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industry
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mice lacking the NAD(P)H oxidase gp91phox subunit respond to exposure to single-walled carbon nanotubes with a marked accumulation of polymorphnuclear neutrophils and elevated levels of apoptotic cells in the lungs, production of pro-inflammatory cytokines, decreased production of the anti-inflammatory and pro-fibrotic cytokine, TGF-beta, and significantly lower levels of collagen deposition
synthesis
usage of the enzyme for regeneration of both NADP+ and NAD+ in alcohol dehydrogenase-catalyzed enantioselective oxidation of racemic 1-phenylethanol. NADP+ regeneration at 30°C by TkNOX coupled with (R)-specific ADH from Lactobacillus kefir results in successful acquisition of optically pure (S)-1-phenylethanol, or at 45-60°C with moderately thermostable (S)-specific ADH from Rhodococcus erythropolis in optically pure (R)-1-phenylethanol, giving the possibility to operate the enantioselective bioconversion accompanying NAD+ regeneration at high temperatures, advantage of the combination of thermostable enzymes
additional information
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NADPH oxidase but not myeloperoxidase is required for host defense in lymphopenic mice. Lymphocytes and NADPH oxidase may compensate for each other's deficiency in providing resistance to spontaneous bacterial infections
agriculture
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both genes coding for NAD(P)H oxidases, Nox1 and Nox2, are independently required for pathogenicity of Magnaporthe grisea. Mutants lacking either nox1 or nox2 are incapable of causing plant disease because of unability to bring about appresorium-mediated cuticle penetration
agriculture
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infection by the pathogen Phytophthora infestans results in a radical burst mediated by mitogen-activated protein kinase cascades MEK2-SIPK/NTF4 and MEK1-NTF6. Silencing of the NAD(P)H oxidase Respiratory Burst Oxidase Homolog B, RBOHB eliminates generation of reactive oxygen speicies. INF1 elicitin, produced by the pathogen, regulates reactive oxygen species generation through mitogen-activiated protein kinase cascades
agriculture
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an approximately twofold increase in NADPH oxidase in radicles and epicotyls is observed with Cr(VI) treatment. Cr(VI) elicits H2O2 production in plants, which is suppressed by NaHS and also by an inhibitor of NADPH oxidase (NOX). These effects are correlated with relative changes in carbomyl and thiol groups
medicine
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administration of thrombin to endothelial cells leads to upregulation of enzyme subunit p22phox accompanied by a delayed increase in generation of reactive oxygen species and enhanced proliferation. Existence of a positive feedback mechanism, whereby reactive oxygen species lead to elevated levels of p22phox and thus, sustained generation of reactive oxygen species as is observed in endothelial dysfunction
medicine
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mutations in enzyme gene should be considered as the molecular cause of congenital hypothyroidism in young patients with thyroid dyshormogenesis
medicine
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proliferation of microglial cells induced by fibrillar beta-amyloid peptide Abeta1-40 is mediated both by microglial release of TNF-alpha and by production of hydrogen peroxide by enzyme. TNF-alpha and enzyme, and its products, are potential targets to prevent Abeta-induced inflammatory neurodegeneration
medicine
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TNF-alpha activates enzyme, resulting in an increase in intracellular H2O2 that stimulates Ca2+ sparks and transient Kca currents, leading to a reduction in global concentration of Ca2+ and vasodilation
medicine
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(pro)renin receptor is constitutively expressed in renal glomeruli and tubules. Expression of the receptor is upregulated in diabetes via enhancement of angiotensin subtype 1 receptor-NADPH oxidase activity
medicine
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after 14 days, local treatment with apocynin via the adventitia, reduces superoxide generation. Apocynin significantly reduces neointima formation and proliferation of cells in both the neointima and adventitia. Nitric oxide-dependent vasorelaxation to acetylcholine, which is normally impaired in collared arteries, is improved, and apocynin suppresses the endothelial expression of intracellular adhesion molecule- and vascular cell adhesion molecule-
medicine
