AUTOLYSIS OF THE LIVER 95 



and others. The lecithin disintegrates somewhat more completely, about one- 

 half or two-thirds beinp disintegrated by the time nuclear destruction is complete, 

 after whicli this and all other autolytic change is slow. The change from coagul- 

 able to non-coagulable forms of nitrogen was as follows: Normal spleen, non- 

 coagulable nitrogen, 5.7 per cent, of the total; stage of marked pycnosis, without 

 rhexis or lysis, 7.4 per cent.; stage of karyonhexis and early karyolysis, 2(j.5 jjer 

 cent. ; stage of complete karyolysis, ;^0.3 per cent. That is, when nuclear structures 

 in the spleen have lost their staining properties entirely through autolysis, about 

 72 per cent, of the nuclein nitrogen, 50 per cent, of the insoluble phosphorus com- 

 pounds. 70 per cent, of the coagulable nitrogen, and about two-thirds of the 

 lecithin are still intact. 



Liver Degenerations. — ^Thc 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^^ found that the livers of dogs, taken just as the 

 animals were dying of phosphorus-poisoning, contained free leucine 

 and tyrosine; 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 proc- 

 ess. 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 enzj^mes is an important factor in the liver degen- 

 eration. 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 chloro- 

 form poisoning may, perhaps, be explained in a similar way, the cells 

 behaving exactly as bacteria would do under the same conditions. 

 Taylor^^ has analyzed several livers in degenerative conditions for 

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

 probabl}^ due to chloroform poisoning, and which was from a case 

 clinically resembling acute yellow atrophy. Here he obtained 4 gm. 

 of leucine, 2.2 gm. of tyrosine, and 2.3 gm. of arginine nitrate. Wald- 

 vogel and Tintemann,^* in phosphorus livers, found an increase in 

 protagon, jecorin, fatty acids, cholesterol, and neutral fat, while 

 lecithin w^as decreased. Wakeman" found arginine, histidine, and ly- 

 sine decreased in phosphorus livers in proportion to the total nitro- 

 gen, indicating that the protein-splitting enzyme in this condition 

 either picks out certain varieties of proteins first, or removes the 

 nitrogen-rich constituents most rapidly. ^^ 



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



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



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



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



5^ Considerable quantities of amino-acids of various sorts have been isolated 

 from the liver in acute vellow atrophv and chloroform necrosis bv Wells (Jour. 

 Exper. Med., 1907 (9), 627; Jour. Biol. Chem., 190S (5), 1-29); but the value of 

 these figures is questionable because it is possible that the alcohol in which the 

 tissues were kept before analysis was not strong enough entirely to prevent au- 

 tolysis (Wells and Caldwell. Jour. Biol. Chem., 1914 (19), 57). 



