Chronic ethanol reduces immunologically detectable Gq alpha/11 alpha in NG108-15 cells.
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.
Williams
R J
RJ
Department of Pharmacology, School of Medical Sciences, University of Bristol, England, UK.
Kelly
E
E
D004591:Electrophoresis, Polyacrylamide Gel; D000431:Ethanol / Q000494:pharmacology*; D019204:GTP-Binding Proteins / Q000378:metabolism*; D005910:Glioma / Q000378:metabolism* / Q000473:pathology; D006822:Hybrid Cells; D015151:Immunoblotting; D009447:Neuroblastoma / Q000378:metabolism* / Q000473:pathology; D013997:Time Factors; D014407:Tumor Cells, Cultured
D000431:Ethanol; D019204:GTP-Binding Proteins