86 The Chemistry of the Injured Cell 



failure of ketogenesis, lipogenesis and oxidation of acetate to C0 2 

 (Rosecan et al., 1955) . Mitochondria isolated from the liver at this 

 stage show impaired succinic dehydrogenase activity, presumably 

 because of altered permeability especially when diphosphopyridine 

 nucleotide is added to the medium (Corwin and Schwarz, 1959) . 



Quite recently our colleague Dr. Andre McLean has made an 

 important contribution to our knowledge of the pre-necrotic stage. 

 He has studied the water and ion balance of liver slices incubated 

 in Ringer solution. Slices from pre-necrotic liver are unable to 

 maintain their internal potassium concentration. Slices from con- 

 trol animals, given vitamin E, show no such defect. 



This defect is found long before the respiratory decline de- 

 scribed by Schwarz's group. McLean suggests that respiratory de- 

 cline is secondary to alteration of water and ion distribution in the 

 liver slices. (See also Chapter I.) 



The finding that selenium prevents dietary necrosis but has 

 no effect on any of the biochemical lesions so far discovered suggests 

 that we have not yet defined the biochemical lesion of dietary liver 

 necrosis. However, the description of a lesion that affects primarily 

 intracellular water and ion balance is of interest. Such lesions may 

 well be found in other pathological states. 



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 Daft, F. S., Sebrell, W. H. and Lillie, R. D. (1942) : Proc. Soc. exp. Biol 



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