Effects of membrane charges and hydroperoxides on Fe(II)-supported lipid peroxidation in liposomes.

The processes in producing a lag phase in Fe2+-supported lipid peroxidation in liposomes were investigated. Incorporation of phosphatidylserine (PS) or dicetyl phosphate (DCP) into phosphatidylcholine [PC(A)] liposomes, which have arachidonic acid, produced a marked lag phase in Fe(2+)-supported peroxidation, where PS was more effective than DCP. Phosphatidylcholine dipalmitoyl [PC(DP)] with a net-neutral charge was still effective in producing a lag phase, though weak. Increasing concentrations of PS, DCP, and PC(DP) prolonged the lag period. Initially after adding Fe2+, slight oxygen consumption occurred in PC(A)/PS liposomes including hydroperoxides, followed by a lag phase. An increase in the hydroperoxide resulted in a shortening of the lag period. The initial events of Fe2+ oxidation accompanied by oxygen consumption were dependent on the hydroperoxide content, but significant changes in diene conjugation and hydroperoxide levels at this stage were not found. The molar ratios of both disappeared Fe2+ and consumed O2 to preformed hydroperoxide in liposomes with or without tert-butylhydroxytoluene were constant, regardless of the different amounts of lipid hydroperoxides. The antioxidant completely inhibited the propagation of lipid peroxidation in the lipid phase, following a lag phase. In a model system containing 2,2'-azobis (2-amidinopropane) dihydrochloride, Fe2+ were consumed. We suggest that Fe2+ retained at a high level on membrane surfaces play a role in producing a lag phase following the terminating behavior of a sequence of free radical reactions initiated by hydroperoxide decomposition, probably by intercepting peroxyl radicals.