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after addition of thrombin to cell culture, expression of NADPH oxidase subunits p47phox and p67phox occurs, accompanied by up-regulation in the expression of cytosolic enzyme components Rac 1 and p67phox, and the translocation of cytosolic subunits p47phox and p67phox to the membrane. Thrombin-induced reactive oxygen species production, protein oxidation, and loss of cultured hippocampal neurons are partially attenuated by NADPH oxidase inhibition and/or by several antioxidants
medicine
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after myocardial infarction, NAD(P)H oxidase activity is markedly increased in remote left ventricular myocardium of wild-type mice but not in mice deficient in subunit p47phox. Increased myocardial xanthine oxidase activity is observed in wild-type, but not in p47phox-deficient mice after myocardial infarction. Left ventricular cavity dilatation and dysfunction 4 weeks after infarction are markedly attenuated in p47phox-deficient mice and cardiomyocyte hypertrophy, apoptosis, and interstitial fibrosis are substantially reduced as compared with wild-type. The survival rate is markedly higher in mice deficient in subunit p47phox
medicine
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analysis of pre-interventional intravascular ultrasound images and histological specimens obtained by directional coronary artherectomy of patients with atherosclerosis. Reactive oxygen positive area ratio in directional coronary artherectomy probes correlates positiviely with vessel cross-sectional area, and relative plaque area. The area immunopositive for subunit p22phox also correlates positively with vessel cross-sectional area, and relative plaque area
medicine
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angiotensin-(1-7) decreases the elevated levels of renal NADPH oxidase activity and attenuates the activation of subunit NOX-4 gene expression in the diabetic hypertensive kidney. Angiotensin-(1-7) treatment increases sodium excretion but does not affect mean arterial pressure in diabetic hypertensive rats. The significant increase in urinary protein in the diabetic compared to control hypertensive rat is reduced by angiotensin-(1-). Angiotensin-(1-7) treatment also attenuates the diabetes-induced increase in renal vascular responsiveness to endothelin-1, norepinephrine, and angiotensin II in hypertensive rats, but significantly increases the vasodilation of the renal artery of hypertensive and diabetic hypertensive rats to the vasodilator agonists
medicine
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aortas of transgenic rats harboring the mouse renin transgene exhibit greater NADPH oxidase activity, reactive oxygen species levels, C-reactive protein, tumor necrosis factor-alpha expression, apoptosis, and wall thickness, which are significantly attenuated by in vivo treatment with angiotensin type 1 receptor blockade by valsartan or the superoxide dismutase/catalase mimetic tempol
medicine
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apocynin reduces avascularity and apoptosis in the oxygen-indunced retinopathy model. The antioxidant properties of N-acetylcysteine are not effective in reducing intravitreous neovasicularization or avascular retina
medicine
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application of HIV regulatory protein Tat to microglia or macrophages causes dose- and time-dependent increases in superoxide formation that are prevented by both pharmacologic NADPH oxidase inhibitors and by specific decoy peptides gp91ds. Inhibition of NADPH oxidase attenuates Tat-induced release of IL-6 and TNFalpha, and MCP-1, and decreases microglial-mediated neurotoxicity. Macrophages derived from NADPH oxidase deficient mice display reduced superoxide production, released lower levels of cytokines/chemokines, and induce less neurotoxicity in response to Tat compared to wild-type macrophages
medicine
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characterization of mutant V674G. Thyroid glands of mutant mice are goitrous and contain few normal follicles, anterior pituitaries are dysplastic. Serum thyroxine in homozygotes is about one-tenth the level of controls.. the weight of adult mutant mice is approximately half that of littermate controls, and serum IGF-I is reduced. The cochleae of mutant mice exhibit abnormalities characteristic of hypothyroidism, including a delayed formation of the inner sulcus and tunnel of Corti and an abnormally thickened tectorial membrane. Hearing thresholds of adult mutant mice are on average 50-60 decibels above those of controls
medicine
