GEORGE T. SCOTT AND HUGH K. HAYWOOD 



47 



nal concenlralion, continues in running sea water in tlie light for about 2 

 hours. At this point a gradual but definite and reproducible re-accumulation 

 begins, the full extent of which could not be measured because of termination 

 of the experiments (fig. 8). 



The cellular sodium concentration after 16 hours in o.ooi m/1. iodoacetate 

 in the dark is increased to 30% above the control level. In contrast to the potas- 



10 20 



HOURS IN LIGHT and 



30 



RUNNING 



50 



Fig. 8. Influence of light and running sea water on the potassium content of Ulva pre- 

 viously maintained for 16 hours in sea water containing o.ooi m/1. iodoacetate in the dark. 

 Zero time on the graph represents time of transfer to running sea water and light. Control 

 samples were illuminated after 16 hours in the dark. 



sium, the net movement of sodium against its concentration gradient begins 

 immediately when the cells are returned to light and running sea water, and 

 restoration of the normal level reaches completion in about 4 hours (fig. 9). 



These experiments indicate that although the iodoacetate causes a marked 

 loss of potassium and gain of sodium by the cell, this effect of iodoacetate can 

 apparently be 'washed out' of the cell in running sea water in the presence of 

 light. Potassium loss ceases whereas sodium ion is secreted out of the cells 

 against its concentration gradient. Attention is directed to the diflFerential 

 behavior of the cell as regards sodium and potassium movements in these experi- 

 ments; i.e. although potassium is progressively lost from the cell for 25 hours 

 sodium is excreted to the normal level within 4 hours. 



Influence of Arsenate on Ion Shifts Caused by Iodoacetate. Two types of 



