Inhibition of gap junctional intercellular communication in human teratocarcinoma cells by organochlorine pesticides.
Inhibition of intercellular communication, as measured by metabolic cooperation between 6-thioguanine-sensitive and 6-thioguanine-resistant Chinese hamster V79 cells, has been previously shown to be correlated with a large variety of known tumor promoters, including some of the organochlorine pesticides. Since further evidence concerning the effects of those known or suspected animal tumor promoters on human cells is needed, three organochlorine pesticides, dieldrin, aldrin, and 1,1,1-trichloro-2,2-bis(p-chlorophenyl)ethane (DDT), were tested for their ability to inhibit metabolic cooperation between 6-thioguanine-sensitive (6TGs, HTP3-4) and 6-thioguanine-resistant (6TGr, HTXTG-1) human teratocarcinoma cells. Similar to the effect of the known mouse skin tumor promoter 12-tetradecanoyl phorbol-13-acetate (TPA), all three pesticides inhibited gap junctional intercellular communication within a noncytotoxic dose range. The dose-response curves of these chemicals were similar to those of other known tumor promoters on Chinese hamster V79 cells. In addition, the transfer of [3H]uridine between teratocarcinoma cells in contact was reduced after pesticide treatment.
D000452:Aldrin / Q000633:toxicity; D002450:Cell Communication / Q000187:drug effects*; D002460:Cell Line; D003634:DDT / Q000633:toxicity; D004026:Dieldrin / Q000633:toxicity; D006801:Humans; D007306:Insecticides / Q000633:toxicity*; D007365:Intercellular Junctions / Q000187:drug effects / Q000502:physiology*; D007700:Kinetics; D013724:Teratoma / Q000503:physiopathology*; D014316:Tritium; D014529:Uridine / Q000378:metabolism
D007306:Insecticides; D014316:Tritium; D003634:DDT; D004026:Dieldrin; D000452:Aldrin; D014529:Uridine