FURTHER-STUDIES ON THE ANTIOXIDANT ROLE OF PYROPHOSPHATE IN MODEL MEMBRANES

Our previous studies (G. Cervato et al., Chem. Phys. Lipids 56 (1990), 91-99) demonstrated that 100 muM pyrophosphate (PPi) inhibits Fe2+/as corbate-induced peroxidation of arachidonic acid (AA) inserted in unil amellar liposomes (SUVs) of dipalmitoylphosphatidylcholine (DPPC), by chelating ferrous ions in the aqueous phase. In this work we demonstra te that the kinetics of AA peroxidation in DPPC SUVs are strongly affe cted by PPi, also at very low concentration (1 muM). In fact at low PP i concentration there is a longer lag-phase, while the maximum of thio barbituric acid reactive substances (TBARS) is similar in both the pre sence and absence of 1 muM PPi. The lag-phase of peroxidation of AA in lysophosphatidylcholine (palmitoyl) (LysoPC) micelles is also prolong ed. The AA peroxidation in membrane models without choline as the pola r headgroup (dipalmitoylphosphatidylethanolamine (DPPE) SUVs, or Trito n X-100 micelles), or in which AA is not free but esterified with glyc erol (stearoylarachidonylphosphatidylcholine (SAPC)), is unaffected by the presence of 1 muM PPi.