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Respiratory burst (is 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 macrophages, 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 (particularly 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 one of these free radicals, 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.
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:, PMID 12874436 Free full text
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