IRON(III) STIMULATION OF LIPID HYDROPEROXIDE-DEPENDENT LIPID-PEROXIDATION

In an experimental system where both Fe2+ autoxidation and generation of reactive oxygen species is negligible, the effect of FeCl2 and FeCl 3 on the peroxidation of phosphatidylcholine (PC) liposomes containing different amounts of lipid hydroperoxides (LOOH) was studied; Fe2+ ox idation, oxygen consumption and oxidation index of the liposomes were measured. No peroxidation was observed at variable FeCl2/FeCl3 ratio w hen PC liposomes deprived of LOOH by triphenylphosphine treatment were utilized. By contrast, LOOH containing liposomes were peroxidized by FeCl2. The FeCl2 concentration at which Fe2+ oxidation was maximal, de fined as critical Fe2+ concentration [Fe2+], depended on the LOOH con centration and not on the amount of PC liposomes in the assay. The LOO H-dependent lipid peroxidation was stimulated by FeCl3 addition; the o xidized form of the metal increased the average length of radical chai ns, shifted to higher values the [Fe2+] and shortened the latent peri od. The iron chelator KSCN exerted effects opposite to those exerted b y FeCl3 addition. The experimental data obtained indicate that the kin etics of LOOH-dependent lipid peroxidation depends on the Fe2+/Fe3+ ra tio at each moment during the time course of lipid peroxidation. The r esults confirm that exogenously added FeCl3 does not affect the LOOH-i ndependent but the LOOH-dependent lipid peroxidation; and suggest that the Fe3+ endogenously generated exerts a major role in the control of the LOOH-dependent lipid peroxidation.