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chronic administration of agents that induce hypertension can also produce changes in the subcellular localization in subunit p47phox in dorsomedial nucleus tractus solitarius neurons. Systemic hypertension may produce alterations in the trafficking of proteins associated with superoxide production in central autonomic neurons. Administration of angiotensin over 7 days, which produces elevated systemic blood pressure, is associated with a redistribution of p47phox immunolabeling away from intracellular organelles in the distal dendritic compartment, and toward non-vesicular targets in less distal, intermediate areas of dorsomedial nucleus tractus solitarius neurons. Chronic administration of phenylephrine, which produces increases in systolic blood pressure, is associated with a repartitioning of p47phox immunolabeling away from intracellular organelles in distal dendritic areas, andtoward the plasma membrane of intermediate dendritic areas of dorsomedial nucleus tractus solitarius neurons
medicine
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diabetes-induced translocation of protein kinase C, specifically PKC-alpha to renal membranes is associated with increased NADPH-dependent superoxide production. In both diabetic animals and in advanced glycation end products-treated mesangial cells, blockade of NADPH oxidase or PKC-alpha attenuates cytosolic superoxide and protein kinase C activation and increases vascular endothelial growth factor
medicine
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experimental model of spontaneous intracranial hemorrhage in transgenic mice expressing human renin and human angiotensinogen treated with high-salt diet and Nomega-nitro-L-arginine methyl ester. In these mice, NAD(P)H oxidase activity is significantly increased. Increased enzyme activity preceeds signs of spontaneous intracranial hemorrhage and increases further whith development of intracranial hemorrhage
medicine
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exposure of porcine coronary artery endothelial cells, PCAECs, to hypoxia for 2 h followed by 1 h of reoxygenation significantly increases reactive oxygen species formation. Pretreatment with the NADPH oxidase inhibitors, diphenyleneiodonium and apocynin, significantly attenuates hypoxia/reoxygenation-induced reactive oxygen species formation. Exposure of PCAECs to hypoxia/reoxygenation causes a significant increase in serine-threonine kinase Akt and ERK1/2 activation. Exposure of PCAEC spheroids to hypoxia/reoxygenation significantly increases endothelial spheroid sprouting and vessel outgrowth, whereas pharmacological inhibition of NADPH oxidase or genetic deletion of the NADPH oxidase subunit p47phox significantly suppresses these changes
medicine
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expression of isoform Nox4 mRNA in glioblastomas of WHO grade IV is significantly higher than other astrocytomas of WHO grades II and III. Knock-down of isoform Nox4 expression by RNAi results in cell-growth inhibition and enhances induction of apoptosis by chemotherapeutic agents in cultured glioma cell lines
medicine
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glucose-mediated down-regulation of protein kinase G-I expression in vascular smooth muscle cells occurs through protein kinase C-dependent activation of NAD(P)H oxidase derived superoxide production, contributing to diabetes-associated vessel dysfunctions
medicine
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hydrophobic, proapoptotic bile salts induce hepatocyte shrinkage largely through NADPH oxidase-derived oxidative stress. Because cell shrinkage in turn activates NADPH oxidase, which blunts cell volume recovery, a vicious cycle ensues between oxidative stress and cell shrinkage, which propagates CD95 activation and may finally lead to apoptosis
medicine
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hypoosmotic swelling of cardiac myocytes activates volume-sensitive Cl- current via the angiotensin II-reactive oxygen species signalling cascade. In several models of cardiac disease, volume-sensitive Cl- current is persistently activated
medicine
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hypoxic conditions lead to upregulation exclusively of NOX4 mRNA in lung, concomitant with increased levels in microdissected pulmonary arterial vessels. NOX4 mRNA and protein are localized predominantly in the media of small pulmonary arteries, with increased labeling intensities after chronic exposure to hypoxia. In isolated pulmonary arterial smooth muscle cells, NOX4 is localized primarily to the perinuclear space
medicine
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in brain capillary endothelial cells, hypoxia/reoxygenation induces translocation of the NAD(P)H oxidase activator Rac-1 to the membrane. Inhibition of Rac-1 prevents the ischemia/reperfusion-induced blood-brain barrier disruption. Activation of NAD(P)H oxidase promotes cerebral reactive oxygen species formation, which then leads to Rho kinase-mediated endothelial cell contraction and disruption of the blood-brain barrier
medicine
