title: Nonchelational cell growth inhibition by EDTA.
abstract: The ability of the dinitrilotetraacetates EDTA, CDTA, and EGTA to inhibit the growth of rat C6 glioma cells was not proportional to their chelational stability constants, suggesting a nonchelational mechanism of action. Ion antagonization studies supported this hypothesis. Growth inhibition did not appear to be caused by an EDTA-ion coordination complex. The chemical structure of the DNTAs suggests that they might act by: increasing zeta potential electronegativity and altering local physical properties; macromolecular crosslinking; and disrupting hydrogen bonds and hydrophobic interactions. Interestingly, their ability to inhibit growth paralleled their hydrophobic surface areas.
mesh_terms: D000818:Animals; D002412:Cations; D002455:Cell Division / Q000187:drug effects; D002460:Cell Line; D004492:Edetic Acid / Q000031:analogs & derivatives / Q000037:antagonists & inhibitors / Q000494:pharmacology*; D004533:Egtazic Acid / Q000494:pharmacology; D005910:Glioma / Q000473:pathology*; D008670:Metals / Q000494:pharmacology; D051381:Rats
chemical_list: D002412:Cations; D008670:Metals; C005390:CDTA; D004533:Egtazic Acid; D004492:Edetic Acid