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EFFECTS OF SELECTED ANTI-TUMOR-PROMOTING CHEMICALS ON METABOLIC COOPERATION BETWEEN CHINESE HAMSTER V79 CELLS
Citation:
Mills, L.J., S. Nelson, AND A. Malcolm. EFFECTS OF SELECTED ANTI-TUMOR-PROMOTING CHEMICALS ON METABOLIC COOPERATION BETWEEN CHINESE HAMSTER V79 CELLS. U.S. Environmental Protection Agency, Washington, D.C., EPA/600/J-94/482 (NTIS PB95136867), 1994.
Description:
Many tumor-promoting chemicals inhibit gap junctional communication between cells. we investigated the possibility that antipromoting chemicals may act inversely and enhance gap junctional communication. he V79/metabolic cooperation assay is an in vitro test that measures pp junctional communication indirectly by determining the extent of metabolic cooperation between mutant and wild-type V79 Chinese hamster lung fibroblasts in culture. ix in vivo antipromoters (caffeine, 3-isobutyl-l-methylxanthine (IBMX), phenidone, dibromoacetophenone, tosylphenylalanine chloromethyl ketone (TPCK), and acetic acid) were tested in this assay to assess their effects on metabolic cooperation. affeine, IBMX, phenidone, and dibromoacetophenone had no effect on metabolic cooperation, while TPCK slightly inhibited metabolic cooperation in one V79 assay. cetic acid appeared to facilitate metabolic cooperation. n tests where an antipromoter was combined with the established tumor promoter phorbol 12-myristate 13-acetate (PMA), acetic acid, caffeine, and IBMX counteracted PMA-induced inhibition of metabolic cooperation, while phenidone, dibromoacetophenone, and TPCK had little effect. hese results indicate that sonic antipromoters interfere with the ability of a tumor-promoting chemical to inhibit metabolic cooperation and suggest that alteration of gap junctional communication can be a mechanism of antipromoter action.