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in cells continuously treated with nitric oxide donors, including nitroglycerin, over 2-3 days, basal production of nitrite and nitrate is diminished. The diminished basal nitric oxide levels are mitigated by intermittent treatment allowing an 8-h daily nitrate-free interval during the 2- to 3-day treatment period. Addition of the NAD(P)H oxidase inhibitor apocynin restores the basal levels of nitric oxides that are decreased by continuous nitroglycerin treatment. Apocynin causes significant improvement of increased mRNA and protein levels of endothelial nitric oxide synthase in cells given nitroglycerin continuously over the treatment period. Apocynin also reduces endothelial production of reactive oxygen species after continuous nitroglycerin treatment
medicine
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in lungs from patients with idiopathic pulmonary arterial hypertension, expression levels of NOX4, which is localized in the vessel media, are 2.5-fold upregulated
medicine
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in macula densa, increasing luminal NaCl induces superoxide anion production during tubuloglomerular feedback. Superoxide anion generated by the macula densa is primarily derived from NAD(P)H oxidase and is induced by depolarization
medicine
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in obese, diabetic, leptin-receptor deficient db-/db- mice, mRNA levels of enzyme subunits Nox-1, Nox-2, and Nox-4 as well as Nox-2 protein expression are elevated, whereas aortic Cu/Zn superoxide dismutase protein and PPARgamma mRNA levels are reduced
medicine
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in peripheral blood lymphocytes from children with acute asthma, activity of NAD(P)H oxidase is significantly increased. Plasma levels of malondialdehyde, and nitric oxide are also markedly elevated, while catalase activity is decreased. Treatment of lymphocytes with salbutamol at 10 microg per ml, prevents the attenuation of catalase activity but significantly increases the levels of nitroc oxide and NAD(P)H oxidase activity. Levels of isoform NOX-1 mRNA are significantly increased in peripheral blodd lymphocytes following treatment with NO donor, S-nitroso-N-acetyl penicillamine. Subunit gp91phox protein is also two- to threefold increased following treatment with S-nitroso-N-acetyl penicillamine and leads to increased NAD(P)H oxidase activity
medicine
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in rabbits with heart failure induced by myocardial infarction, treatment with inhibitor apocynin reduces NADPH oxidase activity, subunit p47phox protein, oxidative stress, myocyte apoptosis, and Bax protein, increases Bcl-2 protein, and ameliorates left ventricular dilatation and dysfunction
medicine
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in sarcoplasmic reticulum vesicles isolated after exercise and tachycardia, increase in NAD(P)H oxidase activity, ryanodine receptor-2 S-glutathionylation, and calcium release rates. Apocynin prevents the increase in ryanodine receptor-2 S-glutathionylation, reduced calcium release activity, and completely prevents the protective effects of exercise and tachycardia on infarct size
medicine
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increased oxidative stress in the vasculature of streptozotocin-induced diabetic apoE-deficient mice is linked to changes in endothelial nitric oxide synthase, superoxide dismutase and NADPH oxidase expression
medicine
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increases in myocardial serine-threonine kinase Akt and ERK1/2 activation and vascular endothelial growth factor expression are markedly blunted in the subunit p47phox-deficient mouse subjected to myocardial ischemia-reperfusion compared with the wild-type mouse
medicine
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incubation of microglial cultures in the presence of fibrillar amyloid beta1-42 induces the assembly and the activation of NADPH oxidase, and triggers the production of superoxide anion-derived reactive oxygen species. Pretreatment of microglia with melatonin dosedependently prevents the activation of NADPH oxidase and decreases the production of reactive oxygen species. Melatonin inhibits the phosphorylation of the p47phox subunit of NADPH oxidase via a PI3K/Akt-dependent signalling pathway, blocks the translocation of p47phox and p67phox subunit to the membrane, down-regulates the binding of p47phox to gp91phox, and impairs the assembly of NADPH oxidase
medicine
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induction of sterile hyperinflammation by injection of fungal cell wall preparations in chronic granulomatous disease mouse model. Preparations from Aspergillus fumigatus, Candida albicans, or Saccharomyces cerevisiae cause prolonged and severe skin inflammation, but not preparations from bacteria such as Staphylococcus aureus, Pseudomonas aerginosa, or Escherichia coli. Components most responsible for the inflammatory effect are branched fungal beta-glucans
medicine
