Abstract: Background and purpose: Gap junctions (GJ) could enhance cytotoxicity induced by chemotherapeutic agents. Previous studies have showed that some of anesthetics exerted effect on GJ and thereby affected the cytotoxicity of X-ray. However, it is still unclear whether etomidate, a commonly used anesthesia adative agent, could alter GJ intercellular communication in tumor cells. This study explored the effect of etomidate on GJ composed of connexin 43 in U87 malignant glioma cells to provide mechanism clues for studies on the effect of anesthetics on the toxicity induced by chemotherapeutic agents. Methods: Sulforhodamine B was used to examine the toxicity of etomidate on U87 malignant glioma cells. The effect of etomidate on GJ function was determined by parachute dye-coupling assay. Results: Pretreatment of etomidate at the concentration of 0.1, 0.5, 1 or 5 μmol/L for 4 h did not induce cytotoxicity in U87 cells. So etomidate at these concentrations would not reduce the amount of GJ on U87 cell membranes. Parachute dye-coupling assay had showed that treatment with 0.5 and 1 μmol/L etomidate for 4 h significantly decreased the dye spread through GJ in U87 cells, while 0.1 μmol/L etomidate had no effect on dye spread of U87 cells through GJ. Conclusion: Etomidate inhibits GJ function in glioma cells.

Key words: Etomidate, Glioma cell, Gap junction