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Mitochondrial uncoupling is the main, but not exclusive, way through which hypoxia causes ROS formation . The crosstalk between dysfunctional mitochondria and NADPH oxidase in the plasma membrane  engages this enzyme as an additional ROS source . NADPH oxidase 4 responds directly to the O2 lack , thus constituting a major ROS source in hypoxia [55,56], and nearly doubles in the brains of mice exposed to 5900 m/10.0 %O2 for 4 weeks . NADPH oxidase 4 is antagonized by the nuclear factor erythroid 2-related factor 2 (Nrf2), which in rat brains responds to 12 h hypoxia  and upregulates the antioxidant defenses . Another protective factor, protein kinase B or Akt, is a serine/threonine-specific protein kinase that plays a key role in neuroprotection by inhibiting apoptosis [60,61] and revealed protective features even in chronic situations, possibly overriding the protection elicited by Nrf2 . Mild 5900 m/10.0 %O2 hypoxia increases both ROS production and defense mechanisms, but since the first is stronger, at least for 4-week hypoxia, the redox imbalance results worsened with the onset of clear signs of oxidative stress . 041b061a72