Inhibition of gap-junctional intercellular communication between Chinese hamster lung fibroblasts by di(2-ethylhexyl) phthalate (DEHP) and trisodium nitrilotriacetate monohydrate (NTA).
Di(2-ethylhexyl)phthalate and trisodium nitrilotriacetate monohydrate, two apparently nongenotoxic carcinogens, were tested for effects on gap-junctional communication between Chinese hamster V79 lung fibroblasts. Both compounds inhibited gap-junctional communication in a concentration-dependent manner. The inhibiting effects of these chemicals on gap-junctional communication in vitro correlate with their tumor-promoting activity. Such results further support the hypothesis that inhibition of gap-junctional communication is an in vitro biomarker for some tumor-promoting chemicals.
Environmental Research Laboratory, U.S. EPA, Narragansett, Rhode Island.
A R
AR
Malcolm
L J
LJ
Mills
D000085:Acetates / Q000494:pharmacology*; D000818:Animals; D015197:Carcinogenicity Tests / Q000379:methods; D002450:Cell Communication / Q000187:drug effects*; D002470:Cell Survival / Q000187:drug effects; D006224:Cricetinae; D003412:Cricetulus; D004051:Diethylhexyl Phthalate / Q000494:pharmacology*; D005347:Fibroblasts / Q000187:drug effects; D066298:In Vitro Techniques; D007365:Intercellular Junctions / Q000187:drug effects*; D008168:Lung / Q000166:cytology; D009571:Nitrilotriacetic Acid / Q000494:pharmacology*; D010795:Phthalic Acids / Q000494:pharmacology*
D000085:Acetates; D010795:Phthalic Acids; D004051:Diethylhexyl Phthalate; D009571:Nitrilotriacetic Acid