Glucose and other transportable sugars and polyols inhibited Clinflux very soon after addition to mycelium in the process of Claccumulation. Under the usual experimental conditions (0.1 mM KCl, glucose 2 2 mM) the mean percentage of inhibition of Cl-influx by glucose was 54.1 + 8.0 (±+ standard error; N = 26). Transport of the exogenous carbohydrate was necessary for inhibition of Clinflux. Thus, the estimated Ki for glucose inhibition of Clinflux (28 ,uM) was close to the Km for glucose transport; glycerol did not inhibit Cl-influx unless it was itself transported, and the degree of inhibition exerted by various carbohydrates correlated with their uptake rates. Inhibition was not caused by the accumulated sugar itself, as high levels (ca. 60 mM) of intramycelial 3-0methylglucose gave rise to a stimulation of Clinflux when the exogenous sugar was removed. It is suggested that interaction of Cl-and carbohydrate transport arises from competition for a common energy-coupling mechanism in the cell membrane. Both glucose and 3-0-methylglucose elicited Cl-efflux, but the maximal Clefflux rates were observed only after 40 min of incubation and only in the presence of the readily metabolizable glucose. Removal of the exogenous glucose, even after maximal Clefflux had been established, resulted in the rapid cessation of efflux. Studies under anaerobic conditions gave further evidence that glucose uptake was necessary and that efflux was not due to temporary depletion of energy reserves. It is proposed that glucose-induced leakage of Clis due to reversal of the Cluptake system, even though the Km for efflux is much greater than that for influx.