Effect of biological toxins on gap-junctionai intercellular communication in Chinese hamster V79 cells |
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Authors: | Cyrenius Jone Laurie Erickson James E. Trosko Chia C. Chang |
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Affiliation: | (1) Department of Pediatrics and Human Development Center of Environmental Toxicology College of Human Medicine, Michigan State University, East Lansing, Michigan;(2) Department of Pediatrics/Human Development, Michigan State University, B240 Life Sciences Building, 48824 East Lansing, MI |
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Abstract: | 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.Abbreviations 6-TG 6-thioguanine - TPA 12-0-tetradecanoylphorbol-13-acetate |
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Keywords: | aplysiatoxin gap junctions metabolic cooperation T2 toxin vomitoxin |
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