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长期乙醇暴露后糖蛋白残基作为钙离子受体位点的修饰。

Modification of glycoprotein residues as Ca2+ receptor sites after chronic ethanol exposure.

作者信息

Ross D H, Kibler B C, Cardenas H L

出版信息

Drug Alcohol Depend. 1977 Sep-Nov;2(5-6):305-15. doi: 10.1016/0376-8716(77)90033-3.

Abstract

Previous studies have demonstrated that chronic low-dose administration of ethanol in the drinking fluid of rats produces an increase in content of calcium on synaptic membranes. In the present study, ethanol was studied in vitro and in vivo for its effects on Ca2+ binding to a high affinity receptor site on synaptic membranes. Ethanol (1-50 micrometer) significantly inhibits the binding of Ca2+ in non-competitive fashion, together with inhibiton of a cooperative mechanism for Ca2+ binding. Ruthenium red and neuraminidase were used to probe surface glycoprotein sites as receptors for Ca2+. Use of these probes together with ethanol in vitro or in vivo suggests that increases in Ca2+ receptor sites after chronic ethanol exposure are related to an increase in sialic acid exposure, possibly as a result of conformational changes in membrane protein. These findings are consistent with the hypothesis that chronic low-dose exposure to ethanol causes changes in proteins of synaptic membranes, which may in turn regulate the cellular adaptation to ethanol.

摘要

先前的研究表明,在大鼠饮水中长期低剂量给予乙醇会使突触膜上的钙含量增加。在本研究中,对乙醇在体外和体内对Ca2+与突触膜上高亲和力受体位点结合的影响进行了研究。乙醇(1 - 50微米)以非竞争性方式显著抑制Ca2+的结合,同时抑制Ca2+结合的协同机制。钌红和神经氨酸酶被用于探测作为Ca2+受体的表面糖蛋白位点。在体外或体内将这些探针与乙醇一起使用表明,长期乙醇暴露后Ca2+受体位点的增加与唾液酸暴露的增加有关,这可能是膜蛋白构象变化的结果。这些发现与以下假设一致,即长期低剂量暴露于乙醇会导致突触膜蛋白发生变化,这可能进而调节细胞对乙醇的适应性。

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