THE METABOLISM OF THE PURIN BODIES 427 



In passing, it may be mentioned here that a synthesis of 

 uric acid from glycin and urea has also been supposed to exist 

 in mammals. These two bodies can be combined into uric acid 

 in the laboratory (Horbaczewski). Glycin (amido acetic acid, 

 CH 2 NH 2 COOH), it will be remembered, enters into yet another 

 synthetic process in the organism ; it unites with benzoic acid to 

 form hippuric acid, so that, if benzoic acid be present in excess in 

 the tissues, an increased excretion of hippuric acid results. If uric 

 acid is also formed from glycin, we would expect its excretion to be 

 diminished when the available glycin in the organism is all com- 

 bined with benzoic acid to form hippuric acid as by feeding with 

 benzoic acid. In other words, we would expect the uric and 

 hippuric acid excretions to bear an inverse ratio to one another. 

 Such is, however, not the case. Feeding with substances containing 

 benzoic acid, or which yield it in the process of their metabolism, 

 cause a marked increase in hippuric acid excretion without causing 

 any change in that of uric acid. 1 That urea and glycin when 

 given in excess to mammals do not influence the uric acid excretion 

 has moreover been shown by Horbaczewski and Weiss ( 20 ). 



The urinary purins of mammals are practically all pro- 

 duced by some process different from that obtaining in birds. 

 This process we have seen to be an oxidative one, and the sub- 

 stances which are thus oxidised to be other purin bodies. The 

 purin bodies which are constituent parts of the animal tissues 

 are the oxy-purins (xanthin and hypoxanthin) most abundant in 

 muscle, and the amido -purins (guanin and adenin), integral parts 

 of nuclein. From these two sources, then from nuclein and 

 from muscular tissue endogenous purins might be derived. 



Among the tissue nucleins which are constantly undergoing dis- 

 integration are those of the leucocytes ; an increased leucolysis 

 cell destruction elsewhere remaining constant should consequently 

 run parallel with raised endogenous purin excretion. Now, in- 

 creased leucolysis occurs in certain forms of leucocythaemia, and 

 one of the first indications of the origin of endogenous purins was 

 furnished in 1866 by the discovery of Bartels ( 20 ), that a large 



1 A diet of fruits has been said to diminish the excretion of uric acid and 

 increase that of hippuric acid, because of an organic acid which they contain. 

 This acid is converted into benzoic acid in its passage through the tissues, hence 

 the increase of hippuric acid. The supposed diminution of uric acid, however, 

 has recently been shown to be incorrect. 



