27057461 | Interferon gamma/NADPH oxidase defense system in immunity and cancer |
27057461 | As a part of cellular pathogen defense, IFNgamma triggers induction of NADPH oxidase NOX2, which produces superoxide into phagosomes of immune cells |
27057461 | IFNgamma is capable of inducing expression of constitutively active NADPH oxidase NOX4 in tumor cells leading to generation of reactive oxygen species (ROS) damaging DNA, activation of DNA damage response and cell cycle arrest/premature cellular senescence |
26734996 | ENO1 silencing increased reactive oxygen species that were mainly generated through the sorbitol and NADPH oxidase pathways, as well as autophagy and catabolic pathway adaptations, which together affect cancer cell growth and induce senescence |
26333813 | The autofluorescence emission spectrum of sperm of the common bedbug, Cimex lectularius, was consistent with the presence of flavins and NAD(P)H |
26333813 | 80 ns) suggest the presence of NAD(P)H and flavins and show that sperm metabolism can be characterized using fluorescence lifetime imaging |
26078718 | In this study, we report that expression of NAD(P)H: quinone oxidoreductase 1 (NQO1), a cytoplasmic 2-electron reductase, is induced during oncogene-induced senescence (OIS) |
25982278 | Using human and mouse normal and cancer cell models, we now show that TNFalpha and IFNgamma induce NADPH oxidases Nox4 and Nox1, reactive oxygen species (ROS), DDR signaling and premature senescence |
25982278 | In contrast to mouse B16 cells, inability of TC-1 cells to respond to IFNgamma/TNFalpha by DDR and senescence correlated with the lack of TGFbeta and Nox4 response, supporting the role of ROS induced by NADPH oxidases in cytokine-induced senescence |
25982278 | Overall, our data reveal differences between cytokine effects in mouse and human cells, and mechanistically implicate the TGFbeta/SMAD pathway, via induction of NADPH oxidases and suppression of ANT2, as key mediators of IFNgamma/TNFalpha-evoked genotoxicity and cellular senescence |
25879533 | Intermittent high glucose implements stress-induced senescence in human vascular endothelial cells: role of superoxide production by NADPH oxidase |
25879533 | Intermittent but not constant high glucose strikingly up-regulated the expression of p22phox, an NADPH oxidase component, increasing superoxide |
25735595 | A combination of the superoxide dismutase mimetic 1-Oxyl-2,2,6, 6-tetramethyl-4-hydroxypiperidine (TEMPOL) and the nicotinamide adenine dinucleotide phosphate (NADPH) oxidase inhibitor apocynin significantly improved endothelium-dependent vasodilation in aged wildtype and Terc(-/-) G3 mice compared to untreated controls |
25655936 | Greater endothelial oxidative stress with aging is a result of augmented production from the intracellular enzymes NADPH oxidase and uncoupled eNOS, as well as from mitochondrial respiration in the absence of appropriate increases in antioxidant defenses as regulated by relevant transcription factors, such as FOXO |
25526894 | Epigenetic mechanisms regulate NADPH oxidase-4 expression in cellular senescence |
25526894 | Recent studies implicate the reactive oxygen species (ROS)-generating enzyme, NADPH oxidase 4 (Nox4) in cellular senescence |
25192254 | Overexpression of Sirt3 or treatment with NADPH oxidase inhibitor apocynin (Apo, 200 and 400 microM) rescued these abnormalities |
25033544 | NADPH oxidase NOX4 is a source of reactive oxygen species in many tissue of human body |
24727683 | We recently reported that indoxyl sulfate (IS), a uremic toxin, directly activates aryl hydrocarbon receptor (AhR) and generates oxidative stress through NADPH oxidase-4 in human umbilical vein endothelial cells (HUVECs) |
24727683 | The intracellular nicotinamide phosphoribosyltransferase (iNampt) activity, cellular NAD()/NADPH ratio and Sirt1 activity were analyzed according to a colorimetric assay to determine the mechanism of cellular senescence |
24727683 | RESULTS: IS decreased the iNampt activity, NAD()/NADPH ratio and Sirt1 activity, resulting in an increase in the percentage of SA beta-gal-positive cells |
24583638 | We also show that oncogenic Ras-induced ROS are produced in a Rac1 and NADPH oxidase (Nox4)-dependent manner |
24204728 | CONCLUSIONS: Bradykinin, acting through BK B2 receptor induced NO release, upregulated antioxidant Cu/Zn-SOD and Mn-SOD activity and expression while downregulating NADPH oxidase activity and subsequently inhibited ROS production, and finally protected against cardiomyocytes senescence induced by oxidative stress |
24191234 | Our previous data highlighted a role for angiotensin II in the induction of telomere-dependent and -independent premature senescence of human vascular smooth muscle cells and suggested this was due to production of superoxide by NADPH oxidase |
