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Efficient electron transfer and conversion of L -arginine to L -citrulline and nitric oxide (NO • ) by neuronal nitric oxide synthase (nNOS) requires calmodulin (CaM) binding. The present study focused on electron transfer ability of resting state CaM-free nNOS in presence of dinitrobenzene isomers (DNBs). NADPH oxidation (NADPH  ox  ) and acetylated cytochrome- c reduction (AcCyt- c   red  ) catalyzed by nNOS and the CaM binding sequence-deficient nNOS reductase construct (nNOS-FP) were estimates of total electron flux and [Formula: see text] production, respectively. All the DNBs ( o -, m -, p -) independently stimulated rates of NADPH  ox  by CaM-free nNOS and by nNOS-FP in isomer- and concentration-dependent manner. Blocking nNOS heme by imidazole or L -arginine did not affect CaM-free nNOS-catalyzed NADPH  ox  stimulated by DNBs. This stimulated electron flux by DNBs did not support NO • formation by CaM-free nNOS. The DNBs, like FeCN, extract electrons from both FMN and FAD of the nNOS reductase domain. All three DNBs greatly stimulated nNOS and nNOS-FP catalyzed AcCyt- c   red  that was significantly inhibited by SOD demonstrating [Formula: see text] formation. Thus, in presence of DNBs, resting-state CaM-deficient nNOS efficiently transfers electrons generating [Formula: see text], inferring that additional metabolic roles for nNOS exist that are not yet explored.

DINITROBENZENES STIMULATE ELECTRON FLUX WITHIN NEURONAL NITRIC OXIDE SYNTHASE IN THE ABSENCE OF CALMODULIN