Hunter C K, Treanor L L, Gray J P, Halter S A, Hoyumpa A, Wilson F A
Biochim Biophys Acta. 1983 Jul 13;732(1):256-65. doi: 10.1016/0005-2736(83)90210-9.
Ethanol, at concentrations found in the intestinal lumen after moderate drinking, has been shown to inhibit carrier-mediated intestinal transport processes. This inhibition could occur by direct interaction with membrane transporters, dissipation of the energy producing Na+ electrochemical gradient and/or nonspecific alteration of membrane integrity. The latter alteration may be reflected by changes in membrane fluidity, chemical composition or vesicular size. These possibilities were examined with studies in purified brush border membrane vesicles of rat intestine. Ethanol inhibited concentrative Na+-dependent D-glucose uptake in a dose-dependent manner. In contrast, ethanol did not inhibit concentrative D-glucose uptake under conditions of D-glucose trans-stimulation in the absence of a Na+ electrochemical gradient. Ethanol also inhibited initial, concentrative Na+-dependent taurocholic acid uptake, as well as equilibrium uptake. That ethanol exerted a dual effect on transport by increasing membrane conductance for Na+ while decreasing intravesicular space was supported by direct studies of Na+ uptake. Morphometric analysis confirmed that ethanol-treated membranes had a decreased intravesicular size when compared to untreated membranes. Finally, membrane fluidity measured by EPR showed that ethanol had a significant fluidizing effect without producing qualitative changes in membrane proteins, as determined by SDS gel electrophoresis. These results suggest that ethanol inhibits carrier-mediated transport by dissipation of the Na+ electrochemical gradient and alteration of membrane integrity rather than by direct interaction with membrane transporter.
适度饮酒后在肠腔中发现的乙醇浓度已被证明可抑制载体介导的肠道转运过程。这种抑制可能通过与膜转运蛋白的直接相互作用、产生能量的Na +电化学梯度的耗散和/或膜完整性的非特异性改变而发生。后者的改变可能通过膜流动性、化学成分或囊泡大小的变化来反映。通过对大鼠肠道纯化刷状缘膜囊泡的研究来检验这些可能性。乙醇以剂量依赖的方式抑制Na +依赖性D -葡萄糖的浓缩摄取。相比之下，在没有Na +电化学梯度的D -葡萄糖反刺激条件下，乙醇不抑制D -葡萄糖的浓缩摄取。乙醇还抑制初始的、Na +依赖性牛磺胆酸的浓缩摄取以及平衡摄取。通过对Na +摄取的直接研究支持了乙醇通过增加Na +的膜电导同时减小囊泡内空间对转运产生双重作用。形态计量分析证实，与未处理的膜相比，乙醇处理的膜囊泡内大小减小。最后，通过电子顺磁共振测量的膜流动性表明，乙醇具有显著的流化作用，而通过SDS凝胶电泳测定，膜蛋白没有发生定性变化。这些结果表明，乙醇通过耗散Na +电化学梯度和改变膜完整性来抑制载体介导的转运，而不是通过与膜转运蛋白的直接相互作用。