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induction of superoxide production by doxorubicin is much higher in hearts of wild-type mice than in subunit gp91phox knock-out mice. Superoxide production is similarly induced by addition of NADPH cytochrome P450 reductase
medicine
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inhibition of NAD(P)H oxidase by apocynin in ischemia-induced mice prevents blood-brain barrier damage in the ischemic hemisphere I after reperfusion. In mice deficient in subunit gp91phox, middle cerebral artery occlusion-induced blood-brain barrier disruption and lesion volume in ischemia-induced animals are largely attenuated. Activation of NAD(P)H oxidase promotes cerebral reactive oxygen species formation, which then leads to Rho kinase-mediated endothelial cell contraction and disruption of the blood-brain barrier
medicine
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inhibition of subunit Nox4 expression by small interfering RNA reduces angiogenic responses, in both human microvascular and umbilical vein endothelial cells. Overexpression of wild-type Nox4 enhances, whereas expression of a dominant negative form of Nox4 suppresses the angiogenic responses in endothelial cells. These effects are mimicked by exogenous H2O2 and the antioxidant compound ebselen, respectively. Overexpression of Nox4 enhances receptor tyrosine kinase phosphorylation and the activation of extracellular signal-regulated kinase. Nox4 expression also promotes proliferation and migration of endothelial cells, and reduces serum deprivation-induced apoptosis
medicine
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intrarenal infusions of angiotensin II both in vitro and in vivo increase renal vascular resistance, and alpha2-adrenoceptor agonist UK14,304 enhances this response. The interaction between angiotensin II and UK14,304 is blocked by inhibitors of NAD(P)H oxidase
medicine
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intravitreal injections of angiotensin II can result in retinal leukostasis, which appears to be mediated via increasing superoxide generation by NAD(P)H oxidase, and by vasular endothelial growth factor. The activity of NAD(P)H oxidase is required for leukostasis to occur in the diabetic retina
medicine
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isoform Nox4 is expressed at high levels in white and brown preadipocytes. Differentiation into adipocytes results in a decrease in their NOX4 mRNA content. In intact adipose tissue, the majority of NOX4 expressing cells are localized within the preadipocyte containing stromal/vascular fracftion. Alterations in NOX4 expression reflects changes in the ratio of adipocyte/interstitial fractions
medicine
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isoobtusilactone A elicits a concentration-dependent growth impediment with IC50 value of 37.5 microM. Treated cells also display transient increase of reactive oxygen species during the earlier stage of the experiment, followed by the disruption of mitochondrial transmembrane potential. The presence of a reactive oxygen species scavenger N-acetyl-L-cysteine and the inhibitor of NADPH oxidase diphenyleneiodonium chloride block reactive oxygen species production and the subsequent apoptotic cell death
medicine
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long-term survival mechanisms in niacin deficient HaCaT keratinocyte cells involve accumulation of reactive oxygen species and increased DNA damage with concomitant increase in expression and activity of NAD(P)H oxidase
medicine
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mice deficient in NAD(P)H oxidase p47phox show an increase of 17% of the area occupied by airway smooth muscle cells in trachea, compared with wild-type. They exhibit a significantly reduced airway smooth muscle cell relaxation during electric field stimulation and after the end of stimulation. NAD(P)H oxidase may have a role in the structural arrangement and mechanical properties of the airway tissue
medicine
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mice lacking the NAD(P)H oxidase gp91phox subunit respond to exposure to single-walled carbon nanotubes with a marked accumulation of polymorphnuclear neutrophils and elevated levels of apoptotic cells in the lungs, production of pro-inflammatory cytokines, decreased production of the anti-inflammatory and pro-fibrotic cytokine, TGF-beta, and significantly lower levels of collagen deposition
medicine
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microinjection of lipopolysaccharide bilaterally into the rostral ventrolateral medulla induces progressive hypotension, bradycardia, and reduction in sympathetic vasomotor outflow. This is accompanied by an increase in superoxide anion production for 60-240 min, alongside phosphorylation of subunits p47phox or p67phox, upregulation of gp91phox or p47phox protein, and increase in Rac-1 or NADPH oxidase activity during 60-120 min, and a depression of mitochondrial respiratory enzyme activity during 120-240 min. Inhibition of NADPH oxidase or knockdown of the gp91phox or p47phox gene blunts the early phase of 60-150 min, coenzyme Q10 or mitochondrial KATP channel inhibitor antagonizes the delayed phase of 120-240 min of lipopolysaccharide-nduced increase in superoxide anion production in rostral ventrolateral medulla and cardiovascular depression
