552 ABNORMALITIES IN METABOLISM 



which can be demonstrated in the urine of dogs poisoned with phos- 

 phorus, and which represents a simple deaminization of tyrosine without 

 further oxidation. It is evident from the urinary findings, therefore, 

 that oxidation is decreased, which is presumably because of the de- 

 struction of liver tissue with its important oxidizing functions. The 

 reduction of oxidation can also be shown experimentally by studying 

 the respiratory exchange, Welsch having found the oxidation decreased 

 by from ^ to }i in phosphorus poisoning. Carbamates do not seem to 

 be present in recognizable amounts, and sugar is also absent. 



In phosphorus poisoning the urinary findings are similar, but with marked 

 quantitative differences. Tyrosine cannot usually be detected, at least by ordinary 

 methods, being found by Riess in but 7 of 36 cases of (human) phosphonis poison- 

 ing, and in but 4 of these was it abvmdant. Leucine is even less frequently found. 

 With experimental animals glycine and other amino-acids have been found" in the 

 urine, and they could probably be found in acute hepatic atrophy if the same 

 delicate methods were employed. Wohlgemuth'^ has indeed found glycine, 

 alanine, and arginine in human urine after phosphorus poisoning. The small 

 quantity of amino-acids in phosphorous poisoning is probably due to the relative 

 slowness of the autolytic changes. On the other hand, the deficiency of oxidation 

 in phosphorus poisoning is shown by the abundant elimination of organic acids, 

 Riess having obtained as high as 4 to 6 grams of the zinc salt of paraladic acid 

 from the urine (per liter) in human cases, and its presence seems to be constant. 



The Liver.2^ — In the liver may be found an abundance of the free 

 amino-acids that have not yet escaped by diffusion, their presence 

 having been first detected by Frerichs microscopically. Taylor-^ was 

 able to isolate from a liver weighing 900 grams, 0.35 gm. of leucine 

 and 0.612 gm. aspartic acid, which probably represent much less than 

 the total amount present. Deuteroalbumose was also found, but no 

 peptone, arginine, histidine, or lysine, and glycogen was also absent. 

 In another case that appeared to be the result of chloroform intoxi- 

 cation, Taylor^" obtained 4 grams of leucine, 2.2 grams of tyrosine, 

 and 2.8 grams of arginine nitrate. Wells found several amino-acids 

 free in sufficient quantity to identify in the liver in cases of acute yellow 

 atrophy and chloroform necrosis, an increase in gelatigenous substance 

 in the former, and of organic non-lipoidal phosphorus in both, sulphur 

 being unchanged. The increase in tissue phosphorus is striking, and 

 agrees with Slowtzoff's and Wohlgemuth's^^ finding that the tissue 

 phosphorus persists in experimental phosphorus poisoning. Wake- 

 man^2 found that in phosphorus poisoning of dogs the liver shows 

 a diminution of the hexonc bases as a whole, the arginine being espe- 



28 Abderhalden and Barker, Zeit. physiol. Chem., 1904 (42), 524; Abderhalden 

 and Bergell, ibid., 1903 (39), 464. 



" Zeit. physiol. Chem., 1905 (44), 74. 



" Full analyses and discussion of the chemistry of the liver in acute >ellow 

 atrophy and choloroform necrosis given by Wells, Jour. lOxper. Med., 1907 (9), 

 027; Arch. int. Med., 1908 (1), 5S9; Jour. Biol. Cliem., 190S (5), 129. 



2» Zeit. physiol. Cliem., 1902 (34), 5S0; Jour. Mod. Ucscarcli, 1902 (S), 424. 



3" Univ. of Calif. Publications (Pathol.), 1904 (1), 43. 



3> Biocheiii. Zeit., 1911 (32), 172. 



3^ Jour. Expcr. Mod., 1905 (7), 292; Jour. Biol. Chem., 1908 (4), 119. 