24191234 | These data suggest that mitochondrial superoxide is necessary for the induction of stress-induced premature senescence by angiotensin II and taken together with other data suggest that mitochondrial cross-talk with NADPH oxidases, via as yet unidentified signalling pathways, is likely to play a key role |
24096100 | The enzyme displays a dimer-tetramer equilibrium and NADPH (but not NADP) reduces the rate of approach to equilibrium, while 6PG is able to antagonize the NADPH effect |
24096100 | The different behaviour of the two forms of coenzyme appears to be related to the differences in DeltaCp, with NADP binding DeltaCp closer to what is expected of crystallographic structures, while NADPH DeltaCp is three times larger |
24030923 | Pharmacological therapies with beta-adrenoceptor antagonists, resveratolol, anti-obesity agents, nifedipine, and NADPH oxidase inhibitors may also be effective; however, these treatments have to be utilized under the basis of exercise and dietary controls |
23997094 | Interestingly, inhibition of NAD(P)H oxidase with apocynin or gp91ds-tat improved endothelial function in MnSOD(+/+) mice but significantly impaired endothelial function in MnSOD(+/-) mice at both ages |
23974111 | Erlotinib and gefitinib alone did not promote differentiation, yet stimulated the acquisition of morphological and biochemical maturation markers (including the expression of CD11b and CD14 as well as increased NADPH oxidase activity) when combined with either ATRA or VD |
23941874 | Our results demonstrated that the total antioxidant capacity and mRNA levels of thioredoxinreductase and glucose-6-phosphate dehydrogenase as well as the ratio of NADPH/NADP were decreased markedly in fibroblasts from patients with type 2 diabetes (DFs) |
23514110 | Mitochondrial respiratory chain complex I is inactivated by NADPH oxidase Nox4 |
23514110 | ROS (reactive oxygen species) generated by NADPH oxidases play an important role in cellular signal transduction regulating cell proliferation, survival and differentiation |
23514110 | Nox4 (NADPH oxidase 4) induces cellular senescence in human endothelial cells; however, intracellular targets for Nox4 remained elusive |
23478296 | A recent study published in Nature reveals a novel connection between p53 and metabolism: p53 transcriptionally represses the expression of malic enzymes and associated NADPH production, which in turn triggers a positive feedback loop resulting in sustained p53 activation, cellular senescence, and tumor suppression |
23334421 | Both malic enzymes are important for NADPH production, lipogenesis and glutamine metabolism, but ME2 has a more profound effect |
22907303 | Western blot was used to analyze the expression levels of xanthine oxidase (XOD), manganese-superoxide dismutase (Mn-SOD) and the subunits p67(phox) of nicotinamide adenine dinucleotide phosphate (NADPH) oxidase in the HUVECs |
22335598 | Concomitantly, translocation of Rac1 to the plasma membrane, which leads to the activation of NADPH oxidases and generation of ROS, was significantly attenuated |
22284404 | This study was undertaken to investigate the effects of resveratrol (Res) on amelioration of vascular cell aging and the role of SIRT1/nicotinamide adenine dinucleotide phosphate (NADPH) oxidase pathway |
22284404 | Res protected against HFS- or high-glucose-induced increase in NADPH oxidase p47phox expression and decrease in SIRT1 level |
22284404 | Apocynin, a NADPH oxidase inhibitor, down-regulated p47phox protein expression, but had no influence on SIRT1 protein; sirtinol, a SIRT1 inhibitor, aggravated the decrease in SIRT1 protein level and the increase in p47phox protein expression induced by high glucose |
22279170 | Using time-resolved microfluorimetry, we found a negative correlation between metabolic rate (proportion of protein-bound NAD[P]H) and in situ intracellular oxygen radicals production in freshly ejaculated sperm |
21841319 | Correlation of different NADPH oxidase homologues with late endothelial progenitor cell senescence induced by angiotensin II: effect of telmisartan |
20523116 | NADPH oxidase 4 is an oncoprotein localized to mitochondria |
20523116 | Initially ROS-producing NADPH oxidase (NOX) proteins were thought to be present in phagocytes |
19906512 | Further, T-oligo increases cellular ROS levels via a p53-dependent pathway, and these increases are abrogated by the NAD(P)H oxidase inhibitor diphenyliodonium chloride |
19841470 | Data demonstrate that 1) the toxic effects of epirubicin mainly occur through NAD(P)H oxidase activation; 2) the erbB2 overexpression induced by epirubicin is a redox-sensitive mechanism largely dependent on NAD(P)H oxidase; 3) the loss of erbB2-related functions caused by B10 determines marginal cellular changes in untreated cells, but causes massive death by apoptosis in cells previously exposed to a prosenescent dose of epirubicin, 4) dexrazoxane promotes survival pathways, as demonstrated by the activation of Akt and the PI3K-dependent erbB2 overexpression; and 5) it also prevents epirubicin-induced senescence and renders epirubicin-treated cells more resistant to treatment with B10 |
