The powerful neutrophil-derived oxidant hypochlorous acid HOCl/OCl- is assumed to contribute to tissue injury in a number of pathological states accompanied by massive accumulation of neutrophils. The production of malondialdehyde to indicate lipid peroxidation was studied in egg yolk phosphatidylcholine liposomes upon treatment with NaOCl as a source for hypochlorous acid. Its accumulation was inhibited by alpha-tocopherol and butylated hydroxytoluene. Singlet oxygen, hydroxyl radicals or superoxide anion radicals derived from direct reactions of hypochlorous acid seem not to be involved in initiation of lipid peroxidation because the malondialdehyde accumulation was unaffected by hydrogen peroxide, catalase, superoxide dismutase, ferrous sulphate or ferric chloride. Double bonds of fatty acid residues seem to be the primary target for NaOCl. Their number is continuously diminished in liposomes (2 mg lipids/ml) after incubation with increasing amounts of NaOCl at 37 degrees C for 40 min as detected by two independent methods (iodine bromide reduction and 1H-NMR spectroscopy). A 1:1 molar ratio between the loss of double bonds and NaOCl added was found only at low NaOCl concentrations. Then double bonds are decreased with a lower efficiency. A continuous increase of lipid peroxidation products was only observed up to 0.5-0.7 mmol/l NaOCl. The yield of lipid hydroperoxides kept constant at higher NaOCl concentrations. However, diene conjugates and malondialdehyde exhibit a maximum at 0.7-1 mmol/l or 0.5 mmol/l NaOCl, respectively, while the concentration of these products decreases at higher doses of NaOCl. The decrease of malondialdehyde was more pronounced than for diene conjugates. These results were discussed from the background that at minimum two (diene conjugates) or three (malondialdehyde) double bonds in a fatty acid residue are necessary for formation of lipid peroxidation products.