408 h'KTh'OflHESSnE CHANGES 



goes on, and are built up into fat by tlie cell lipase, for in anemic areas 

 the intracellular oxidases cannot destroy these substances as they nor- 

 mally do, because of lack of oxygen. The accumulation of fat in dead 

 areas depends, therefore, on the fact that the constituents of fat can 

 diffuse into the dead tissue, whereas the oxyg-en, being held in the cor- 

 puscles, cannot enter the anemic area.^- It is also possible that where 

 fat is set free by autolysis of dead tissue, or when for any cause free 

 fat or lipoid material is present in the vicinity of living cells, it may 

 be phag:ocyted or in some way infiltrate the cells, causing a fatty meta- 

 morphosis by absorption (Dietrich). 



It is to be supposed that poisons also cause fatty degeneration in 

 a similar way — by interfering with oxidation. We have much evi- 

 dence that in phosphorus, chloroform, and other poisoning associated 

 with fatty degeneration of the liver, oxidation is impaired.^^ If we 

 imagine for a moment, a cell in which oxidation is checked by any 

 means, we shall have in this cell the lipase and the proteolytic en- 

 zymes not balanced, as they normally are by the action of the oxi- 

 dases, and hence the processes of cell autolysis and of the accumula- 

 tion of fat by the lipase will go on uncontrolled. The result will be 

 a disintegrated cell containing- many fat-droplets, i. e., fatty degen- 

 eration.^* In cloudy swelling there also appear droplets stained with 

 osmic acid but not by sudan III, which Hess and Saxl ^^ have shown 

 to result from intravitam cell autolysis, and to be a precursor of true 

 fatty degreneration. 



Work with cells in tissue cultures indicates that fatty changes of 

 all types may occur independently of the circulation. Lambert ^^"^ 

 states that the amount of fat in the culture cells is roughly propor- 

 tional to the amount in the culture medium, and cells rich in fat may 

 move actively and undergo normal mitosis. Lewis, however, observed 

 fatty changes in cells growing in fat-free media, and made the espe- 

 cially interesting observation that cells grown in 2.5-3 per cent, alco- 

 liol will show a rich fat accumulation. Also, an accumulation of fats 



32 See Griesser, Ziegler's Beitr., mil (51), 11.5. 



■■^3 See Welsch, Arch. int. de pliarm. et therap., 1905 (14). 211. 



•"•* Interference with oxidation does not necessarily imply destruction of the 

 oxidases. As yet we know practically notliinn; concerninsi the oxidases of the 

 cells in disease, and the above hyjiothesis has yet to be demojistrated. Duccheschi 

 and Almafjia (Arch. Ttal. Biol., 100.3 (.SO), 20) found the normal amount of 

 lipase in phosphorus-livers, but also observed no decrease in ability to oxidixo 

 salicylic aldehyde, which, however, ''ocs not prove a normal ])ower io oxidize fats. 

 Gierke's observation (Zieji-ler's Bcif'., 1005 (37), 502) tliat "rlycoiren and fat 

 accumulate imdcr identical conditions mifiht be cit(>d as judical injr decreased oxi- 

 dative power. Wells (.Tour. Exper. ^Med., 1010 (12), 007) found that the power 

 of liver tissue to oxidize i)urines was Tiot decreased bv the maximum dearee of 

 fatty defjeneration, but Waldvo<rel (Deut. Arch. klin. ]\Ied., 1007 (SO), :?42) found 

 that obese persons can burn fatty acids which arise in metabolism less readily 

 than normal; and Quinan (Jour. Med. Bes., 1015 (.32), 73) found the ester- 

 splittinp lipolytic enzymes of tlie liver much reduced in the liver of chloroform 

 necrosis, but the relation of these esterases to true lipases is Tiot known. 



3n Virchow's Arch., 1010 (202), 140. 



35n Trans. Assoc. Amer. I'hys., 1013 (0), 03; Jour. Exp. Afcd.. 1014 (10). 30S. 



