Jones D P, Miller L A, Chesney R W
Department of Pediatrics, University of Tennessee, Memphis 38163, USA.
Pediatr Res. 1995 Feb;37(2):227-32. doi: 10.1203/00006450-199502000-00017.
Taurine is a beta-sulfonic amino acid that serves as a nutrient important for developing brain and retina and as an osmolyte in the medullary collecting duct. The activity of the taurine transport system is regulated by substrate supply and by the external osmolality; these two stimuli induce changes in taurine transport. Increased medium osmolality (500 mosmol) stimulates taurine uptake into MDCK cells but not LLC-PK1 cells. The enhanced taurine uptake that occurs in response to hyperosmolality is localized primarily to the basolateral surface of MDCK cells, whereas the adaptive response to medium taurine concentration is expressed on both the apical and the basolateral surfaces of both cell lines. The response of MDCK cells to medium osmolality requires protein synthesis and RNA transcription and is expressed in the presence of microtubular toxins. When cell monolayers were loaded with taurine by incubation in high-taurine medium before increasing medium osmolality, the expected increase in taurine uptake was blunted. Similarly, increased external beta-alanine (500 microM) also prevented the anticipated increase in taurine accumulation in response to hypertonicity; aminoisobutyric acid and betaine (500 microM) partially prevented the increase in taurine transport after hypertonicity, whereas L-alanine had no effect. The concentration of taurine or structurally similar analogs in the external medium might modify the response of taurine accumulation after exposure to hypertonic medium, in that taurine-replete cells behave differently than taurine-depleted cells. These studies indicate that there are at least tow distinct mechanisms involved in the regulation of taurine transport: external taurine concentration and medium osmolality, with taurine concentration seeming to be the predominant stimulus.(ABSTRACT TRUNCATED AT 250 WORDS)
牛磺酸是一种β-磺酸氨基酸，它是发育中的大脑和视网膜所需的重要营养素，也是髓质集合管中的一种渗透溶质。牛磺酸转运系统的活性受底物供应和外部渗透压调节；这两种刺激会引起牛磺酸转运的变化。中等渗透压升高（500毫渗量）会刺激牛磺酸摄取进入MDCK细胞，但不会刺激其进入LLC-PK1细胞。高渗引起的牛磺酸摄取增强主要定位于MDCK细胞的基底外侧表面，而两种细胞系对培养基中牛磺酸浓度的适应性反应则表现在顶端和基底外侧表面。MDCK细胞对培养基渗透压的反应需要蛋白质合成和RNA转录，并且在存在微管毒素的情况下也会表现出来。当在增加培养基渗透压之前通过在高牛磺酸培养基中孵育使细胞单层加载牛磺酸时，预期的牛磺酸摄取增加会减弱。同样，增加外部β-丙氨酸（500微摩尔）也可防止因高渗而预期的牛磺酸积累增加；氨基异丁酸和甜菜碱（500微摩尔）可部分防止高渗后牛磺酸转运的增加，而L-丙氨酸则无作用。外部培养基中牛磺酸或结构相似类似物的浓度可能会改变暴露于高渗培养基后牛磺酸积累的反应，因为富含牛磺酸的细胞与缺乏牛磺酸的细胞表现不同。这些研究表明，至少有两种不同的机制参与牛磺酸转运的调节：外部牛磺酸浓度和培养基渗透压，其中牛磺酸浓度似乎是主要刺激因素。（摘要截短于250字）
