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- Abdel-Rahman 2016 Oxid Med Cell Longev + (Disruption of cellular redox homeostasis i β¦ Disruption of cellular redox homeostasis is implicated in a wide variety of pathologic conditions and aging. A fundamental factor that dictates such balance is the ratio between mitochondria-mediated complete oxygen reduction into water and incomplete reduction into superoxide radical by mitochondria and NADPH oxidase (NOX) enzymatic activity. Here we determined mitochondrial as well as NOX-dependent rates of oxygen consumption in parallel with H<sub>2</sub>O<sub>2</sub> generation in freshly isolated synaptosomes using high-resolution respirometry combined with fluorescence or electrochemical sensory. Our results indicate that, although synaptic mitochondria exhibit substantially higher respiratory activities (8-82 folds greater than NOX oxygen consumption depending on mitochondrial respiratory state), NADPH-dependent oxygen consumption is associated with greater H<sub>2</sub>O<sub>2</sub> production (6-7 folds higher NOX-H<sub>2</sub>O<sub>2</sub>). We also show that, in terms of the consumed oxygen, while synaptic mitochondria βleakedβ 0.71% Β± 0.12 H<sub>2</sub>O<sub>2</sub> during NAD<sup>+</sup>-linked resting, 0.21% Β± 0.04 during NAD<sup>+</sup>-linked active, and 0.07% Β± 0.02 during FAD<sup>+</sup>-linked active respirations, NOX converted 38% Β± 13 of O<sub>2</sub> into H<sub>2</sub>O<sub>2</sub>. Our results indicate that NOX rather than mitochondria is the major source of synaptic H<sub>2</sub>O<sub>2</sub>. The present approach may assist in the identification of redox-modulating synaptic factors that underlie a variety of physiological and pathological processes in neurons.of synaptic H<sub>2</sub>O<sub>2</sub>. The present approach may assist in the identification of redox-modulating synaptic factors that underlie a variety of physiological and pathological processes in neurons.)