Nonchelational cell growth inhibition by EDTA.
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.
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
D002412:Cations; D008670:Metals; C005390:CDTA; D004533:Egtazic Acid; D004492:Edetic Acid