since nothing indicates the destruction of the hypothetical antidigestive enzymes through lack of oxygen. The recent work of Bradley and Morse[298] and of Bradley[299] 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/200 HCl 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 CO₂, 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 formation of lactic acid continues, but the acid is not oxidized to CO₂ 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 contained in the cells themselves could not attack formerly, becomes possible. Acid increases the digestibility of a protein, probably by salt formation. Theoretically we should not be surprised that while in the liver an increase in the C_{H} favours autolysis in other tissues the same result is produced by the reverse effect. We might say that the preservation of a certain C_{H} probably at or near the point of neutrality during life prevents self-digestion, while the gross alteration of the C_{H} in either direction after death (or after the cessation of oxidations in the tissues) induces autolysis. Bradley indeed suggests that many of the phenomena of autolysis during lifetime, such as atrophy, necrosis, involution, might be due to an increase in the C_{H} in the tissues. [298] Bradley, H. C., and Morse, M., _Jour. Biol. Chem._, 1915, xxi., 209. [299] Bradley, H. C., _ibid._, 1915, xxii., 113. These facts agree with the suggestion of Fermi that in the living cell the proteins cannot be attacked by the digestive enzymes but relieves us of the necessity of making the monstrous assumption of a “living molecule” of proteins as distinct from a “dead” molecule. The difference between life and death is not one between living and dead molecules, but more likely between the excess of synthetic over hydrolytic processes.