| Main Title |
Effects of Selected Anti-Tumor-Promoting Chemicals on Metabolic Cooperation between Chinese Hamster V79 Cells. |
| Author |
Mills, L. J. ;
Nelson, S. M. ;
Malcolm, A. R. ;
|
| CORP Author |
Science Applications International Corp., Narragansett, RI.;Environmental Research Lab., Narragansett, RI. |
| Publisher |
c1994 |
| Year Published |
1994 |
| Report Number |
EPA-68-C1-0005; EPA/600/J-94/482 ; ERLN-1434 |
| Stock Number |
PB95-136867 |
| Additional Subjects |
Anticarcinogenic agents ;
Metabolism ;
Gap junctions ;
Antitumor drug screening assays ;
Biomedical measurement ;
Hamsters ;
Cells(Biology) ;
Biological effects ;
Synaptic transmission ;
Neural inhibition ;
In vivo analysis ;
In vitro analysis ;
Reprints ;
Metabolic cooperation ;
V79 Chinese hamster cells
|
| Holdings |
| Library |
Call Number |
Additional Info |
Location |
Last
Modified |
Checkout
Status |
| NTIS |
PB95-136867 |
Some EPA libraries have a fiche copy filed under the call number shown. |
|
07/26/2022 |
|
| Collation |
9p |
| Abstract |
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. |
