GEORGE T. SCOTT AND HUGH R. HAYWOOD 



45 



A logical explanation of the action of iodoacetate in the dark is that the 

 glycolytic breakdown of carboliydrate is blocked at the level of phosphoglycer- 

 aldehyde dehydrogenase, the principal site of attack of this inhibitor (14). 

 Accordingly, metabolic energy apparently required for cation regulation is no 

 longer supplied; potassium is lost and sodium gained by the cell. 



The prevention of these ions shifts by light further supports this hypothesis, 

 since phosphoglyceric acid, the compound which is formed by the action of 

 phos{)hoglyceraldehyde dehydrogenase, has been shown to be the first stable 

 product formed in the photosynthetic reduction of carbon dioxide (3, 13). 



4 00 



Fig. 5. Influence of o.oi m/1. iodoacetate on the potassium and sodium content of Valonia 

 macrophysa in the light and dark. 



Hence, in the light, even in the presence of the inhibitor, which prevents the 

 glycolytic formation of phosphoglyceric acid, this intermediate is made avail- 

 able to cellular metabolism by photosynthesis. 



The postulated reactions are summarized in figure 21. 



In the interpretation of the prevention by light of the iodoacetate effect it is 

 essential to know whether or not the cell when illuminated is permeable to the 

 inhibitor. In order to examine this problem the inhibitor was added to samples 

 of Ulva in the light and maintained for 12 hours. At this time samples were 

 transferred to sea water without the inhibitor and placed in the dark. Typical 

 results are presented in figures 6 and 7, indicating a marked loss of potassium 

 and gain of sodium after transfer to the inhibitor-free medium in the dark. 



Washing-out of the iodoacetate elBfect. It is of interest to determine whether 

 or not the ion shifts caused by iodoacetate in the dark are permanent or whether. 



