50 ELECTROLYTES IN BIOLOGICAL SYSTEMS 



It is to be noted that the sodium movements in these cells are of a distinctly 

 different nature from those of potassium. Thus in the dark arsenate affords 

 no protection against continued sodium entry resulting from the iodoacetate, 

 while in the light a dramatic secretion of sodium to the control level occurs 

 within several hours. 



The action of arsenate in these experiments is presumably to be explained 

 by a mechanism proposed by Warburg and Christian (46) ; that is, arsenolysis 

 at the level of 3-phosphoglyceraldehyde dehydrogenase, with the formation of 

 i-arseno,3-phosphoglyceric acid, and subsequent spontaneous decomposition 

 of this to 3-phosphoglyceric acid. It has been observed in yeast (17) that 

 arsenate offers complete protection against the loss of potassium and gain of 

 sodium usually observed aerobically with iodoacetate. It was proposed, then, 

 that arsenate allows the metabolic pattern to circumvent the site of iodoacetate 

 inhibition and that the 3-phosphoglyceric acid formed is further metabolized 

 via the usual Embden-Meyerhof scheme. 



Several features of the experiment described by figure 10 should be pointed 

 out. First, it is apparent that, so far as the potassium-regulating mechanism is 

 concerned, 3-phosphoglyceraldehyde dehydrogenase is the only enzyme blocked 

 by iodoacetate. Since arsenate is effective when given after iodoacetate (figs. 

 II and 12), the possibility that arsenate acts by preventing the iodoacetate 

 from attacking the enzyme in the first place is not tenable. The most plausible 

 explanation, then, is the one outlined above. The fact that arsenate does not 

 protect against the sodium increase with iodoacetate suggests that the iodo- 

 acetate may be acting on another sulfhydryl enzyme — one which would be 

 essential for an effective sodium pump in the dark, and not necessary for potas- 

 sium accumulation — at a site where this special relief by arsenate is not possible. 

 In accordance with this hypothesis is the observation that added phospho- 

 glycerate in the presence of iodoacetate resulted in no protection against 

 sodium gain but did allow protection against potassium loss. 



Such an interpretation is consistent with the data shown in figures 11 and 

 12. Again the arsenate relieves the potassium loss resulting from iodoacetate. 

 It is important to note that this relief is almost certainly in no part due to a 

 washing out of the inhibitor since profound potassium loss occurs for many 

 hours after transfer from iodoacetate to light and running sea water as already 

 described. Furthermore, as mentioned above, iodoacetate inhibition is essen- 

 tially irreversible. The protection in the dark after transfer to arsenate would be, 

 according to the hypothesis, a measure of arsenolysis of cellular carbohydrate 

 reserves. The additional protection in the light (to the extent of an actual 

 slight reaccumulation) would be the result of additional phosphoglycerate 

 formed in the cells during photosynthesis (3, 13, 35). It should be noted that 

 these samples in the light were actively photosynthesizing, as judged by the 

 formation of gas bubbles on the under surfaces of the samples. 



