Respiratory burst
Oxford Dictionary of Biochemistry:
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respiratory burst
a phase of elevated oxygen consumption that occurs in neutrophils, monocytes, and macrophages shortly after phagocytosing material. This is associated with increased activity of the hexose monophosphate shunt and production of NADPH(see pentose phosphate pathway). An NADPH oxidase complex passes electrons from the NADPH to O2 creating the reactive sueroxide (O2 −) ion and H2 O2 in the vacuole. Patients with chronic granulomatous disease never produce a respiratory burst. The patients suffer an accumulation of mononuclear cells at sites of chronic inflammation, forming granulomas. See phagocyte NADPH oxidase.
| respiration, resorcinol, resorb | |
| respiratory chain, respiratory complex, respiratory control |
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Respiratory burst
Respiratory burst (sometimes called oxidative burst) is the rapid release of reactive oxygen species (superoxide radical and hydrogen peroxide) from different types of cells.
Usually it denotes the release of these chemicals from immune cells, e.g., neutrophils and monocytes, as they come into contact with different bacteria or fungi. They are also released from the ovum of higher animals after the ovum has been fertilized. These substances can also be released from plant cells.
Respiratory burst plays an important role in the immune system. It is a crucial reaction that occurs in phagocytes to degrade internalized particles and bacteria.
NADPH oxidase, an enzyme family in the vasculature (in particular, in vascular disease), produces superoxide, which spontaneously recombines with other molecules to produce reactive free radicals. The superoxide reacts with NO, resulting in the formation of peroxynitrite, reducing the bioactive NO needed to dilate terminal arterioles, feed arteries and resistance arteries. Superoxide anion, peroxynitrite, and other reactive oxygen species also lead to pathology via peroxidation of proteins and lipids, and via activation of redox sensitive signaling cascades and protein nitrosylation. NADPH oxidase activation has been suggested to depend on prior PKC activation.[1] Myeloperoxidase uses the reactive oxygen species hydrogen peroxide to produce hypochlorous acid. Many vascular stimuli, including all those known to lead to insulin resistance, activate NADPH oxidase via both increased gene expression and complex activation mechanisms.
To combat infections, immune cells use NADPH oxidase to reduce O2 to oxygen free radical and then H2O2. Neutrophils and monocytes utilize myeloperoxidase to further combine H2O2 with Cl- to produce hypochlorite, which plays a role in destroying bacteria. Absence of NADPH oxidase will prevent the formation of reactive oxygen species and will result in chronic granulomatous disease.
References
- ^ Inoguchi T, Sonta T, Tsubouchi H, Etoh T, Kakimoto M, Sonoda N, Sato N, Sekiguchi N, Kobayashi K, Sumimoto H, Utsumi H, Nawata H (2003). "Protein kinase C-dependent increase in reactive oxygen species (ROS) production in vascular tissues of diabetes: role of vascular NAD(P)H oxidase". J. Am. Soc. Nephrol. 14 (8 Suppl 3): S227–32. doi:10.1097/01.ASN.0000077407.90309.65. PMID 12874436. Free full text
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