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首页> 外文期刊>American Journal of Physiology >Transport model of the human Na+-coupled L-ascorbic acid (vitamin C) transporter SVCT1
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Transport model of the human Na+-coupled L-ascorbic acid (vitamin C) transporter SVCT1

机译：Na +偶联的L-抗坏血酸（维生素C）转运蛋白SVCT1的转运模型

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First published December 19, 2007; doi:10.1152/ajpcell.00439.2007.-Vitamin C (L-ascorbic acid) is an essential micronutrient that serves as an antioxidant and as a cofactor in many enzymatic reactions. Intestinal absorption and renal reabsorption of the vitamin is mediated by the epithelial apical L-ascorbic acid cotrans-porter SVCT1 (SLC23A1). We explored the molecular mechanisms of SVCTl-mediated L-ascorbic acid transport using radiotracer and voltage-clamp techniques in RNA-injected Xenopus oocytes- L-Ascorbic acid transport was saturable (K0.5 approx = 70 muM), temperature dependent (Q10 approx = 5), and energized by the Na+ electrochemical potential gradient. We obtained a Na+-L-ascorbic acid coupling ratio of 2:1 from simultaneous measurement of currents and fluxes. L-Ascorbic acid and Na+ saturation kinetics as a function of cosubstrate concentrations revealed a simultaneous transport mechanism in which binding is ordered Na+, L-ascorbic acid, Na+. In the absence of L-ascorbic acid, SVCT1 mediated pre-steady-state currents that decayed with time constants 3~(-1)5 ms. Transients were described by single Boltzmann distributions. At 100 mM Na+, maximal charge translocation (Smax) was 25 nC, around a midpoint (V0.5) at -9 mV, and with apparent valence approx =-1. Qmax was conserved upon progressive removal of Na+, whereas V0.5 shifted to more hyperpolarized potentials. Model simulation predicted that the pre-steady-state current predominantly results from an ion-well effect on binding of the first Na+ partway within the membrane electric field. We present a transport model for SVCT1 that will provide a framework for investigating the impact of specific mutations and polymorphisms in SLC23A1 and help us better understand the contribution of SVCT1 to vitamin C metabolism in health and disease.
机译：首次发布于2007年12月19日; doi：10.1152 / ajpcell.00439.2007.-维生素C（L-抗坏血酸）是一种必不可少的微量营养素，可在许多酶促反应中充当抗氧化剂和辅助因子。维生素的肠吸收和肾脏重吸收是由上皮根尖的L-抗坏血酸共转运蛋白SVCT1（SLC23A1）介导的。我们使用放射性示踪剂和电压钳技术探索了RNA注射非洲爪蟾卵母细胞中SVCT1介导的L-抗坏血酸运输的分子机制-L-抗坏血酸运输是饱和的（K0.5大约= 70μM），温度依赖性（Q10大约10） = 5），并由Na +电化学势梯度激发。通过同时测量电流和磁通，我们获得了Na + -L-抗坏血酸的耦合比为2：1。 L-抗坏血酸和Na +饱和动力学作为共底物浓度的函数揭示了一种同时转运机制，其中结合是有序的Na +，L-抗坏血酸，Na +。在缺少L-抗坏血酸的情况下，SVCT1介导的稳态前电流随时间常数3〜（-1）5 ms衰减。瞬态通过单个玻尔兹曼分布来描述。在100 mM Na +下，最大电荷移位（Smax）为25 nC，在-9 mV处的中点（V0.5）附近，表观价大约为-1。逐步去除Na +后，Qmax得以保留，而V0.5转移至更多的超极化电位。模型仿真预测，稳态前电流主要来自离子阱对膜电场中第一个Na +结合的影响。我们提出了SVCT1的运输模型，该模型将提供一个框架来研究SLC23A1中特定突变和多态性的影响，并帮助我们更好地了解SVCT1对健康和疾病中维生素C代谢的贡献。

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