Effect of biological toxins on gap-junctional intercellular communication in Chinese hamster V79 cells.
Since chemical modulation of gap-junctional intercellular communication has been implicated in several toxicological endpoints, a study to examine the ability of several biological toxins to inhibit this process was undertaken. Eight biological toxins were tested for their ability to inhibit metabolic cooperation, a measure of gap-junctional intercellular communication, in the Chinese V79 cell system. Aplysiatoxin, anhydrodebromoaplysiatoxin and debromoaplysiatoxin showed the strongest ability to inhibit metabolic cooperation while T2-toxin and vomitoxin inhibited metabolic cooperation to a lesser degree. Aflatoxin B1, aflatoxin B2 and palytoxin were inactive in the Chinese V79 system. Palytoxin, which was extremely cytotoxic, might act as a tumor promoter if it induces compensatory hyperplasia in vivo.
D000818:Animals; D002470:Cell Survival / Q000187:drug effects; D002478:Cells, Cultured; D006224:Cricetinae; D003412:Cricetulus; D007365:Intercellular Junctions / Q000187:drug effects*; D008387:Marine Toxins / Q000378:metabolism / Q000633:toxicity*; D009183:Mycotoxins / Q000378:metabolism / Q000633:toxicity*; D012717:Sesquiterpenes / Q000633:toxicity*; D014255:Trichothecenes / Q000378:metabolism / Q000633:toxicity*
D008387:Marine Toxins; D009183:Mycotoxins; D012717:Sesquiterpenes; D014255:Trichothecenes; C007262:deoxynivalenol