title: Fenton reagents may not initiate lipid peroxidation in an emulsified linoleic acid model system.
abstract: This study includes two parts. First, the Fe2+ autooxidation and chelation processes in the presence of the chelators ethylenediaminetetraacetic acid (EDTA) and diethylenetriamine pentaacetic acid (DTPA) were studied by measuring UV light absorbance alterations. Competition for Fe3+ between chelators and water or phosphate buffer (PB) ions was confirmed. The addition of EDTA or DTPA to Fe3+ in water or PB only slowly turned the water/PB-Fe3+ complexes to EDTA-Fe3+ or DTPA-Fe3+ complexes. In the second part of this study, the initiation mechanisms of Tween 20 emulsified linoleic acid peroxidation under stimulation by chelator-Fe-O2 complexes were studied by measuring changes in UV light absorbance following diene conjugation. Fe3+ in the presence of EDTA or DTPA did not stimulate diene conjugation. Fe2+ (0.10 mM) and EDTA (0.11 mM) stimulated diene conjugation of the linoleic acid emulsion, but only after apparent Fe2+ autooxidation. Fe2+ and DTPA, as well as premixed DTPA-Fe2+ complex, resulted in very fast diene conjugation in a wide range of concentrations. A nonlinear, mainly square root relation between Fe2+ concentration and peroxidation rate was noted. Superoxide dismutase (SOD), catalase, and mannitol did not prevent the lipid peroxidation. H2O2 substantially decreased the DTPA-Fe2+ stimulated, otherwise rapid, diene conjugation but slightly enhanced the slower one stimulated by EDTA-Fe2+. Without ambient oxygen, Fenton reagents did not result in .H abstraction-related diene conjugation. The findings suggest that .OH resulting from Fenton reagents may not be the main cause for the initiation of peroxidation in this model system. Furthermore, a study with different combinations of Fe2+ and Fe3+ did not support the Fe2+/Fe3+ (1:1) optimum ratio hypothesis. We therefore conclude that perferryl ions or chelator-Fe-O2 complexes may be responsible for the first-chain initiation of lipid peroxidation, at least in this model system.
authors.affiliation: Department of Pathology, Linköping University, Sweden.
authors.forename: D
authors.initials: D
authors.lastname: Yin
authors.forename: H
authors.initials: H
authors.lastname: Lingnert
authors.forename: B
authors.initials: B
authors.lastname: Ekstrand
authors.forename: U T
authors.initials: UT
authors.lastname: Brunk
mesh_terms: D000818:Animals; D002374:Catalase / Q000378:metabolism; D002417:Cattle; D002614:Chelating Agents; D004492:Edetic Acid; D004655:Emulsions; D004912:Erythrocytes / Q000201:enzymology; D006861:Hydrogen Peroxide; D007501:Iron; D007700:Kinetics; D019787:Linoleic Acid; D008041:Linoleic Acids / Q000737:chemistry*; D015227:Lipid Peroxidation; D008099:Liver / Q000201:enzymology; D008954:Models, Biological; D004369:Pentetic Acid; D013482:Superoxide Dismutase / Q000097:blood
chemical_list: D002614:Chelating Agents; D004655:Emulsions; C045076:Fenton's reagent; D008041:Linoleic Acids; D004369:Pentetic Acid; D004492:Edetic Acid; D019787:Linoleic Acid; D006861:Hydrogen Peroxide; D007501:Iron; D002374:Catalase; D013482:Superoxide Dismutase