Dietary Liver Necrosis 



85 



are constant, but their significance is uncertain since they are met 

 with after any kind of protein deficiency (Kosterlitz, 1947) . 



Massive necrosis sets in explosively. The animal may be in 

 perfect health up to six hours before death, and then suddenly is 

 struck down. In the earliest stages, parenchymal degeneration and 

 necrosis are midzonal and peripheral. Many contiguous liver 

 lobules are soon destroyed while the central and middle zones of 

 many other lobules are involved. Necrosis is coagulative to begin 

 with, and is accompanied by severe nuclear degeneration, but there 

 is little inflammatory reaction, no disturbance in the bile ducts or 

 blood vessels. Later the liver cells break up into a pale, eosinophilic 

 debris stippled with nuclear fragments, while glycogen is com- 

 pletely lost in necrotic cells and is much reduced in surviving cells 

 around the portal tracts (Himsworth, 1950; Abell et al, 1950). 

 Calcification of cellular debris is not uncommon and fat heaps up 

 within unaffected liver and Kupffer cells. Regeneration is promi- 

 nent in surviving cells after a few days and may lead to the forma- 

 tion of regeneration nodules in the stage of post-necrotic scarring. 



CHEMISTRY OF THE LIVER CELLS DURING 

 DIETARY NECROSIS 



Little is known about the chemical changes preceding and ac- 

 companying dietary necrosis. In the pre-necrotic period there is an 

 initial and proportional fall in both dry and wet liver weights. Total 

 lipids, neutral fat, total fatty acid and cholesterol esters show pro- 

 gressive increase, but no additional significant change is found 

 until the onset of necrosis. Glycogen and phospholipid levels re- 

 main unchanged. 



With massive necrosis water and plasma accumulate in the organ 

 giving a considerable increase in wet and dry weights. Free choles- 

 terol is increased, but phospholipid and glycogen greatly diminish 

 in amount (Abell and Beveridge, 1950) . 



Liver slices from pre-necrotic animals consume oxygen at a 

 normal rate for approximately thirty minutes, but the oxygen 

 uptake declines to 30-50 per cent normal during the following hour 

 (Chernick et al, 1955) . This metabolic defect is prevented by 

 agents that prevent liver necrosis. Dying livers also show progressive 