medicine
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monocytes from sickle cell disease patients show higher levels of NAD(P)H oxidase subunit gp91phox gene expression and p47phox phosphorylation, along with increased interferon-gamma release by lymphocytes
medicine
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N-[2-(4-hydroxy-phenyl)-ethyl]-2-(2, 5-dimethoxy-phenyl)-3-(3-methoxy-4-hydroxy-phenyl)-acrylamide i.e. FLZ, squamosamide derivative. FLZ inhibits the translocation of the cytosolic subunit p47phox to the membrane and thus inhibits the activation of NAD(P)H oxidase. In vivo, FLZ significantly protects against 1-methyl-4-phenyl-1, 2, 3, 6-tetrahydropyridine-induced dopaminergic neuronal loss
medicine
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NADPH oxidase is involved in killing of Candida albicans by dendritic cells, which is increased by interferon-alpha or interferon-gamma. However, Candida escapes the oxidative damage by inhibiting NADPH oxidase and by entering dendritic cells through receptors not involved in NADPH oxidase activation
medicine
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neuroblastoma cell, cells differentiated by retinoic acid die after exposure to glycated albumin, a model of advanced glycation end product-modified protein. Undifferentiated cells are resistant to glycated albumin. Differentiated cells pre-treated with NAD(P)K oxidase inhibitor diphenyleneiodinium or with rottlerin, an inhibitor of protein kinase C delta, are able to prevent neuronal death induced by glycated albumin
medicine
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neutrophil cytosolic factor 1-deficient mice lacking functional NADPH oxidase are resistant to skin blistering by the passive transfer of antibodies against type VII collagen. Recruitment of granulocytes into the skin is required for tissue injury, as demonstrated by the resistance to experimental blistering of wild-type mice depleted of neutrophils and of CD18-deficient mice. Granulocyte-derived NADPH oxidase is a key molecular effector engaged by pathogenic autoantibodies and provides relevant targets for prevention of tissue damage in granulocyte-mediated autoimmune diseases
medicine
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neutropjhil NAD(P)H oxidase activation, induced by hemorrhagic shock/resuscitation and as mediated by high-mobility group box HMGB1/TLR4 signaling, is an important mechanism responsible for hemorrhagic shock/resuscitation-mediated inflammation and organ injury after hemorrhage
medicine
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on a high-salt diet of 4% NaC1, male and obese rats have significantly higher mean arterial blood pressure relative to female and lean rats and reduced renal cortical nitric oxide synthase activity. Lean female rats have the highest outer medullary protein levels of several NADPH oxidase subunits, including gp91phox, p47phox, and p67phox, however, renal NADPH activity is not increased in lean females, but is significantly increased in obese rats of both sexes
medicine
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overweight and obese adults demonstrate increased vascular endothelial expression of NAD(P)H oxidase subunit p47phox and evidence of endothelial oxidative stress, with selective compensatory upregulation of antioxidant enzymes and Ser1177-phosphorylated endothelial nitric oxide synthase. Endothelin-1 and nuclear factor kappaB protein expression also appear to be elevated in obese compared with lean adults
medicine
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pharmacological inhibition or deficiency of human NADPH oxidase abolishes dermal-epidermal separation caused by autoantibodies and granulocytes ex vivo. Granulocyte-derived NADPH oxidase is a key molecular effector engaged by pathogenic autoantibodies and provides relevant targets for prevention of tissue damage in granulocyte-mediated autoimmune diseases
medicine
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pivotal role of myeloid Src family kinases and complement receptor 3 in mounting an effective defense against infection with Streptococcus pneumonia by regulating phagocytosis and NADPH oxidase-dependent superoxide production. Leukocyte recruitment into the cerebrospinal fluid space and bacterial clearance is hampered in mice deficient in all three myeloid Src family kinases during pneumococcal meningitis. The mice develop increased intracranial pressure and a worse clinical outcome with increased neurologic deficits and mortality, compared with wildtype mice. In neutrophils of mice deficient for myeloid Src family kinases p59/61hck, p58c-fgr, and p53/56lyn, phosphorylation of NAD(P)H oxidase subunit p40phox is absent, indicating a defect in enzyme activation
