12 The Chemistry of the Injured Cell 



specificity as expansion of the sodium-rich at the expense of the 

 potassium-rich zone. As a result, potassium uptake would be slowed 

 due to fewer potassium-binding sites and to increased difficulty in 

 reaching the inner potassium-rich zone. Simultaneously, more of 

 the sodium ions normally entering the cell will remain in the cell 

 because of more sodium-binding sites. Thus sodium would displace 

 potassium in the intracellular fluid. These changes would explain 

 the observed facts that in cells so injured there is reduced output 

 of sodium, increased output of potassium and that the net loss of 

 potassium equals the net gain of sodium. 



It is clear that there are two rival views of the mechanism 

 whereby cells maintain electrolyte gradients. One view takes the 

 membrane to be the major factor and the internal electrolytes to be 

 freely diffusible. The opposing theory believes specific ion-binding 

 within the cell to be of greater importance. It is obvious that any 

 explanation of electrolyte movements in cell injury must be based 

 on one or the other of these hypotheses. 



The ion-binding theory has been criticised by Rothstein (1959) 

 chiefly on the grounds that no evidence is available of specific 

 potassium or sodium binding by cell constituents. However, since 

 it is now necessary for the protagonists of the membrane theory to 

 postulate specific transport systems or "pumps" for ions other than 

 sodium, a similar objection applies to the membrane hypothesis. 



A dispassionate study of the recent literature reveals that there 

 is much to be said for and against both theories. Electron micro- 

 scopy is now revealing that the cell membrane is not merely a 

 boundary structure but is on the contrary in intimate and variable 

 contact with all parts of the cell interior, as well as being the seat 

 of many metabolic reactions and containing ion-binding radicles. 

 This new concept of the membrane as both cell boundary and an 

 actively metabolising part of the cell interior may perhaps serve to 

 bridge the gap between the two hypotheses of electrolyte transport. 



The relation between in vitro injury such as chilling of tissue 

 slices and injury in vivo may be indicated by some recent experi- 

 ments carried out at University College Hospital by McLean. 

 Young rats fed on the deficient diet described by Himsworth de- 



