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首页> 外文期刊>Alcohol >Effect of ethanol administration on Mg(2+) transport across liver plasma membrane.
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Effect of ethanol administration on Mg(2+) transport across liver plasma membrane.

机译：乙醇给药对Mg（2+）跨肝质膜转运的影响。

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Acute and chronic ethanol administration results in a decrease in cellular Mg(2+) content and an alteration of Mg(2+) transport in liver cells. In this study we investigated the extent to which ethanol affects the Mg(2+) transport mechanisms in the liver cell membrane. The functionality of these transport mechanisms was assessed in plasma membrane vesicles purified from livers acutely perfused with varying concentrations of alcohol, livers of animals fed with 6% ethanol for 3 weeks, and the respective controls. Acute alcohol administration had little or no effect on the Mg(2+) extrusion mechanisms present in the apical and basolateral domains of the hepatocyte but completely impaired the Mg(2+) entry mechanism present in the basolateral side of the cell. This effect was already evident at a dose of alcohol as small as 0.01% (~1.5mM). The chronic administration of ethanol, instead, impaired all the Mg(2+) transport mechanisms irrespective of the location and directionality in a time-dependent manner. Taken together, these data indicate a selective sensitivity of the Mg(2+) entry mechanism to acute alcohol administration, whereas the Mg(2+) extrusion mechanisms are affected only after prolonged exposure to alcohol. These results suggest that the defect in hormone-activated Mg(2+) transport observed in the chronic EtOH model [Young, A., Cefaratti, C., & Romani, A. (2003). Chronic EtOH administration alters liver Mg(2+) homeostasis. Am J Physiol 284, G57-G67] depends not only on a reduced cellular Mg(2+) content but also on the impaired Mg(2+) transport mechanisms present in the hepatocyte plasma membrane, in particular the Mg(2+) entry pathway, which prevents the liver cell from restoring cellular Mg(2+) homeostasis.
机译：急性和慢性乙醇管理导致肝细胞中细胞Mg（2+）含量降低和Mg（2+）转运改变。在这项研究中，我们调查了乙醇影响肝细胞膜Mg（2+）传输机制的程度。在从用不同浓度的酒精急性灌注的肝脏，饲喂6％乙醇3周的动物肝脏和各自的对照组中纯化的质膜囊泡中评估了这些转运机制的功能。急性酒精管理对肝细胞的顶端和基底外侧域中存在的Mg（2+）挤压机制几乎没有影响，但完全损害了在细胞基底外侧中存在的Mg（2+）进入机制。在低至0.01％（〜1.5mM）的酒精剂量下，这种效果已经很明显。乙醇的长期管理，相反，损害了所有Mg（2+）的运输机制，而与时间和位置有关的位置和方向无关。综上所述，这些数据表明Mg（2+）进入机制对急性酒精管理的选择性敏感性，而Mg（2+）挤出机制仅在长时间暴露于酒精后才会受到影响。这些结果表明，在慢性EtOH模型中观察到了激素激活的Mg（2+）转运缺陷[Young，A.，Cefaratti，C.，＆Romani，A.（2003）。长期给予EtOH会改变肝脏Mg（2+）的体内稳态。 Am J Physiol 284，G57-G67]不仅取决于减少的细胞Mg（2+）含量，而且取决于肝细胞质膜中存在的受损的Mg（2+）转运机制，特别是Mg（2+）进入通路，阻止肝细胞恢复细胞Mg（2+）稳态。

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