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Effects of membrane charges and hydroperoxides on Fe(II)‐supported lipid peroxidation in liposomes
Author(s) -
Tampo Yoshiko,
Yonaha Masanori
Publication year - 1996
Publication title -
lipids
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.601
H-Index - 120
eISSN - 1558-9307
pISSN - 0024-4201
DOI - 10.1007/bf02522459
Subject(s) - chemistry , liposome , lipid peroxidation , phosphatidylcholine , tert butyl hydroperoxide , phospholipid , oxygen , antioxidant , membrane , chromatography , organic chemistry , biochemistry , catalysis
The processes in producing a lag phase in Fe 2+ ‐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 Fe 2+ , 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 Fe 2+ 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 dis‐appeared Fe 2+ and consumed O 2 to preformed hydroperoxide in liposomes with or without tert ‐butylhydroxytoluene were constant, regardless of the different amounts of lipid hydroper‐oxides. 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, Fe 2+ were consumed. We suggest that Fe 2+ 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 decompositin, probably by intercepting peroxyl radicals.