Inhibition of intercellular gap junctional communication by alkyl ethers and its modulation by cAMP.
The inhibition of intercellular gap junctional communication (IGJC) by alkyl ethers (ethylene glycol, monomethyl ether, polyethylene glycol 1,000 and polyethylene glycol 6000) was examined using V79 Chinese hamster cells in vitro. Ethylene glycol and monomethyl ether inhibited IGJC very strongly, whilst the other agents inhibited IGJC only insignificantly. When the cells were treated with the combination of two agents, ethylene glycol and monomethyl ether, a significant increase in the inhibition of IGJC occurred. This was probably the result of potentiation rather than an addition effect. The effect of ethylene glycol was antagonized by dibutyryl cyclic adenosine monophosphate (DbcAMP). This effect was most intensive when the cells were treated with both agents at the same time and, in other experimental combinations, the effect was lower but also significant. Caffeine did not influence IGJC either in combination with DbcAMP or by itself.
Vítek
J A
JA
Research Institute of Child Health, Brno, Czech Republic.
D000818:Animals; D003994:Bucladesine / Q000037:antagonists & inhibitors / Q000494:pharmacology / Q000633:toxicity*; D002110:Caffeine / Q000494:pharmacology; D002450:Cell Communication / Q000187:drug effects*; D002460:Cell Line; D006224:Cricetinae; D004305:Dose-Response Relationship, Drug; D004347:Drug Interactions; D019855:Ethylene Glycol; D005026:Ethylene Glycols / Q000037:antagonists & inhibitors / Q000633:toxicity*; D007365:Intercellular Junctions / Q000187:drug effects* / Q000502:physiology; D008738:Methyl Ethers / Q000037:antagonists & inhibitors / Q000633:toxicity*; D011092:Polyethylene Glycols / Q000633:toxicity; D013997:Time Factors
D005026:Ethylene Glycols; D008738:Methyl Ethers; D002110:Caffeine; D011092:Polyethylene Glycols; D003994:Bucladesine; D019855:Ethylene Glycol