Respiratory burst

Lucas, M., and Solano, F. (1992). Coelenterazine is a superoxide anion-sensitive chemiluminescent probe its usefulness in the assay of respiratory burst in neutrophils. Anal. Biochem. 206 273-277. 

CC, and one CX3C and XC chemokine receptors have been cloned so far [2]. Receptor binding initiates a cascade of intracellular events mediated by the receptor-associated heterotrimeric G-proteins. These G-protein subunits trigger various effector enzymes that lead to the activation not only of chemotaxis but also to a wide range of fimctions in different leukocytes such as an increase in the respiratory burst, degranulation, phagocytosis, and lipid mediator synthesis. 

Superoxide is formed (reaction 1) in the red blood cell by the auto-oxidation of hemoglobin to methemo-globin (approximately 3% of hemoglobin in human red blood cells has been calculated to auto-oxidize per day) in other tissues, it is formed by the action of enzymes such as cytochrome P450 reductase and xanthine oxidase. When stimulated by contact with bacteria, neutrophils exhibit a respiratory burst (see below) and produce superoxide in a reaction catalyzed by NADPH oxidase (reaction 2). Superoxide spontaneously dismu-tates to form H2O2 and O2 however, the rate of this same reaction is speeded up tremendously by the action of the enzyme superoxide dismutase (reaction 3). Hydrogen peroxide is subject to a number of fates. The enzyme catalase, present in many types of cells, converts... 

NADPH-oxidase j 2O2 + NADPH 20p + NADP -F H+ Key component of the respiratory burst Deficient in chronic granulomatous disease... 

The Respiratory Burst of Phagocytic Cells Involves NADPH Oxidase Helps Kill Bacteria... 

The electron transport chain system responsible for the respiratory burst (named NADPH oxidase) is composed of several components. One is cytochrome 6558, located in the plasma membrane it is a heterodimer, containing two polypeptides of 91 kDa and... 

Leukocytes are activated on exposure to bacteria and other stimuh NADPH oxidase plays a key role in the process of activation (the respiratory burst). Mutations in this enzyme and associated proteins cause chronic granulomatous disease. 

Arthur, M.J.P., Kowalski-Saunders, P. and Wright, R. (1986a). C. /Mm -elicited hepatic macrophages demonstrate enhanced respiratory burst activity compared with resident Kupffer ceUs in the rat. Gastroenterology 91, 174-181. 

Baldassano, R.N., Schreiber, S., Johnston, R.B. and MacDermott, KP. (1991). Increased respiratory burst activity from Crohn s disease peripheral blood mononuclear ph o-cytes. Gastroenterology 100, A559. 

Mahida, Y.R., Wu, K.C. and Jewell, D.P. (1989). Respiratory burst activity of intestinal macrophages in normal and inflammatory bowel disease. Gut 30, 1362-1370. 

Suematsu, M., Suzuki, M., Kitahora, T. et al. (1987a). Increased respiratory burst of leukocytes in inflammatory bowel disease - the analysis of free radical generation by using chemiluminescence probe. J. Clin. Lab. Immunol. 24, 125-128. 

Polymorphonuclear leucocytes (PMNs) employ a system comprising myeloperoxidase, hydrogen peroxide, and a halide factor to kill microorganisms and tumour cells. This process is sometimes loosely called the respiratory burst , which refers to the sudden rise in oxygen consumption by the phagocytosing neutrophils that is independent of the mitochondrial electron transport chain. 

Chronic granulomatous disease is a rare inherited disorder characterized by the failure of neutrophils, eosinophils, monocytes and macrophages to produce the respiratory burst (Curnutte and Babior, 1987) this leads to recurrent bacterial and fungal infections often starting within the first year of life. 

Baggiolini, M. and Thelen, M. (1991). The phagocytes and the respiratory burst. In Oxidative Stress (ed. H. Sies) pp. 399-420. Academic Press, London. 

In addition to the well-characterized role of iron in catalysing redox interactions, other metallic contaminants, for example, nickel, may also contribute. In vivo toxicity studies have demonstrated the capacity of nickel particulate compounds to induce tumours following intraperitoneal injection (Pott etal., 1987). Such activity is proportional to their phagocytic uptake, and to the associated respiratory burst and generation of PMN-derived reactive oxygen metabolites (ROMs), a proposed pathogenic mechanism (Evans et al., 1992a). 

Inflammatory injury is tied to both neutrophil release of neutral proteinases and a respiratory burst with production of superoxide anion and hydrogen peroxide... 

Inflammatory cell phenomenon are also contributors to lipid peroxidation. Activated neutrophils may adhere to damaged endothelium and amplify traumatic, ischaemic or ischaemia-reperfiision injury. Many cyclooxygenase products of the metabolism of atachidonic acid modulate the inflammatory responses of cells. Macrophages, neutrophils and microglia are important sources of reactive oxygen at the injury site. When activated, they produce a respiratory burst that is traced to activated nicotinamide adenine dinucleotide (NADPH/NADH) oxidase. 

The mammalian immune system protects the body from infection by many complex strategies. The most vigorous defense is performed by white blood cells known as granulocytes. These cells consume oxygen in response to microbial infections. This oxidative process, called the respiratory burst, has recently been proven to produce stabilized hvDOchlorite antimicrobials (bredominantlv bv neutroDhils) and stabilized... 

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