EFFECTS ON PERMEABILITY AND ACTIVE TRANSPORT 185 



acetate and 2,4-dinitrophenol, but floride can inhibit Na+ transport com- 

 pletely while having only a minor effect on K+ uptake (Schultz and Solo- 

 mon, 1961). 



Correlations between Transport Inhibition and Depression of Glycolysis 



Many workers have claimed to have established the basis for transport 

 inhibition by iodoacetate as the EM pathway — e.g., in yeast (Pulver and 

 Verzar, 1940), duck erythrocytes (Tosteson and Johnson, 1957), human 

 erythrocytes (Wilbrandt, 1940), toad muscle (Muller, 1962), Ehrlich ascites 

 cells (Maizels et al, 1958), calf lens (Kinoshita et al., 1961), rat diaphragm 

 (Del Monte, 1961), and nerve (Shanes, 1952), but in most instances the 

 only evidence has been that a depression of glucose uptake, lactate forma- 

 tion, or CO2 release occurs simultaneously with the inhibition of the trans- 

 port. There is seldom quantitative correlation between the inhibitions and 

 none would be expected: sometimes glycolysis is reduced much more than 

 transport — as in ascites cells, where glycolysis is inhibited 60% and Na+ 

 efflux 36% by 0.07 raM iodoacetate, and in duck erythrocytes, where gly- 

 colysis is inhibited 96% and K+ influx 50% by 1 m.M iodoacetate; but in 

 other cases it seems that rather slight glycolytic inhibition causes marked 

 changes in transport — as in calf lens, where a 31% depression of gly- 

 colysis is accompanied by a marked block of K+ accumulation, or in toad 

 muscle, where a 34% inhibition of glycolysis is again accompanied by severe 

 loss of K+ and gain of Na+. Thus these data alone do not signify the mech- 

 anism of the inhibition at all. A good example of this is given by Craig 

 (1959), who found that perfused frog liver loses K+ as lactate formation 

 is inhibited by iodoacetate, and indeed the concentrations necessary to pro- 

 duce comparable inhibitions are roughly the same; one might conclude that 

 the accumulation of K+ is dependent on glycolysis. However, when the 

 iodoacetate is washed out, the loss of K+ stops while the block of glycolysis 

 persists, leading Craig to conclude that K+ movements are really not re- 

 lated to lactate formation. In at least one case, rabbit kidney slices, 1 n\M 

 iodoacetate has no effect on K+ concentrations, K+ flux, or the exchange- 

 able and nonexchangeable fractions, so that it was concluded that K+ trans- 

 port here is independent of glycolysis (Mudge, 1953). 



Efforts have been made to correlate the effects of iodoacetate on transport 

 and respiration, but it is clear from what has previously been said about 

 respiratory inhibition (page 111) that any relationship observed would be 

 fortuitous. One might predict respiration to be depressed less than transport, 

 and this is borne out in several studies. The following may be cited (in each 

 case the inhibition of transport is given first and then the respiratory inhi- 

 bition): Br- uptake in barley roots (30%-18% by 0.01 mM iodoacetate, 

 90%-62% by 0.05 mM iodoacetate) (Machlis, 1944), K+ uptake by barley 

 roots (81%-24% by 1 mM iodoacetate) (Ordin and Jacobson, 1955), glycine 



