Lactobionic and gluconic acid complexes of FeII and FeIII; control of oxidation pathways by an organ transplantation preservant

摘要: Lactobionic acid, [4-beta-(galactosido)-D-gluconic acid] = LBA, is the major component of Wisconsin organ transplantation preservant fluid and may suppress oxygen radical-induced tissue damage upon reperfusion by control FeII autoxidation. FeIII complexes LBA related gluconic acid (GLC) have been studied herein titrimetric, infrared, electrochemical methods (CV; DPP). FeII(GLC) forms quickly at pH 7, but FeII(LBA) reacts in two steps, second requiring 4 hr. The initial complex lacks coordination carboxylate (C-1) bound "2,3,5" hydroxyl groups. slow rearrangement a "1,2,3,6" chelate which shares common with donor set FeIII(LBA) complex. Titration data shows removal three protons from through 5 an additional proton 6 to 9 indicative [FeIII(LBA)(OH)(H2O)]- formulation donating positions. more stable, form has investigated its oxidation mechanisms H2O2 O2 using selected trapping agents for HO. ferryl intermediates. Eighty-six percent events FeII(LBA)/H2O2 occurs steps involving formation reduction freely diffusible HO.. These pathways are altered known traps t-butanol, dmso, ethanol, methanol manner predictable beta-oxidizing radicals (from t-butanol or dmso) alpha-reducing ethanol methanol). Fourteen reaction via FeIVO intermediates not trapped intercepted primary secondary alcohols. generating responsible competitive ligand C-2 position HO., formed within original cage. Competitive absent FeII(LBA)/O2 autoxidation, different redox mechanism. rate first-order each insensitive presence as trap. observations support intermediate autoxidation pathway absence free during Although chelation hard donors such edta4-, Cl-, HPO4(2-) accelerate FeII, carboxylate, alkoxy, does implications these findings, inner-sphere role 4-beta-(galactosido) functionality toward action fluids, discussed.