EFFECTS OF MEMBRANE PEROXIDATION ON [H-3] ACETYLCHOLINE-RELEASE IN RAT CEREBRAL CORTICAL SYNAPTOSOMES

[H-3]Acetylcholine (ACh) release, malonaldehyde formation and calcium- 45-uptake were measured in rat cerebral cortical nerve terminal that w ere exposed to various concentrations of ferrous and ascorbate ions. A t a constant molar ratio of 25:1, ferrous:ascorbate, these ions increa sed malonaldehyde (MA) synthesis in a concentration-dependent manner. Treatment with these ions in the same ratio also induced a dose-relate d inhibition of the K+-depolarization-induced release of newly synthes ized [H-3]ACh. Combined exposure to Fe2+/ascorbate also reduced calciu m ionophore A23187-induced [H-3]ACh release. Neither ferrous nor ascor bate ions alone altered depolarization- or ionophore-induced [H-3]ACh release over this concentration range. Depolarization- and A23187-indu ced calcium-45 uptake were not affected by peroxidation, suggesting th at membrane peroxidation influenced some process in the release-proces s subsequent to calcium influx in a manner similar to what is observed during aging.