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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 and 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.

In plants

Reactive oxygen species (ROS) in plants are important in various signaling cascades and are continuously produced by cells as byproducts of various metabolic pathways.[2] They were mostly shown to be massively produced after the detection of PAMPs by cell-surface located receptors (e.g. FLS2 or EFR).[3][4][5] The production of reactive oxygen species is mediated by the NADPH oxidase, and in plant immunity the subunits RbohD and RbohF have overlapping functions but are expressed in different tissues and in different levels.[6][7] ROS production can be used as a readout for successful pathogen recognition via a luminol-peroxidase based assay.[8]

References

  1. ^ 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
  2. ^ Apel, Klaus; Hirt, Heribert (2004). "REACTIVE OXYGEN SPECIES: Metabolism, Oxidative Stress, and Signal Transduction". Annual Review of Plant Biology. 55 (1): 373–399. doi:10.1146/annurev.arplant.55.031903.141701. PMID 15377225.
  3. ^ Doke, N. (1985-11-01). "NADPH-dependent O2− generation in membrane fractions isolated from wounded potato tubers inoculated with Phytophthora infestans". Physiological Plant Pathology. 27 (3): 311–322. doi:10.1016/0048-4059(85)90044-X.
  4. ^ Bradley, Desmond J.; Kjellbom, Per; Lamb, Christopher J. (1992-07-10). "Elicitor- and wound-induced oxidative cross-linking of a proline-rich plant cell wall protein: A novel, rapid defense response". Cell. 70 (1): 21–30. doi:10.1016/0092-8674(92)90530-P.
  5. ^ Jabs, Thorsten; Tschöpe, Markus; Colling, Christiane; Hahlbrock, Klaus; Scheel, Dierk (1997-04-29). "Elicitor-stimulated ion fluxes and O2− from the oxidative burst are essential components in triggering defense gene activation and phytoalexin synthesis in parsley". Proceedings of the National Academy of Sciences. 94 (9): 4800–4805. doi:10.1073/pnas.94.9.4800. ISSN 0027-8424. PMC 20805. PMID 9114072.
  6. ^ Torres, Miguel Angel; Dangl, Jeffery L.; Jones, Jonathan D. G. (2002-01-08). "Arabidopsis gp91phox homologues AtrbohD and AtrbohF are required for accumulation of reactive oxygen intermediates in the plant defense response". Proceedings of the National Academy of Sciences. 99 (1): 517–522. doi:10.1073/pnas.012452499. ISSN 0027-8424. PMC 117592. PMID 11756663.
  7. ^ Morales, Jorge; Kadota, Yasuhiro; Zipfel, Cyril; Molina, Antonio; Torres, Miguel-Angel (2016-03-01). "The Arabidopsis NADPH oxidasesRbohDandRbohFdisplay differential expression patterns and contributions during plant immunity". Journal of Experimental Botany. 67 (6): 1663–1676. doi:10.1093/jxb/erv558. ISSN 0022-0957.
  8. ^ Keppler, L. Dale (1989). "Active Oxygen Production During a Bacteria-Induced Hypersensitive Reaction in Tobacco Suspension Cells". Phytopathology. 79 (9): 974. doi:10.1094/phyto-79-974.

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