FORMATION OF FERMENTS OF GASTRIC JUICE. 543 



pepsin, but would yield the same under appropriate treatment. The 

 differentiation of the one from the other was further advanced by 

 Langley and Edkins. 1 They confirmed the observation, that alkalies 

 and alkaline salts rapidly destroy pepsin. The conditions influencing 

 the rate of destruction by sodium carbonate were found to be the 

 strength of the solution of the alkaline salt, the time during which it is 

 allowed to act, the temperature of the mixture, and finally the amount 

 of proteids present. By mere neutralisation of an acid solution of 

 pepsin, a considerable amount might be destroyed. If equal volumes of 

 an extract of pepsin and of a 1 per cent, solution of sodium carbonate 

 were mixed, in fifteen seconds as much as 97 per cent, of the pepsin 

 might be destroyed. The greater the amount of proteid present, the 

 greater the amount of sodium carbonate necessary to cause destruction. 

 The difference between pepsin and pepsinogen in their behaviour with 

 different reagents is merely one of degree. Pepsinogen is destroyed 

 also by alkalies, but the destruction is so slow as compared with that of 

 pepsin, that this reaction furnishes a useful method of distinguishing 

 the one from the other. Since the aqueous extract of the gastric 

 mucous membrane of a fasting animal loses but very little peptic 

 power on brief treatment with 1 per cent, sodium carbonate, it follows 

 that pepsinogen, but little or no pepsin, is present in the gastric glands 

 in hunger. Schiff stated that "propepsin" was slowly converted into 

 true pepsin. Langley and Edkins found that the conversion of 

 pepsinogen into pepsin is one of great rapidity. All the pepsinogen 

 present in an aqueous extract of a cat's gastric mucous membrane 

 may be converted into pepsin by treatment with 1 per cent, hydro- 

 chloric acid in sixty seconds. With reference to the point as to 

 whether pepsin is present in the gland cells during digestion, no definite 

 result was arrived at. Pepsin can be obtained from the gastric 

 mucous membrane of an animal in digestion, but not invariably, and 

 such as is found may have been produced by the acid in the lumen of 

 the tubes affecting the pepsinogen in the contiguous chief cells. In the 

 oesophagus of the frog, where no acid is secreted, but only ferment, 

 injection of commercial peptone causes no accumulation of pepsin in 

 the gland cells. Carbonic acid destroys pepsinogen more rapidly than 

 pepsin ; but if only a small quantity of peptone is present, there is 

 practically no destruction. Finally, it is observed that both pepsin and 

 pepsinogen are rapidly destroyed on heating to a temperature of 55 

 57 C. 



(b) The conditions of formation ofrennin (rennet-ferment). -An enzyme 

 which has the property of causing milk or the separated caseinogen 

 to undergo coagulation, is found in the stomachs of almost all animals. 

 As regards the secretion of rennin, there is an important resemblance 

 to that of pepsin, inasmuch as, in the case of the former, there is a 

 precursor of the actual ferment existent in the glands of the stomach 

 which has the power, under the influence of acid, of producing the 

 active enzyme. It was in the case of the rennin that it first was 

 shown that -many of the ferments of the alimentary canal have a 

 zymogen stage. Hammarsten, 2 in 1872, pointed out that the gastric 

 glands of many animals contain reimet-zyniogen, but do not contain 

 rennet-ferment. The zymogens of pepsin and trypsin were not 



1 "Pepsin and Pepsinogen," Journ. Pkysiol., Cambridge and London, 1886, vol. vii. 

 - Jahresb. ii. d. Fortschr. d. Thicr-Chem., Wiesbaden, 1872. 



