Oxidation of ferrous iron during peroxidation of lipid substrates.

Abstract Oxidation of Fe 2+ in solution was dependent upon medium composition and the presence of lipid. The complete oxidation of Fe 2+ in 0.9% saline was markedly accelerated in the presence of phosphate or EDTA and the ferrous oxidation product formed was readily recoverable as Fe 2+ by ascorbate reduction. In contrast, in the presence of either brain synaptosomal membranes, phospholipid liposomes, fatty acid micelles or H 2 O 2 , less than 50% of the Fe 2+ oxidized during an incubation could be recovered as Fe 2+ via reduction with ascorbate. In the presence of unsaturated lipid, oxidation of Fe 2+ was associated with peroxidation of lipid, as assessed by the uptake of O 2 and formation of thiobarbituric acid-reactive products during incubations. Although relatively little Fe 2+ oxidation or lipid peroxidation occurred in saline with synaptosomes or linoleic acid micelles during an incubation with Fe 2+ alone, significant Fe 2+ oxidation and lipid peroxidation occurred in incubations containing a 1:1 ratio of Fe 2+ and Fe 2+ . Extensive Fe 2+ oxidation and lipid peroxidation also occurred with Fe 2+ alone in saline incubations with either linolenic or arachidonic acid acid micelles or liposomes prepared from dilinoleoylphosphatidylcholine. While a 1:1 ratio of Fe 2+ and Fe 3+ enhanced thiobarbituric acid-reactive product formation in incubations containing linolenic or arachidonic micelles, it reduced the rate of O 2 consumption as compared with Fe 2+ alone. The results demonstrate that oxidation of Fe 2+ in incubations containing lipid substrates is linked to and accelerated by peroxidation of those substrates. Furthermore, the results suggest that oxidation of Fe 2+ in the presence of lipid or H 2 O 2 creates forms of iron which differ from those formed during simple Fe 2+ autoxidation.