[Mechanisms of the inhibition of Fe2+-induced oxidation of phosphatidylcholine by polyhydroxynaphthoquinones].

The kinetics of egg phosphatidylcholine oxidation induced by an artificial prooxidant Fe2+--ascorbate system or hematine was followed by oxygen uptake. The protective effect of natural free radical scavangers--polyhydroxynaphthoquinones, ionol (BHT), alpha-tocopherol and EDTA was estimated by the decrease of the phosphatidylcholine oxidation rate. EDTA was shown to inhibit the Fe2+--ascorbate-induced oxidation but had no effect on the hematine-induced oxidation. The inhibiting effect of polyhydroxynaphthoquinones on Fe2+--ascorbate-induced oxidation was 10-100 times as high as that on hematine-induced oxidation. The effects of BHT and alpha-tocopherol were the same in both models. Natural polyhydroxynaphthoquinones interacted with the free radical diphenylpicrylhydrazyl in stoichiometric ratios coinciding with the number of beta-hydroxyls in naphthoquinone molecules; the methylation of these hydroxyls fully suppressed such an interaction. Two possible mechanisms of action of polyhydroxynaphthoquinones as antioxidative agents are discussed. The first of these is coupled with the formation of Fe2+--PHNQ complexes, while the second one--with their effect as free radical scavengers. In both cases, beta-hydroxyls of naphthoquinone molecules were shown to play a key role.