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Effect of biological toxins on gap-junctionai intercellular communication in Chinese hamster V79 cells

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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. Afatoxin B1, afatoxin 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.

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Abbreviations

6-TG:

6-thioguanine

TPA:

12-0-tetradecanoylphorbol-13-acetate

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Jone, C., Erickson, L., Trosko, J.E. et al. Effect of biological toxins on gap-junctionai intercellular communication in Chinese hamster V79 cells. Cell Biol Toxicol 3, 1–15 (1987). https://doi.org/10.1007/BF00117821

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