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-α-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 Km 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.
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机译:浸泡在1X溶液中的甘蔗(Saccharum officinarum L.)叶薄壁组织细胞在黑暗中的平均膜电位为-135毫伏。在克隆51 NG 97和H50 7209之间未发现膜电位的差异。一个电泵似乎有助于这些细胞的膜电位。外部添加的糖(25毫摩尔)在克隆51 NG 97中引起以下膜电位去极化(以毫伏为单位):葡萄糖,18±4;半乳糖,24±7; 3-O-甲基葡萄糖,10±4;蔗糖,22±3;果糖,21±7;棉子糖,9±3;甘露醇,0;乳糖,0; melibiose,0;和1-O-甲基-α-半乳糖,0。甘氨酸(25毫摩尔)和丝氨酸(10毫摩尔)分别引起47±7和23±2毫伏的去极化。去极化显示相对于葡萄糖浓度的饱和动力学,Km为3至6毫摩尔。代谢抑制剂KCN和水杨基异羟肟酸共同引起膜电位去极化,并通过25毫摩尔葡萄糖和25毫摩尔棉子糖大大抑制了去极化。在一系列替代实验中,葡萄糖(25毫摩尔)几乎完全抑制了棉子糖,蔗糖和3-O-甲基葡萄糖(均为25毫摩尔)的去极化作用,但仅部分抑制了25毫摩尔甘氨酸的去极化作用。甘氨酸(25毫摩尔)也仅能部分抑制25毫摩尔葡萄糖的去极化作用。完全去极化至25毫摩尔甘氨酸和25毫摩尔葡萄糖相当于由1毫摩尔KCN加1毫摩尔水杨基异羟肟酸引起的膜电位的去极化量。结果与膜运输的共运输机制一致,糖和氨基酸通过单独的载体系统运输。
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