MECHANISM OF HYPOCHLORITE-INDUCED PEROXID ATION IN PHOSPHOLIPID LIPOSOMES

Mechanisms of lipid peroxidation induced by HOCl/OCl- were studied in liposomes composed of egg yolk phosphatidylcholine. The incubation of liposomes with different amounts of HOCl/OCl- causes the accumulation of primary (diene conjugates and oxygen-containing compounds) and seco ndary (thiobarbituric acid (TBA)-reactive compounds) products of lipid peroxidation (LPO). The reaction is accompanied by the decrease in th e number of double bonds in phospholipids and by the formation of free radicals, because butylated hydroxytoluene (BHT) and alpha-tocopherol in low concentrations (0.7 and 10 mu M, respectively) completely inhi bit the accumulation of the secondary products of LPO induced by 50 mu M NaOCl. However, BHT does not inhibit the accumulation of the oxygen -containing LPO primary products in liposomes. The accumulation of the TEA-reactive LPO products is not affected by the preliminary addition of H2O2, catalase, superoxide dismutase, Fe2+, or Fe3+ to the incubat ion medium. Therefore, possible intermediates that are generated by th e reactions of HOCl/OCl- with H2O2, O-2(radical anion), Fe2+, or Fe3don't play any role in the initiation of LPO by HOCl/OCl-. Based on th ese data, HOCl/OCl- was suggested to interact directly with the double bonds of the fatty acid acyl chains of phospholipids or with admixtur es that are present in the lipid phase of liposomes, thereby causing t he formation of the primary oxygen-containing LPO products that are co nverted into the secondary products via free-radical mechanisms.