This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Landesman, J. M. Articles by Mossman, B. T. Search for Related Content PubMed PubMed Citation Articles by Landesman, J. M. Articles by Mossman, B. T.

Induction of Ornithine Decarboxylase in Hamster Tracheal Epithelial Cells Exposed to Asbestos and 12-O-Tetradecanoylphorbol-13-acetate¹

Department of Pathology, University of Vermont College of Medicine, Burlington, Vermont 05405

Crocidolite and chrysotile asbestos and the tumor promoter, 12-O-tetradecanoylphorbol-13-acetate (TPA), induce ornithine decarboxylase (ODC) in hamster tracheal epithelial cells (HTE-B). When added at the time cells were plated, non-growth-inhibitory amounts of crocidolite (0.64 to 1.28 µg/sq cm) and chrysotile (0.064 to 0.13 µg/sq cm) asbestos increased ODC activity 2- to 3-fold after 24 to 30 hr. The effect was dose dependent. The nonfibrous mineral hematite (0.64 to 1.28 µg/sq cm) had no effect.

Asbestos-stimulated induction did not occur in confluent monolayers unless fresh medium was added simultaneously. Under these conditions, both crocidolite (3-fold increase) and chrysotile (4-fold increase) induced ODC.

TPA (0.1 µg/ml medium) produced a rapid, transient increase in ODC activity in both logarithmically growing (6-fold increase) and confluent (30-fold increase) HTE-B. When TPA and fresh medium were combined, a synergistic effect was noted both in 24-hr cultures (22-fold increase) and at confluency (72- to 92-hr cultures; 170-fold increase).

The addition of asbestos and TPA alone had no effect on [³H]thymidine incorporation in confluent monolayers; however, a significant mitogenic response was observed when they were added with fresh medium. Under these circumstances, the cells appeared morphologically transformed.

The ability of asbestos to induce ODC and influence proliferation of HTE-B is consistent with the results of previous observations in our laboratory. These studies indicate that asbestos is producing a constellation of changes warranting its classification as a tumor promoter in the respiratory tract.

¹ This research was supported by USPHS Grant R0100888 from the National Institute of Occupational Safety and Health and Contract N01CP33360 from the National Cancer Institute.

² To whom requests for reprints should be addressed.

Received 7/17/81. Accepted 6/ 4/82.