Nicotinamide adenine dinucleotide phosphate oxidase

Cumutte, J. T., Berkow, R. L., Roberts, R. L., Shurin, S. B., Scott, P. J. (1988). Chronic granulomatous disease due to a defect in the cytosolic factor required for nicotinamide adenine dinucleotide phosphate oxidase activation. J. Clin. Invest. 81,606-10. 

Overproduction of superoxide ( Op has been implicated in the pathogenesis of various cardiovascular diseases. The main sources of human superoxide include the nicotinamide adenine dinucleotide phosphate oxidase (NADPH oxidase) enzyme complex, cyclooxygenase, mitochondrial oxidases, xanthine oxidase, and nitric... 

Fortune, A., Beloqui, O., San Jose, G., Moreno, M. U., Zalba, G., Diez, J. (2005). Increased phagocytic nicotinamide adenine dinucleotide phosphate oxidase-dependent superoxide production in patients with early chronic kidney disease. Kidney Inter. SuppL, 99, S71-S75. 

Ying, C. J., Xu, J. W, Ikeda, K., Takahashi, K., Nara, Y, Yamori, Y. (2003). Tea polyphenols regulate nicotinamide adenine dinucleotide phosphate oxidase subunit expression and ameliorate angiotensin 11-induced hyperpermeability in endothelial cells. Hypertens. Res., 26, 823-828. 

NADPH oxidase nicotinamide adenine dinucleotide phosphate oxidase, a primary producer of reactive oxygen species. 

Rusyn, I., Yamashina, S., Segal, B. H., Schoonhoven, R., Holland, S. M., Cattley, R. C., Swenberg, 1. A., and Thurman, R. G. (2000c). Oxidants from nicotinamide adenine dinucleotide phosphate oxidase are involved in triggering cell proliferation in the Uver due to peroxisome prohferators. Cancer Res 60, 4798-4803. 

Kim, C. and Dinauer, M.C. (2001). Rac2 is an essential regulator of neutrophil nicotinamide adenine dinucleotide phosphate oxidase activation in response to specific signaling pathways./. Immunol. 166,1223-1232. 

The resulting oxidized LDL particles trapped in the vessel wall can undergo a number of other reactions including lipolysis, proteolysis and aggregation, which contribute to inflammation and foam cell formation. A multitude of oxidation pathways have been proposed that involve 12/15-lipoxygenase, metals ions, myeloperoxidase producing hypochlorous acid, and NADP (nicotinamide adenine dinucleotide phosphate) oxidase. 

The answers are 34-g, 35-a, 36-d. (Katzung, pp 53—56J There are four major components to the mixed-function oxidase system (1) cytochrome P450, (2) NAD PH, or reduced nicotinamide adenine dinucleotide phosphate, (3) NAD PH—cytochrome P450 reductase, and (4) molecular oxygen. The figure that follows shows the catalytic cycle for the reactions dependent upon cytochrome P450. 

Hexachloroethane is metabolized by the mixed function oxidase system by way of a two-step reduction reaction involving cytochrome P-450 and either reduced nicotinamide adenine dinucleotide phosphate (NADPH) or cytochrome b5 as an electron donor. The first step of the reduction reaction results in the formation of the pentachloroethyl free radical. In the second step, tetrachloroethene is formed as the primary metabolite. Two chloride ions are released. Pentachloroethane is a minor metabolic product that is generated from the pentachloroethyl free radical. 

Curnutte, J. T. (1985). Activation of human neutrophil nicotinamide adenine dinucleotide phosphate, reduced (triphosphopyridine nucleotide, reduced) oxidase by arachidonic acid in a cell-free system. J. Clin. Invest. 75, 1740-3. 

Cassatella, M. A., Hartman, L., Perussia, B., Trinchieri, G. (1989). Tumor necrosis factor and immune interferon synergistically induce cytochrome b.245 heavy-chain gene expression and nicotinamide-adenine dinucleotide phosphate hydrogenase oxidase in human leukemic myeloid cells. J. Clin. Invest. 83,1570-9. 

Cholesterol is transported into the mitochondria of steroidogenic tissue, where side chain cleavage is carried out. In common with other mixed-function oxidase systems, the cholesterol side chain cleavage requires reduced nicotinamide-adenine dinucleotide phosphate... 

Enzymes responsible for metabolism are located at various subcellular sites, for example the cytosol, mitochondria and smooth endoplasmic reticulum. However, it is enzymes derived from endoplasmic reticulum, called mixed function oxidases or monooxygenases , which have been most intensely studied in the past two or three decades. These enzyme systems, which utilize a family of haemoprotein cytochromes, or P-450 as terminal oxidases, require molecular oxygen and reduced nicotinamide adenine dinucleotide phosphate (NADPH) for activity. The overall stoichiometry of the reactions catalyzed by these enzymes is normally represented by equation (1). 

Reduced nicotinamide adenine dinucleotide phosphate (NADPH) oxidase is an enzymatic complex considered the most important source of superoxide... 

The hepatic endoplasmic reticulum possesses oxidative enzymes called mixed-function oxidases or monooxygenase with a specific requirement for both molecular oxygen and a reduced concentration of nicotinamide adenine dinucleotide phosphate (NADPH). Essential in the mixed-function oxidase system is P-450 (Figure 1.12). The primary electron donor is NADPH, whereas the electron transfer involved P-450, a flavoprotein. The presence of a heat-stable fraction is necessary for the operation of the system. 

Conditions for cytosolic incubations depend on the aim of the assay e.g. to cover specific enzymatic activity present in the cytosol. For this purpose it is essential to fortify the incubation medium with the specific cofactor for the reaction-if needed (Ekins 1999). (J> -Nicotinamide adenine dinucleotide (NAD) is needed for alcohol and aldehyde dehydrogenases, flavin adenine dinucleotide (FAD) for polyamine oxidase, P-nicotinamide adenine dinucleotide phosphate (NADPH) for Dihydropyrimidine dehydrogenase. Phase II reactions depend on PAPS (sulfotransferases,... 

Production of ROS, factors involved in the aging process (Finkel and Holbrook, 2000), is elevated in AD brain and may be an important cause of AD (Martins et al., 1986). Elevated levels of oxicUzed hpids (lipid peroxidation, maloncUaldehyde, 4-hydroxynonenal) (Markesbery and Carney, 1999), proteins (advanced glycation end product mocUfications, tyrosine nitration) (Good et al., 1996 Takeda et al., 1998), and nucleic acids (8-hydroxy-deoxyguanosine) have been documented in AD brains (Lyras et al., 1997). Mitochondria and nicotinamide adenine dinucleotide phosphate (NADPH) oxidase complex... 

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