title: The mechanism of Fe(2+)-initiated lipid peroxidation in liposomes: the dual function of ferrous ions, the roles of the pre-existing lipid peroxides and the lipid peroxyl radical.
abstract: The mechanism of Fe(2+)-initiated lipid peroxidation in a liposomal system was studied. It was found that a second addition of ferrous ions within the latent period lengthened the time lag before lipid peroxidation started. The apparent time lag depended on the total dose of Fe(2+) whenever the second dose of Fe(2+) was added, which indicates that Fe(2+) has a dual function: to initiate lipid peroxidation on one hand and suppress the species responsible for the initiation of the peroxidation on the other. When the pre-existing lipid peroxides (LOOH) were removed by incorporating triphenylphosphine into liposomes, Fe(2+) could no longer initiate lipid peroxidation and the acceleration of Fe(2+) oxidation by the liposomes disappeared. However, when extra LOOH were introduced into liposomes, both enhancement of the lipid peroxidation and shortening of the latent period were observed. When the scavenger of lipid peroxyl radicals (LOO(.)), N,N'-diphenyl-p-phenylene-diamine, was incorporated into liposomes, neither initiation of the lipid peroxidation nor acceleration of the Fe(2+) oxidation could be detected. The results may suggest that both the pre-existing LOOH and LOO(.) are necessary for the initiation of lipid peroxidation. The latter comes initially from the decomposition of the pre-existing LOOH by Fe(2+) and can be scavenged by its reaction with Fe(2+). Only when Fe(2+) is oxidized to such a degree that LOO(.) is no longer effectively suppressed does lipid peroxidation start. It seems that by taking the reactions of Fe(2+) with LOOH and LOO(.) into account, the basic chemistry in lipid peroxidation can explain fairly well the controversial phenomena observed in Fe(2+)-initiated lipid peroxidation, such as the existence of a latent period, the critical ratio of Fe(2+) to lipid and the required oxidation of Fe(2+).
authors.affiliation: Institute of Biophysics, Chinese Academy of Sciences, Datun Road 15, Chaoyang District, Beijing 100101, People's Republic of China.
authors.forename: L
authors.initials: L
authors.lastname: Tang
authors.forename: Y
authors.initials: Y
authors.lastname: Zhang
authors.forename: Z
authors.initials: Z
authors.lastname: Qian
authors.forename: X
authors.initials: X
authors.lastname: Shen
mesh_terms: D000818:Animals; D000975:Antioxidants / Q000494:pharmacology; D002645:Chickens; D004305:Dose-Response Relationship, Drug; D004530:Egg Yolk; D007477:Ions; D007501:Iron / Q000378:metabolism*; D007700:Kinetics; D015227:Lipid Peroxidation; D008054:Lipid Peroxides / Q000378:metabolism*; D008081:Liposomes / Q000378:metabolism*; D010100:Oxygen / Q000378:metabolism; D010545:Peroxides / Q000378:metabolism*; D010655:Phenylenediamines / Q000494:pharmacology; D013858:Thiobarbiturates / Q000378:metabolism; D013997:Time Factors
chemical_list: D000975:Antioxidants; D007477:Ions; D008054:Lipid Peroxides; D008081:Liposomes; D010545:Peroxides; D010655:Phenylenediamines; D013858:Thiobarbiturates; C049375:perhydroxyl radical; C004845:N,N'-diphenyl-4-phenylenediamine; D007501:Iron; C029684:thiobarbituric acid; D010100:Oxygen