D. C. TOSTESON 



141 



the rates of the chemical reactions involved and the resistance of the cell 

 membrane to diffusion of the ions. Formulations of cation transport in human 

 red cells somewhat similar to that proposed here have been advanced by 

 Ponder (85), Maizels (60), and Harris (34). As noted above, the hypothesis 

 suggested by Solomon (100) to account for cation transport in human red 

 cells differs from that formulated here in that it requires four different carrier 

 processes and rejects free diffusion as one of the mechanisms of Na and K 

 movement. The observed high apparent activation energies are the main 

 evidence in favor of the idea that K outflux and Na influx involve a carrier 

 process. As noted in the theoretical section, mechanistic interpretation of 

 temperature data is too uncertain to justify rejection of diffusion on this 

 basis alone. 



The addition of butanol to human red cells causes K transport to assume 

 the characteristics of a diffusion process. The mechanism of this effect is not 



Table 3. Effect of k concentration in medium on k content of human red cells 



Normal human red cells were incubated in bicarbonate buffer with glucose as substrate 

 at 37°C. 



known. Any proposed explanation must begin with an assumption about the 

 factors responsible for the high resistance of the normal human red cell mem- 

 brane to cation diffusion. As will be elaborated in detail in the section on 

 models, the red cell membrane is in many ways comparable to a highly se- 

 lective, anion permeable membrane. By analogy with artificial membranes 

 possessing these properties we may suppose that there is a high concentration 

 of fixed positive changes in the channels thru which the ions diffuse. Although 

 the identity of the molecules possessing these positively charged groups is not 

 known, it is conceivable that lipoprotein bonds (presumably sensitive to 

 butanol) are responsible for their orientation in the membrane. 



Potassium and sodium transport in sickled S-S cells may be considered inter- 

 mediate between that observed in normal and butanol treated human cells. 

 Transport by diffusion seems substantially greater than in normal cells but 

 not as great as in the butanol cell. On the other hand, transport by chemical 

 reaction is also substantially greater than normal. It is reasonable to suppose 

 that the extreme distortion of the cell surface produced by sickling reduces 



