Abstract
Abstract—The objective of this work was to study the biological effect of dinitrosyl iron complexes (DNICs) with the glutathione ligand (GSH−DNICs) as a stabilized form of nitric oxide in a rat model of nitric oxide hyperproduction induced by inflammation. Administration of GSH−DNICs in endotoxin shock did not increase the total nitric oxide levels in rat organs, but exerted a protective effect by suppressing nitric oxide hyperproduction in the liver and led to an accumulation of the complexes with protein ligands in the kidney.
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