• Description
    • Phagocytes (e.g., neutrophils, monocytes) ingest pathogens
    • Activation of the NADPH oxidase complex generates and releases reactive oxygen species (ROS; free radicals) that destroy the pathogens in phagosomes
  • Mechanism
    • 1. NADPH Oxidase (located on the phagosome membrane)
      • This is the rate-limiting enzyme and the first step.
      • Converts molecular oxygen (O₂) to superoxide (O₂•⁻).
      • Reaction: O₂ + NADPH → O₂•⁻ + NADP⁺ + H⁺
      • A large amount of NADPH is consumed, leading to ↑ activity in the pentose phosphate pathway (HMP shunt) to regenerate NADPH.
    • 2. Superoxide Dismutase (SOD)
      • Converts superoxide to hydrogen peroxide (H₂O₂).
      • Reaction: 2O₂•⁻ + 2H⁺ → H₂O₂ + O₂
    • 3. Myeloperoxidase (MPO)
      • An enzyme contained within azurophilic granules of neutrophils.
      • Converts H₂O₂ to hypochlorous acid (HOCl, i.e., bleach), a potent antimicrobial agent. MPO gives sputum its characteristic green color.
      • Reaction: H₂O₂ + Cl⁻ + H⁺ → HOCl + H₂O
    • Release of oxidative burst causes K+ influx, which triggers secretion of lysosomal enzymes into the phagosome.
RankROS SpeciesPotency/ReactivityKey USMLE Fact
1Hydroxyl Radical (•OH)ExtremeMost biologically reactive ROS; formed from H2O2 via the Fenton Reaction (non-enzymatic process).
2Hypochlorous Acid (HOCl)Very High”Bleach”; produced by myeloperoxidase in neutrophils to kill pathogens.
3Superoxide (O2•⁻)ModerateInitial ROS made by NADPH oxidase in the respiratory burst.
4Hydrogen Peroxide (H2O2)LowStable precursor to •OH and HOCl; can diffuse across membranes.
  • Associated Disease: Chronic Granulomatous Disease (CGD)
    • Defect: Mutation in NADPH oxidase → absent oxidative burst
    • Inheritance: X-linked (most common) or autosomal recessive
    • Clinical Features:
      • Recurrent infections with catalase-positive organisms (S. aureus, Burkholderia, Serratia, Nocardia, Aspergillus)
      • Granuloma formation (compensatory mechanism)
      • Infections of skin, lungs, liver, bones
    • Diagnosis: Abnormal NBT or DHR test (no color change)
    • Treatment: Prophylactic TMP-SMX + itraconazole, IFN-γ, aggressive infection management
  • Associated Disease: Myeloperoxidase Deficiency
    • Less severe than CGD
    • ↑ susceptibility to Candida infections
    • Most patients asymptomatic (H₂O₂ still produced)