Respiratory burst is due to which enzyme

Phagocytosis: Phagocytosis (Greek word-Phagein-to eat) is the engulfment of large paicles like viruses, bacteria, cells, or debris by macrophages and granulocytes. They extend pseudopodia and surround the paicles to form phagosomes which later fuse with lysosomes to form Phagolysosomes in which the paicles are digested. Biochemical mechanism is called respiratory burst, in which O2 consumption is increased and lead to formation of superoxide ion O2-. Superoxide anion O2- is conveed to H2O2 and other free radicals OH* and OCl-, etc. which are potent microbial agent. O2- + O2- + 2H+ - H2O2 + O2 The electron transpo chain system responsible for the "respiratory burst" is "NADPH oxidase". In resting phagocyte it is in an inactive form, consisting of cytochrome b 558 + two polypeptides (heterodimer). The NADPH oxidase system is activated by recruitment in plasma membrane by two more cytoplasmic polypeptides. Thus: 2 Cytoplasmic polypeptides Cytb558 + 2 Polypeptides _______________________ Cytb588 (Inactive NADPH oxidase) + 4 Polypeptides (Active NADPH oxidase) NADPH oxidase is activated upon contact with various ligands like complement fragment C5a, chemotactic peptides, etc. Events resulting in activation of the NADPH oxidase system involve G proteins, activation of phospholipase C and generation of inositol-1, 4, 5-triphosphate (P3). The P3 mediates a transient increase in the level of cytosolic Ca++, which is essential for the induction of the respiratory burst. Killing of bacteria within phagolysosomes appears to depend on the combined action of elevated pH, superoxide ions or other "free radicals" like H2O2, OH*, and HOCl (hypochlorous acid) and on the action of ceain bactericidal peptides, called defensins and other proteins, e.g. cathepsin G and ceain cationic proteins present in phagocytic cells. Macrophages are extremely active and may ingest 25 percent of their volume per hour. In such a process, a macrophage may internalize 3 percent of its plasma membrane each minute or the entire membrane every 1/2 hour. CLINICAL ASPECT Chronic granulomatous disease has been recently implicated due to defective phagocytosis and respiratory burst. The disease is characterized by * Recurrent infections * Widespread granuloma formation in various tissues like lungs, lymph nodes, skin, etc. Fig. 2.11: Sequence of events that occur in chronic granulomatous disease Defect: The disorder is attributed to mutations in the genes encoding the four polypeptides that constitute the active NADPH oxidase system. The granulomas are formed as attempts to wall off bacteria that have not been killed due to genetic deficiencies in the NADPH oxidase systemRef: MN Chatterjea Textbook of Medical Biochemistry, 8th edition, page no: 18