Inoue M, Arias I M
Department of Biochemistry, Kumamoto University Medical School, Japan.
J Biochem. 1988 Jul;104(1):155-8. doi: 10.1093/oxfordjournals.jbchem.a122413.
To elucidate the mechanism of taurine transport across the hepatic plasma membranes, rat liver sinusoidal plasma membrane vesicles were isolated and the transport process was analyzed. In the presence of a sodium gradient across the membranes (vesicle inside less than vesicle outside), an overshooting uptake of taurine occurred. In the presence of other ion gradients (K+, Li+, and choline+), taurine uptake was very small and no such overshoot was observed. Sodium-dependent uptake of taurine occurred into an osmotically active intravesicular space. Taurine uptake was stimulated by preloading vesicles with unlabeled taurine (transstimulation) in the presence of NaCl, but not in the presence of KCl. Sodium-dependent transport followed saturation kinetics with respect to taurine concentration; double-reciprocal plots of uptake versus taurine concentration gave a straight line from which an apparent Km value of 0.38 mM and Vmax of 0.27 nmol/20 s x mg of protein were obtained. Valinomycin-induced K+-diffusion potential failed to enhance the rate of taurine uptake, suggesting that taurine transport does not depend on membrane potential. Taurine transport was inhibited by structurally related omega-amino acids, such as beta-alanine and gamma-aminobutyric acid, but not by glycine, epsilon-aminocaproic acid, or other alpha-amino acids, such as L-alanine. These results suggest that Na+-dependent uptake of taurine might occur across the hepatic sinusoidal plasma membranes via a transport system that is specific for omega-amino acids having 2-3 carbon chain length.
为阐明牛磺酸跨肝细胞膜转运的机制，分离了大鼠肝窦状隙细胞膜囊泡并分析了转运过程。在膜两侧存在钠梯度（囊泡内钠浓度低于囊泡外）时，牛磺酸出现过摄取。在存在其他离子梯度（K⁺、Li⁺和胆碱⁺）时，牛磺酸摄取量非常小且未观察到这种过摄取现象。牛磺酸的钠依赖性摄取发生在具有渗透活性的囊泡内空间。在NaCl存在下，预先用未标记的牛磺酸预加载囊泡（转刺激）可刺激牛磺酸摄取，但在KCl存在下则不然。钠依赖性转运相对于牛磺酸浓度遵循饱和动力学；摄取量与牛磺酸浓度的双倒数图给出一条直线，由此得到的表观Km值为0.38 mM，Vmax为0.27 nmol/20 s×mg蛋白质。缬氨霉素诱导的K⁺扩散电位未能提高牛磺酸摄取速率，表明牛磺酸转运不依赖于膜电位。牛磺酸转运受到结构相关的ω-氨基酸（如β-丙氨酸和γ-氨基丁酸）的抑制，但不受甘氨酸、ε-氨基己酸或其他α-氨基酸（如L-丙氨酸）的抑制。这些结果表明，牛磺酸的Na⁺依赖性摄取可能通过一种对具有2 - 3个碳链长度的ω-氨基酸特异的转运系统跨肝窦状隙细胞膜发生。
