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pubmed-article:3123331pubmed:abstractTextChelation by citrate was found to promote the autoxidation of Fe2+, measured as the disappearance of 1,10-phenanthroline-chelatable Fe2+. The autoxidation of citrate-Fe2+ could in turn promote the peroxidation of microsomal phospholipid liposomes, as judged by malondialdehyde formation. At low citrate-Fe2+ ratios the autoxidation of Fe2+ was slow and the formation of malondialdehyde was preceded by a lag phase. The lag phase was eliminated by increasing the citrate-Fe2+ ratio, which also increased the rate of Fe2+ autoxidation. The Fe2+ autoxidation product required for the initiation of lipid peroxidation was characterized as being Fe3+. As direct evidence of this, linear initial rates of lipid peroxidation were obtained via the combination of citrate-Fe2+ and citrate-Fe3+, optimum activity occurring at a Fe3+-Fe2+ ratio of 1:1. Evidence is also presented to suggest that the superoxide and the hydrogen peroxide that are formed during the autoxidation of citrate-Fe2+ can either stimulate or inhibit lipid peroxidation by affecting the yield of citrate-Fe3+ from citrate-Fe2+. No evidence was obtained for the participation of the hydroxyl radical in the initiation of lipid peroxidation by citrate-Fe2+.lld:pubmed
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pubmed-article:3123331pubmed:articleTitleAn investigation into the mechanism of citrate-Fe2+-dependent lipid peroxidation.lld:pubmed
pubmed-article:3123331pubmed:affiliationDepartment of Biochemistry, Michigan State University, East Lansing 48824-1319.lld:pubmed
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