NADPH oxidase and myeloperoxidase are enzymes involved in the oxygen-dependent mechanisms for killing bacteria. The most potent bactericidal mechanism is the MPO system. When a bacterium invades, the immune system recognizes it and antibodies attach it to a receptor on a phagocytic cell. Once the microorganism is internalized, NADPH oxidase, located in the leukocyte cell membrane, is activated. It reduces O2 from the surrounding tissue to superoxide ( ), a free radical ROS, while NADPH is oxidized. This rapid consumption of O2 is known as the respiratory burst. Active NADPH oxidase is a membrane-associated complex containing a flavocytochrome and additional peptides. Electrons move from NADPH to O2 via flavin adenine nucleotide (FAD) and heme, . Genetic deficiencies in NADPH oxidase can lead to chronic granulomatous disease (CGD), characterized by severe infections and the formation of granulomas. 

Superoxide is converted to H2O2, either spontaneously or with the help of superoxide dismutase. In the presence of myeloperoxidase (MPO), a heme-containing lysosomal enzyme within the phagolysosome, peroxide and chloride ions react to form hypochlorous acid ([HOCl]), which acts as a bactericidal agent. Peroxide can also be partially reduced to hydroxyl radical (OH•), another ROS, or fully reduced to H2O by catalase or glutathione peroxidase. Deficiencies in MPO do not increase susceptibility to infection as peroxide from NADPH oxidase is still bactericidal. 

In summary, the oxygen-dependent mechanisms involve NADPH oxidase and MPO enzymes. NADPH oxidase produces superoxide, which is converted to H2O2. In the presence of MPO, H2O2 and chloride ions form hypochlorous acid, a bactericidal agent. Deficiencies in these enzymes can lead to diseases such as CGD.
Oxygen-dependent Oxygen-dependent mechanisms include the enzymes NADPH oxidase and myeloperoxidase (MPO) that work together in killing bacteria (Fig. 13.8). Overall, the MPO system is the most potent of the bactericidal mechanisms. An invading bacterium is recognized by the immune system and attacked by antibodies that bind it to a receptor on a phagocytic cell. After internalization of the microorganism has occurred, NADPH oxidase, located in the leukocyte cell membrane, activated and reduces O2 from the surrounding tissue to superoxide ( ), a free radical ROS, as NADPH is oxidized. The rapid consumption of O2 that accompanies formation of is referred to as the respiratory burst. [Note: Active NADPH oxidase is a membrane-associated complex containing a flavocytochrome plus additional peptides that translocate from the cytoplasm upon activation of the leukocyte. Electrons move from NADPH to O2 via flavin adenine nucleotide (FAD) and heme, . Rare genetic deficiencies in NADPH oxidase cause chronic granulomatous disease (CGD) characterized by severe, persistent infections and the formation of granulomas (nodular areas of inflammation) that sequester the bacteria that were not destroyed.] Next, is converted to H2O2 (also a ROS), either spontaneously or catalyzed by superoxide dismutase. In the presence of MPO, a heme-containing lysosomal enzyme present within the phagolysosome, peroxide plus chloride ions are converted to hypochlorous acid ([HOCl] the major component of household bleach), which kills the bacteria. The peroxide can also be partially reduced to the hydroxyl radical (OH•), a
ROS, or be fully reduced to H2O by catalase or glutathione peroxidase. [Note: Deficiencies in MPO do not confer increased susceptibility to infection because peroxide from NADPH oxidase is bactericidal.]
G; NADP(H) = nicotinamide adenine dinucleotide phosphate; = superoxide; H2O2 = hydrogen peroxide; HOCl = hypochlorous acid; OH• = hydroxyl radical.
E. Nitric oxide synthesis