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Proposed mechanism of protection by N,N′-bis(2-mercaptoethyl)isopthalamide (NBMI) and 5-fluoro-2-indolyl des-chlorohalopemide (FIPI) against mercury-induced cytotoxicity in aortic endothelial cells (ECs) through the attenuation of thiol-redox–regulated and extracellular-regulated kinase 1/2 (ERK1/2)–mediated activation of phospholipase D (PLD) and bioactive lipid signal mediator formation.
