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 peroxid ation in liposomes were investigated. Incorporation of phosphatidylser ine IFS) or dicetyl phosphate (DCP) into phosphatidylcholine [PC(A)I l iposomes, which have arachidonic acid, produced a marked lag phase in Fe2+-supported peroxidation, where PS was more effective than DCP. Pho sphatidylcholine dipalmitoyl [PC(DP)] with a net-neutral charge was st ill effective in producing a lag phase, though weak. Increasing concen trations of PS, DCP, and PC(DP) prolonged the lag period. Initially af ter adding Fe2+, slight oxygen consumption occurred in PC(A)/PS liposo mes including hydroperoxides, followed by a lag phase. An increase in the hydroperoxide resulted in a shortening of the lag period. The init ial events of Fe2+ oxidation accompanied by oxygen consumption were de pendent on the hydroperoxide content, but significant changes in diene conjugation and hydroperoxide levels at this stage were not found. Th e molar ratios of both disappeared Fe2+ and consumed O-2 to preformed hydroperoxide in liposomes with or without tert-butylhydroxytoluene we re constant, regardless of the different amounts of lipid hydroperoxid es. The antioxidant completely inhibited the propagation of lipid pero xidation in the lipid phase, following a lag phase. In a model system containing 2,2'-azobis (2-amidinopropane) dihydrochloride, Fe2+ were c onsumed. We suggest that Fe2+ retained at a high level on membrane sur faces play a role in producing a lag phase following the terminating b ehavior of a sequence of free radical reactions initiated by hydropero xide decomposition, probably by intercepting peroxyl radicals.