Inhibition of intercellular gap junctional communication by alkyl ethers and its modulation by cAMP
Language English Country Slovakia Media print
Document type Comparative Study, Journal Article
PubMed
8394517
Knihovny.cz E-resources
- MeSH
- Cell Line MeSH
- Time Factors MeSH
- Bucladesine antagonists & inhibitors pharmacology toxicity MeSH
- Ethylene Glycol MeSH
- Ethylene Glycols antagonists & inhibitors toxicity MeSH
- Caffeine pharmacology MeSH
- Cricetinae MeSH
- Drug Interactions MeSH
- Methyl Ethers antagonists & inhibitors toxicity MeSH
- Cell Communication drug effects MeSH
- Intercellular Junctions drug effects physiology MeSH
- Polyethylene Glycols toxicity MeSH
- Dose-Response Relationship, Drug MeSH
- Animals MeSH
- Check Tag
- Cricetinae MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
- Comparative Study MeSH
- Names of Substances
- Bucladesine MeSH
- Ethylene Glycol MeSH
- Ethylene Glycols MeSH
- Caffeine MeSH
- Methyl Ethers MeSH
- Polyethylene Glycols MeSH
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.
