PROTEIN AND CIRCULATION 71 



ance has been attached as a deaminating agent and 

 during recent years discussion of the so-called defect- 

 ive or insufficient deamination in a series of pathologi- 

 cal conditions has come into vogue. 



In accordance with this idea amino acids have been 

 administered as a test for the functional activity of 

 the liver. Glaessner has shown that normal liver tissue 

 is capable of transforming definite amounts of specific 

 amino acids into urea. In a series of experiments he 

 has shown that in various diseased conditions of the 

 liver, such as fatty liver, in syphilis, cirrhotic liver, and 

 a phosphorus poisoned liver a failure to convert amino 

 acids into urea and a consequent output of amino acids 

 in the urine took place. 



That deamination is undoubtedly an important intra- 

 cellular activity may be derived from a series of experi- 

 ments in which amino acids have been fed and their 

 fate determined. Thus with arginine most of the 

 nitrogen reappears as urea. Probably through the 

 intervention of the enzyme, arginase, a splitting of 

 arginine into urea and orinthine occurs and by deami- 

 nation of the latter more urea is formed. Again, 

 after administration of alanine, lactic acid in the urine 

 has been observed. With the purines also it may be 

 shown that a splitting off of ammonia occurs. One 

 may accept without hesitation that the function of 

 deamination is an important activity of cell life. The 

 contention that certain organs or tissues possess this 

 function more specifically than others has been a matter 

 of controversy. The role played by the intestine in 



