||Effects of Selected Anti-Tumor-Promoting Chemicals on Metabolic Cooperation between Chinese Hamster V79 Cells.
Mills, L. J. ;
Nelson, S. M. ;
Malcolm, A. R. ;
||Science Applications International Corp., Narragansett, RI.;Environmental Research Lab., Narragansett, RI.
||EPA-68-C1-0005; EPA/600/J-94/482 ; ERLN-1434
Anticarcinogenic agents ;
Gap junctions ;
Antitumor drug screening assays ;
Biomedical measurement ;
Biological effects ;
Synaptic transmission ;
Neural inhibition ;
In vivo analysis ;
In vitro analysis ;
Metabolic cooperation ;
V79 Chinese hamster cells
||Some EPA libraries have a fiche copy filed under the call number shown.
||Many tumor-promoting chemicals inhibit gap junctional communication between cells. The authors investigated the possibility that antipromoting chemicals may act inversely and enhance gap junctional communication. The V79/metabolic cooperation assay is an in vitro test that measures gap junctional communication indirectly by determining the extent of metabolic cooperation between mutant and wild-type V79 Chinese hamster lung fibroblasts in culture. Six in vivo antipromotors (caffeine, 3-isobutyl-1-methylxanthine (IBMX), phenidone, dibromoacetophenone, tosylphenylalanine chloromethylketone (TPCK), and acetic acid) were tested in this assay to assess their effects on metabolic cooperation. These results indicate that some antipromoters interfere with the ability of a tumor-promoting chemical to inhibit metabolic cooperation and suggest that alteration of gap junctional communication be a mechansim of antipromoter action.
||Pub. in Toxicology and Applied Pharmacology 126, p338-344 1994. Sponsored by Environmental Research Lab., Narragansett, RI.
|NTIS Title Notes
||Reprint: Effects of Selected Anti-Tumor-Promoting Chemicals on Metabolic Cooperation between Chinese Hamster V79 Cells.
||57Q; 57Y; 57F
||PC A02/MF A01