98 ENZYMES 



caseous areas some slight autolysis does occur. The fact that 

 . tuberculosis is, itself, very poor in proteolytic enzymes as 

 compared with most other bacteria may be another factor. 

 When leucocytes are attracted into a tuberculous focus then 

 softening goes on rapidly, showing that there is no loss of 

 digestibility of the caseous material, but merely a lack of 

 enzymes. Pus from a cold tuberculous abscess will not digest 

 fibrin, but if iodoform is injected, leucocytes enter in great num- 

 bers, softening is rapid, and the pus will then digest fibrin 

 (Heile 1 ). 



I/iver Degenerations. The relation of the disintegration 

 observed in phosphorus-poisoning and acute yellow atrophy to 

 the experimental autolysis of the liver has been the object of 

 much study. Salkowski originally pointed out that the same 

 products were found in the blood, urine, and liver tissue in acute 

 yellow atrophy as are produced in autolysis. Jacoby 2 found 

 that the livers of dogs, taken just as the animals were dying of 

 phosphorus-poisoning, contained free leucin and tyrosin ; also, 

 he found that the rate of autolysis of such livers after removal 

 from the body was much greater than in normal livers. The 

 oxidizing ferments (aldehydase) are not destroyed by the pro- 

 cess. He found that addition of minute amounts of phosphorus 

 to liver enzymes did not increase their proteolytic power; 

 nevertheless, he seems inclined to assume that in phosphorus- 

 poisoning alteration in the autolytic enzymes is an important 

 factor in the liver degeneration. It would seem much more 

 probable that phosphorus is a poison that kills cells and does 

 not destroy their autolytic enzymes, hence favoring autolysis. 

 The liver degeneration following chloroform poisoning may, 

 perhaps, be explained in a similar way, the cells behaving 

 exactly as bacteria would do under the same conditions. Tay- 

 lor 3 has analyzed several livers in degenerative conditions for 

 amino-acids and found them only in one liver, which showed 

 necrosis probably due to chloroform poisoning, and which was 

 from a case clinically resembling acute yellow atrophy. Here 

 he obtained 4 gm. of leucin, 2.2 gm. of tyrosin, and 2.3 gm. of 

 arginin nitrate. Waldvogel and Tintemann, 4 in phosphorus 

 livers, found an increase in protagon, jecorin, fatty acids, cho- 

 lesterin, and neutral fat, while lecithin was decreased. Wake- 

 man 5 found arginin, histidin, and lysin decreased in phospho- 



1 Zeit. klin. Med., 1904 (55), 508. 

 2 Zeit. f. physiol. Chem., 1900 (30), 174. 



3 Univ. of Calif. Public, (pathol.), 1904 (1), 43. 



4 Cent. f. Path., 1904 (15), 97. 

 5 Berl. klin. Woch., 1904 (41), 1067. 



