Effect of sugars and amino acids on membrane potential in two clones of sugarcane.

Sugarcane (Saccharum officinarum L.) leaf parenchyma cells bathed in 1X solution maintained an average membrane potential of -135 millivolts in the dark. No difference in membrane potential was found between clones 51 NG 97 and H50 7209. An electrogenic pump appears to contribute to membrane potential in these cells. Sugars (25 millimolar) added externally caused the following membrane potential depolarizations (in millivolts) in clone 51 NG 97: glucose, 18 +/- 4; galactose, 24 +/- 7; 3-O-methylglucose, 10 +/- 4; sucrose, 22 +/- 3; fructose, 21 +/- 7; raffinose, 9 +/- 3; mannitol, 0; lactose, 0; melibiose, 0; and 1-O-methyl-alpha-galactose, 0. Glycine (25 millimolar) and serine (10 millimolar) caused depolarizations of 47 +/- 7 and 23 +/- 2 millivolts, respectively. Depolarization shows saturation kinetics with respect to glucose concentration, with a K(m) of 3 to 6 millimolar. The metabolic inhibitors KCN and salicyl hydroxamic acid together caused depolarization of the membrane potential and greatly inhibited depolarization by 25 millimolar glucose and 25 millimolar raffinose. In a series of substitution experiments, glucose (25 millimolar) caused almost total inhibition of depolarization by raffinose, sucrose, and 3-O-methylglucose (all 25 millimolar), but only partial inhibition of depolarization to 25 millimolar glycine. Glycine (25 millimolar), also, only partially inhibited depolarization by 25 millimolar glucose. Total depolarization to 25 millimolar glycine and 25 millimolar glucose was comparable to the amount of depolarization of membrane potential caused by 1 millimolar KCN plus 1 millimolar salicyl hydroxamic acid. The results are consistent with a co-transport mechanism of membrane transport, with sugars and amino acids being transported by separate carrier systems.