550 ABNORMALITIES IN MET A BOLISM 



to their acting especially upon the oxidizing enzymes/" leaving the 

 autolytic enzymes and the lipase free to digest the cell and to form 

 fat.^^ That it is particularly the oxidizing enzymes that are attacked 

 is well shown by the chemical findings, and also by Loewy's^^ observa- 

 tion that in poisoning with CNH, which acts by impairing oxidation, 

 the alterations in protein metabolism are very similar to those of 

 phosphorus poisoning.^* To be sure, Lusk^^ found no deficiency in 

 general oxidation in phosphorus poisoning, but this does not signify 

 that the local changes do not depend upon local defective oxidative 

 processes. Furthermore, the marked power of sugar to protect 

 the liver from such poisons as phosphorus and chloroform seems to 

 depend on its furnishing easily oxidizable material to cells with reduced 

 oxidative capacity (Simonds).^^ 



Not only phosphorus but many metals, especially mercurj^, seem 

 able to cause the anatomical changes of acute yellow atrophj-, for 

 the condition has been observed very frequently in persons receiving 

 mercurial and arsenical treatment for syphilis. ^^ Here the syphilis 

 has been held responsible by some, but the fact that in many of the 

 cases the syphilis was quiescent or chronic at the time, and that mer- 

 cury and arsenic are known to kill cells and stimulate autolysis, seems 

 to incriminate the metals, ^'^ at least in some cases. On the other hand, 

 Stewart, ^^'^ calls attention to the fact that acute yellow atrophy occurs 

 especially often after poisoning with picric acid, trinitr o-toluene, dini tro- 

 benzene and aromatic arsenicals; as in all these substances the only 

 common component is the benzene radical, its responsibility is strongly 

 suggested. 



Chemical Changes of Acute Yellow Atrophy 



The Urine. — Most striking, and long regarded as pathognomonic, 

 is the presence of leucine and tyrosine in the urine, first described by 



loSee Verworn, Deut. med. Woch., 1909 (35), 1593; Joannovics and Pick» 

 Arch. ges. Physiol., 1911 (140), 327. 



11 Wells, Jour. Amer. Med. Assoc, 1906 (46), 341. 



12 Cent. f. Physiol., 1906 (19), 23. 



1^ The hypothesis suggested by Quincke (Nothnagel's Handbook, 1899, vol. 18, 

 p. 307) that possibly regurgitation of pancreatic juice up the bile ducts might 

 be responsible for the degenerative changes in the liver, is contradicted by the 

 fact that the bile pressure is greater than the pancreatic juice pressure, and that 

 the bile-ducts and peripheral portions of the lobules are least affected. Nor 

 could Best"" prove that trypsin injected into the liver by way of the bile-ducts is 

 able to cause such changes. (See Wells and Bassoe.^) 



'■* Science of Nutrition, Philadelphia, 1909. 



" Arch. Int. Med., 1919 (23j, 362. P>vin, however, ascribes the protective 

 effect of carbohydrate feeding to the glycogen, which protects the protein-fat 

 emulsion of the liver cell cytoplasm from the action of acids. (Jour. Lab. Clin 

 Med., 1919 (5), 146). 



i« Severin, Zeit. klin. Med., 1912 (76;, 138. Bendig, Mlinch. med. Woch., 1915 

 (62), 1144. 



" Tilcston (Boston Med. and Surg. Jour., 1908 (158), 510) has described a 

 case of acute yellow atrophy from mercurialisin without .svphilis. 



""Stewart, Vining and'Bibby, Jour. Path. Pact., 1919 (.23), Proc. Path. See, 

 p. 120. 



