Ethanol increases hepatocyte water volume.
Ethanol increases hepatocyte water volume.
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乙醇增加肝细胞水量。
DOI：
10.1111/j.1530-0277.1994.tb00110.x
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发表时间：
1994
期刊：
影响因子：
--
通讯作者：
Davis,J
中科院分区：
文献类型：
--
作者：
Wondergem,R;Davis,J
小鼠肝细胞对渗透压应激的反应是跨膜电位Vm的适应性变化，低渗应激使细胞超极化，高渗应激使细胞去极化。Vm的这些变化为离子（如Cl-）的重新分布提供了电动势，这构成了肝细胞体积调节机制的一部分。我们进行了本研究，以确定是否乙醇在体外小鼠肝切片增加肝细胞的水量，以及是否这种肿胀触发适应性变化的Vm。用四甲基铵离子（TMA）负载小鼠肝切片中的细胞。通过离子敏感微电极测量水通量导致的TMA（a1 TMA）细胞内活性变化，计算肝细胞水量变化。乙醇（70 mM）立即增加肝细胞水体积，7 - 8 min达到峰值17%，此时达到平台期。还从预先用4-甲基吡唑（4 mM）处理12小时的小鼠中获得肝切片。乙醇对其肝细胞水体积的影响与未处理小鼠相同，只是开始和峰值延迟2 min。在体积变化过程中，对照组或乙醇处理组细胞之间的肝细胞Vm无差异。相比之下，通过将外部渗透压降低50 mosm而产生的低渗应激使Vm从-30 mV增加至-46 mV。乙醇不抑制这种渗透压应力诱导的超极化，但在257 mM或更高的高浓度下部分抑制。我们推断乙醇诱导的肝细胞肿胀不同于低渗应激引起的肿胀。与细胞内水活性增加相关的细胞事件最有可能引发伴随后者的Vm超极化。因此，我们得出结论，乙醇诱导的肿胀发生时细胞水活性没有变化。这可能是由于乙醇在组成性分泌蛋白质的细胞中保留了大分子。
Mouse hepatocytes respond to osmotic stress with adaptive changes in transmembrane potential, Vm, such that hypotonic stress hyperpolarizes cells and hypertonic stress depolarizes them. These changes in Vmprovide electromotive force for redistribution of ions such as CI−, and this comprises part of the mechanism of hepatocyte volume regulation. We conducted the present study to determine whether ethanol administered in vitro to mouse liver slices increases hepatocyte water volume, and whether this swelling triggers adaptive changes in the Vm. Cells in mouse liver slices were loaded with tetramethylammonium ion (TMA). Changes in hepatocyte water volume were computed from measurements with Ion sensitive micro‐electrodes of changes in intracellular activity of TMA (a1TMA) that resulted from water fluxes. Ethanol (70 mM) increased hepatocyte water volume Immediately, and this peaked at 17% by 7 to 8 min, by which time a plateau was reached. Liver slices also were obtained from mice treated 12 hr prior with 4‐methylpyrazole (4 mM). The effect of ethanol on their hepatocyte water volume was identical to that from untreated mice, except that the onset and peak were delayed 2 min. Hepatocyte Vmshowed no differences between control or ethanol‐treated cells during the course of volume changes. In contrast, hyposmotic stress, created by dropping external osmolality 50 mosm, increased Vmfrom –30 mV to –46 mV. Ethanol did not inhibit this osmotic stress‐induced hyperpolarization, except partially at high concentrations of 257 mM or greater. We infer that ethanol‐induced swelling of hepatocytes differs from that resulting from hyposmotic stress. Cellular events associated with increased activity of intracellular water most likely trigger the hyperpolarization of Vmthat accompanies the latter. We conclude, therefore, that ethanol‐induced swelling occurs without change in cell water activity. This may result from the retention of macromolecules by ethanol in cells that constitutively secrete protein.
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Yoshiro Matsuda：“酒精性肝损伤中肝细胞高尔基体中糖蛋白的积累。”
DOI：
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发表时间：
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期刊：
影响因子：
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作者：
通讯作者：
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高渗介质对肝细胞体积、跨膜电位和细胞内 K 活性的影响。
DOI：
10.1016/0005-2736(91)90123-p
发表时间：
1991
期刊：
Biochimica et biophysica acta
影响因子：
--
作者：
Wang,KN;Wondergem,R
通讯作者：
Wondergem,R
影响因子：
3.4
作者：
KANAL, KM;FULLERTON, GD;CAMERON, IL
通讯作者：
CAMERON, IL
采用直接进样技术对血液和尿液中的酒精进行气相色谱微量分析的简单方法
影响因子：
2.5
作者：
B. Manno;J. E. Manno
通讯作者：
J. E. Manno
影响因子：
13.5
作者：
Ricardo Mastaï;P. Huet;A. Brault;J. Belgiorno
通讯作者：
J. Belgiorno