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The NADH oxidase activity of the plasma membrane of synaptosomes is a major source of superoxide anion and is inhibited by peroxynitrite

Plasma membrane vesicles from adult rat brain synaptosomes (PMV) have an ascorbate‐dependent NADH oxidase activity of 35–40 nmol/min/(mg protein) at saturation by NADH. NADPH is a much less efficient substrate of this oxidase activity, with a Vmax 10‐fold lower than that measured for NADH. Ascorbate‐dependent NADH oxidase activity accounts for more than 90% of the total NADH oxidase activity of PMV and, in the absence of NADH and in the presence of 1 mm ascorbate, PMV produce ascorbate free radical (AFR) at a rate of 4.0 ± 0.5 nmol AFR/min/(mg protein). NADH‐dependent ·O2− production by PMV occurs with a rate of 35 ± 3 nmol/min/(mg protein), and is a coreaction product of the NADH oxidase activity, because: (i) it is inhibited by more than 90% by addition of ascorbate oxidase, (ii) it is inhibited by 1 µg/mL wheat germ agglutinin (a potent inhibitor of the plasma membrane AFR reductase activity), and (iii) the KM(NADH) of the plasma membrane NADH oxidase activity and of NADH‐dependent ·O2− production are identical. Treatment of PMV with repetitive micromolar ONOO– pulses produced almost complete inhibition of the ascorbate‐dependent NADH oxidase and ·O2− production, and at 50% inhibition addition of coenzyme Q10 almost completely reverts this inhibition. Cytochrome c stimulated 2.5‐fold the plasma membrane NADH oxidase, and pretreatment of PMV with repetitive 10 µm ONOO– pulses lowers the K0.5 for cytochrome c stimulation from 6 ± 1 (control) to 1.5 ± 0.5 µm. Thus, the ascorbate‐dependent plasma membrane NADH oxidase activity can act as a source of neuronal ·O2−, which is up‐regulated by cytosolic cytochrome c and down‐regulated under chronic oxidative stress conditions producing ONOO–.