Activation of protein kinase C by crocidolite asbestos in hamster tracheal epithelial cells

Carcinogenesis. 1991 Aug;12(8):1499-502. doi: 10.1093/carcin/12.8.1499.


To determine the mechanisms of cell signalling by asbestos in epithelial cells of the respiratory tract, the activity of protein kinase C (PKC) was examined in hamster tracheal epithelial (HTE) cells exposed to mitogenic concentrations of crocidolite asbestos. In the histone phosphorylation assay, asbestos significantly increased activity of PKC associated with the membrane fraction of HTE cells. However, in contrast to 12-O-tetradecanoylphorbol-13-acetate, which caused redistribution of almost all PKC activity from the cytosolic to the membrane fraction, the majority of the PKC activity was associated with the cytosolic fraction at all time periods examined. Asbestos did not inhibit binding of [3H]phorbol-12,13-dibutyrate to intact HTE cells, whereas binding was inhibited by the phorbol compounds phorbol dibutyrate and phorbol dibenzoate. Thus, crocidolite-induced activation of PKC does not appear to be mediated through the same mechanism as classical phorbol ester tumor promoters, compounds which activate PKC by structurally resembling diacylglycerol.

Publication types

  • Comparative Study
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Animals
  • Asbestos / pharmacology*
  • Asbestos, Crocidolite
  • Cell Line
  • Cricetinae
  • Enzyme Activation
  • Protein Kinase C / biosynthesis*
  • Tetradecanoylphorbol Acetate / pharmacology
  • Trachea / enzymology*


  • Asbestos, Crocidolite
  • Asbestos
  • Protein Kinase C
  • Tetradecanoylphorbol Acetate