Vanadium compounds promote the induction of morphological transformation of hamster embryo cells with no effect on gap junctional cell communication.
Vanadium compounds were found to promote the induction of morphological transformation of hamster embryo cells. Exposure of the cells to Na-O-vanadate, vanadin (V) oxide or vanadin (IV) oxide sulfate following pre-exposure to a low concentration of benzo[a]pyrene, potentiated the induction of transformed colonies similar to 12-O-tetradecanoylphorbol-13-acetate. Unlike this phorbol ester, vanadium compounds did not inhibit intercellular communication, or active protein kinase C. Nor did vanadate influence the reoccurrence of communication after removal of a communication blocking phorbol ester. On the other hand, vanadate showed strong synergism with the phorbol ester on induction of transformed morphology in the phorbol ester sensitive cell line BPNi. This suggests that vanadium and tumor promoting phorbol esters mediate their effect on the induction of morphological transformation of hamster embryo cells through different mechanisms.
Rivedal
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Laboratory for Environmental and Occupational Cancer, Norwegian Radium Hospital, Oslo.
Roseng
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Sanner
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D000818:Animals; D002450:Cell Communication / Q000187:drug effects*; D002471:Cell Transformation, Neoplastic / Q000139:chemically induced*; D002478:Cells, Cultured; D006224:Cricetinae; D004622:Embryo, Mammalian / Q000166:cytology / Q000187:drug effects; D004789:Enzyme Activation; D004815:Epidermal Growth Factor / Q000378:metabolism; D007365:Intercellular Junctions / Q000187:drug effects*; D008647:Mesocricetus; D011493:Protein Kinase C / Q000187:drug effects; D014639:Vanadium / Q000633:toxicity*
D014639:Vanadium; D004815:Epidermal Growth Factor; D011493:Protein Kinase C