Williams R J, Kelly E
Department of Pharmacology, School of Medical Sciences, University of Bristol, England, UK.
J Neurochem. 1993 Sep;61(3):1163-6. doi: 10.1111/j.1471-4159.1993.tb03637.x.
Recent work has shown that chronic ethanol treatment inhibits receptor-stimulated phosphoinositide hydrolysis in NG108-15 cells and that ethanol exerts this effect primarily at the level of the guanine-nucleotide binding protein (G protein). Here we investigated the effects of ethanol exposure on the expression of Gq alpha/11 alpha, two highly homologous G protein alpha-subunits that have been implicated as regulators of phosphoinositidase C. Addition of ethanol (10-200 mM) to the culture medium for 48 h caused a concentration-dependent decrease in the immunologically detectable levels of Gq alpha/11 alpha. A small (approximately 15%) reduction in Gq alpha/11 alpha was observed after only 6 h of exposure to 200 mM ethanol, but membrane levels were reduced by 31% at 48 h. The ethanol-induced loss of Gq alpha/11 alpha was apparently independent of factors present in the foetal calf serum component of the culture medium. These results suggests that the decrease in receptor-mediated phosphoinositide hydrolysis following chronic ethanol treatment of NG108-15 cells may be mediated in part by a reduction in the membrane levels of Gq alpha/11 alpha.
近期研究表明，慢性乙醇处理可抑制NG108 - 15细胞中受体刺激的磷酸肌醇水解，且乙醇主要在鸟嘌呤核苷酸结合蛋白（G蛋白）水平发挥此作用。在此，我们研究了乙醇暴露对Gqα/11α表达的影响，这两种高度同源的G蛋白α亚基被认为是磷脂酶C的调节因子。向培养基中添加乙醇（10 - 200 mM）48小时，导致Gqα/11α的免疫检测水平呈浓度依赖性下降。仅暴露于200 mM乙醇6小时后，Gqα/11α就出现了小幅（约15%）降低，但48小时时膜水平降低了31%。乙醇诱导的Gqα/11α丢失显然与培养基中胎牛血清成分中的因素无关。这些结果表明，慢性乙醇处理NG108 - 15细胞后受体介导的磷酸肌醇水解减少可能部分是由Gqα/11α膜水平降低介导的。
