Glucose at 5 mM inhibited chloride uptake by C h l o r e l l a f u s c a in the light and in the dark by 30-t-10% and acidified the cell interior by 0.2 units (measured with 5.5-dimethyl-oxazolidine-2.4-dione; DMO). Neither effect was shown by the glucose analogues 3-O-methylglucose and 6-desoxyglucose which are transported into the cell but not metabolized. As it was surmised that inhibition of C1-transport was the result of intracellular acidification, the action of other agents on C1transport and intracellular pH was examined. The Tris salts of the permeant acids DMO and propionic acid inhibited C1-transport. The concentration and pH dependence of this effect were consistent with the free acids being the effective agents. At pH 6.7 the 15 mM Tris salts had about the same effect on C1-transport as 5 mM glucose. Under these conditions the intracellular pH (measured by the DMO method) was lowered by 0.2 units with glucose as well as, in presence of the Tris salts. When the algae were gassed with 1.5% CO2 in air, C1-uptake in the light was depressed to 40-50% and the intracellular pH was lowered by 0.4 units. On the basis of these observations and the results from the preceding study, inhibition of C1 transport by glucose is interpreted as inhibition of an ATP-dependent C1-/OH-exchange by intracellular acidification, due to glucose metabolism.