medicine
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platelets and leukocytes from high cholesterol-fed mice exhibit elevated generation of reactive oxygen species compared to normal diet mice. Hypercholesterolemia-induced leukocyte recruitment is attenuated in Cu,Zn-superoxide dismutase transgenic, and NAD(P)H oxidase-knockout mice on high cholesterol diet. Platelets from NAD(P)H oxidase-knockout mice on high cholesterol diet exhibit low levels of adhesion comparable to those of wild-type on normal diet. Overexpression of Cu,Zn-superoxide dismutase or, to a lesser extent, NAD(P)H oxidase subunit gp91 deficiency restores arteriolar vasorelaxation responses toward normal diet wild-type levels
medicine
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pre-treatment of NB-4 cells with inhibitor diphenyleneiodinium blocks arsenic trioxide-induced apoptosis
medicine
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reactive oxygen species produced upstream of Ca2+ influx by NADPH oxidase and downstream of Ca2+ influx by the mitochondria regulate the proinflammatory response of mast cells
medicine
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rosiglitazone activates 5'-AMP-activated protein kinase which, in turn, prevents hyperactivity of NAD(P)H oxidase induced by high glucose, possibly through protein kinase C inhibition. Rosiglitazone protects endothelial cells against glucose-induced oxidative stress with an 5'-AMP-activated protein kinase-dependent and a PPARgamma-independent mechanism
medicine
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rosuvastatin reduces systolic blood pressure in spontaneously hypertensive rats but does not change plasma lipid levels. Rosuvastatin treatment in spontaneously hypertensive rats significantly decreases reactive oxygen species levels , NAD(P)H activity in retinal ganglion cells, and increases retinal plasmalogen content in spontaneously hypertensive rats, but does not modify the electroretinogram response
medicine
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salt sensitivity in the salt-sensitive rat is associated with upregulations of the intrarenal angiotensin system, reactive oxygen species-generating and proinflammatory/profibrotic proteins and an inability to raise antioxidant enzymes and maximally suppress plasma renin activity in response to high salt intake
medicine
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single nucleotide polymorphisms 242C/T and 640A/G in the gene encoding p22phox subunit of NAD(P)H oxidase are marginally significantly associated with asthma, but single nucleotide polymorphisms 640A/G shows a significant association with sensitization to two allergens tested. Haplotype 930G/242T/640A is associated with an increased risk of asthma
medicine
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study on the aggregation of platelets from high-risk cardiac patients with aspirin resistance in presence of adenosine diphosphate, collagen, and epinephrine. Inhibition of NAD(P)H oxidase effectively suppresses collagen and epinephrine-induced aggregation
medicine
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the morphinan analog, sinomenine inhibits NAD(P)H oxidase cytosolic subunit p47phox translocation to the cell membrane and thus reduces lipopolysaccharide-induced extracellular reactive oxygen species production. Sinomenine protects neuron-glial cell cultures at both micro- and sub-picomolar concentrations against dopaminergic neuron death, but not protection is seen at nanomolar concentrations
medicine
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treatment of animals by oral administration of isoobtusilactone A for two weeks does not result in significant difference between control animals and treated animals with respect to the body weight gain, the body weight ratio of liver, spleen and kidney, haematological and clinical chemistry parameters
medicine
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treatment of fibroblasts with tumor necrosis factor induces the formation of a signaling complex containing TNF-R1-associated death domain protein TRADD, receptor interacting protein RIP1, NAD(P)H oxidase Nox1, and the small GTPase Rac1. Formation of this complex plays a key role in tumor necrosis factor-induced necrotic cell death
medicine
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treatment with peptidyl inhibitor gp91ds-tat reduces proliferation and migration of cultured microvascular endothelial cells
medicine
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vascular cell adhesion molecule-1 induction of NADPH oxidase in the endothelium is necessary for the eosinophil recruitment during allergic inflammation
