G proteins coupled to phospholipase C: molecular targets of long-term ethanol exposure

Per Simonsson, F David Rodriguez, Niklas Loman, Christer Alling

Research output: Contribution to journalArticlepeer-review

Abstract

Long-term ethanol exposure is known to inhibit bradykinin-stimulated phosphoinositide hydrolysis in cultures of neuroblastoma x glioma 108-15 cells. In the present study, [3H]bradykinin binding, GTP-binding protein function, and phospholipase C activity were assayed in cells grown for 4 days in 100 mM ethanol with the aim of elucidating the molecular target of ethanol on signal transduction coupled to inositol trisphosphate and diacylglycerol formation. Ethanol exposure reduced guanosine 5'-O-(3-thiotriphosphate) [GTP(S)]- and, to a lesser extent, NaF/AlCl3-stimulated phosphoinositide hydrolysis, whereas it had no effect on the enzymatic activity of a phosphatidylinositol 4,5-bisphosphate-specific phospholipase C. [3H]Bradykinin binding in the absence of GTP(S) was not influenced by ethanol exposure. However, the reduction in [3H]bradykinin binding seen in control cells after addition of GTP analogue was inhibited in cells grown in ethanol-containing medium. The results indicate that long-term ethanol exposure exerts its effects on receptor-stimulated phosphoinositide hydrolysis primarily at the level of the GTP-binding protein.
Original languageEnglish
Pages (from-to)2018-2026
JournalJournal of Neurochemistry
Volume56
Issue number6
DOIs
Publication statusPublished - 1991

Subject classification (UKÄ)

  • Neurosciences

Free keywords

  • Bradykinin
  • Ethanol
  • Phosphatidylinositol 4
  • 5-bisphosphate
  • Phospholipase C
  • GTP-binding protein
  • NG 108–15 cell line

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