medicine
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water-soluble components of cigarette smoke activate the vascular NAD(P)H oxidase. NAD(P)H oxidase-derived H2O2 activates NF-kappaB, leading to proinflammatory alterations in vascular phenotype, which likely promotes development of atherosclerosis
medicine
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wild-type mice fed with high-cholesterol diet exhibit impaired endothelium-dependent vasodilation, enhanced superoxide generation, and increased expression of NAD(P)H oxidase subunit Nox-2 mRNA. In severe combined immunodeficient mice, in mice genetically deficient for interferon IFN-gamma, and CD4+ T-lymphocyte-deficient mice, the impaired endothelium-dependent vasodilation and enhanced superoxide generation are significantly blunted. Effects are similar in high-cholesterol fed mice genetically deficient in NAD(P)H oxidase subunit Nox-2
medicine
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wild-type mice with myocardial infarction display significantly increased gp91phox and 3-nitrotyrosine in the infarcted myocardium, accumulated macrophages and myofibroblasts at the infarct site, abundant apoptotic myocytes primarily at border zones on day 3, and numerous apoptotic inflammatory/myofibroblasts in the later stages. Transforming growth factor 1, tissue inhibitor of metalloprotease 2, and type 1 collagen gene expression is increased, collagen volume in the infarcted myocardium continuously increases, and noninfarcted myocardium displays hypertrophy. Compared to wild-type mice with myocardial infarction, subunit gp91phox knockout mice do not display significant difference in infarct size/thickness, cardiac hypertrophy, myocyte apoptosis, inflammatory/fibrogenic responses, as well as cardiac oxidative stress
medicine
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Burkholderia cenocepacia resides in macrophage vacuoles displaying an altered recruitment of the NADPH oxidase complex at the phagosomal membrane. This phenomenon may contribute to preventing the efficient clearance of this opportunistic pathogen from the infected airways of susceptible patients
medicine
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chronic granulomatous disease is a rare inherited immunodeficiency syndrome caused by mutations in four genes encoding essential nicotinamide adenine dinucleotide phosphate (NADPH) oxidase complex components. Clinical, functional, and molecular investigation of chronic granulomatous disease in nine Jordanian families
medicine
inactivating mutations of Duox2 are linked to congenital hypothyroidism, and epigenetic silencing of Duox is frequently observed in lung cancer
medicine
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as NAD(P)H oxidase activation may have dual actions in diabetes, selective targeting of the deleterious effects of sustained NAD(P)H oxidase activation, such as eNOS uncoupling, mitochondrial dysfunction, and impaired antioxidant gene expression, may prove beneficial in the treatment of diabetes
medicine
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as NAD(P)H oxidase activation may have dual actions in diabetes, selective targeting of the deleterious effects of sustained NAD(P)H oxidase activation, such as eNOS uncoupling, mitochondrial dysfunction, and impaired antioxidant gene expression, may prove beneficial in the treatment of diabetes
medicine
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as NAD(P)H oxidase activation may have dual actions in diabetes, selective targeting of the deleterious effects of sustained NAD(P)H oxidase activation, such as eNOS uncoupling, mitochondrial dysfunction, and impaired antioxidant gene expression, may prove beneficial in the treatment of diabetes
medicine
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as NAD(P)H oxidase activation may have dual actions in diabetes, selective targeting of the deleterious effects of sustained NAD(P)H oxidase activation, such as eNOS uncoupling, mitochondrial dysfunction, and impaired antioxidant gene expression, may prove beneficial in the treatment of diabetes
medicine
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NADPH oxidase type 4 is a major source of oxidative stress and an effective therapeutic target in acute stroke
medicine
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NADPH oxidase type 4 is a major source of oxidative stress and an effective therapeutic target in acute stroke
medicine
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in apolipoprotein E-knockout mice, aequous extract of Tessaria absinthioides and Prosopis strombulifera significantly reduce triglycerides and lipid peroxidation, increase plasma total antioxidant status, and improve glutathione peroxidase activity in the liver. Under high-fat diet, both extracts are able to inhibit O2 anion generation in the aortic tissue and cause a significant regression of atheroma plaques