19841470 | Data underline the importance of NAD(P)H oxidase in epirubicin-induced cardiotoxicity and shed new light on the protective mechanisms of dexrazoxane |
19777843 | Western blot were used to analyse protein expression of NADPH oxidase p47phox, angiotensin type 1 and 2 receptor (AT1R, AT2R) |
19681754 | The NADPH oxidase Nox4 restricts the replicative lifespan of human endothelial cells |
19681754 | Noxs (NADPH oxidases) are well-known sources of superoxide, which contribute to the antimicrobial capabilities of macrophages, a process involving the prototypical member of the family referred to as Nox2 |
19328228 | NADPH oxidases 1 and 4 mediate cellular senescence induced by resveratrol in human endothelial cells |
18976161 | In addition, the role of oxidative stress as a major mediator of senescence and the role of NAD(P)H oxidases and changes to intracellular GSH/GSSG status are reviewed |
18513544 | Therefore, the development of a simultaneous determination of G6PD activity (via the determination of nicotinamide adenine dinucleotide phosphate (NADPH)) in RBCs and the determination of deformation-induced RBC-derived ATP is described |
18513544 | The NADPH and ATP were determined while undergoing a chemically induced aging process via inhibition of G6PD with dehydroepiandroesterone (DHEA) |
18513544 | Upon incubation with DHEA for 30 min, NADPH levels measured in a flow stream decreased to 7 |
18513544 | Upon inhibition with DHEA, NADPH levels decreased to 8 |
18513544 | These values were validated by an examination of NADPH levels in, and ATP release from, RBC fractions containing younger and older cells (separated by cell density centrifugation) |
17928358 | Flavin-dependent enzymes are known to use NAD(P)H to reduce MB to leucomethylene blue (MBH2), whereas cytochrome c reoxidizes MBH2 to MB |
17706954 | Oxidative stress was determined by measuring NADPH oxidase activity and superoxide production |
16978905 | Overproduction of ROS (arising either from mitochondrial electron-transport chain or excessive stimulation of NAD(P)H) results in oxidative stress, a deleterious process that can be an important mediator of damage to cell structures, including lipids and membranes, proteins, and DNA |
16324151 | The superoxide-producing NAD(P)H oxidase Nox4 in the nucleus of human vascular endothelial cells |
16324151 | The superoxide-producing NAD(P)H oxidase Nox4 was initially identified as an enzyme that is highly expressed in the kidney and is possibly involved in oxygen sensing and cellular senescence |
14980702 | Glucose-6-phosphate dehydrogenase (G6PD) is involved in the generation of reduced nicotinamide adenine dinucleotide phosphate (NADPH) and the maintenance of cellular redox balance |
14980702 | In the present study, we demonstrate abatement of both the intracellular G6PD activity and the ratio NADPH/NADP(+) during the serial passage of G6PD-deficient cells |
14980702 | Decreases in both the intracellular G6PD activity and the NADPH/NADP(+) ratio were concomitant with an increase in 8-OHdG level in H(2)O(2)-induced senescent cells |
11074618 | While the NAD(P)H metabolic transients have been studied before, our emphasis in this article is on very rapidly scanned fluorescence images related to organelle integration and photoinduced cellular senescence |
10980404 | Glucose-6-phosphate dehydrogenase (G6PD) is involved in the generation of reduced nicotinamide adenine dinucleotide phosphate (NADPH) and the maintenance of the cellular redox balance |
10869423 | Identification of renox, an NAD(P)H oxidase in kidney |
10869423 | Data suggest that a phagocytic-like NAD(P)H oxidase producing reactive oxygen species serves as a primary sensor for oxygen |
10869423 | Renox is homologous to gp91(phox) (91-kDa subunit of the phagocyte oxidase), the electron-transporting subunit of phagocytic NADPH oxidase, and contains all of the structural motifs considered essential for binding of heme, flavin, and nucleotide |
18649853 | During inflammation, or upon interaction with soluble or particulate stimuli and consequent phagocytosis, macrophages undergo respiratory burst activation, producing large quantities of superoxide anions by NADPH oxidase |
3613687 | In this paper we have used a new method which allows the simultaneous extraction and HPLC determination of ATP, ADP, AMP, NADP, NADPH, NAD and NADH to evaluate the changes in concentration of these compounds during maturation of rabbit reticulocytes and cell aging |
3613687 | The results show a significant increase of ATP concentration, higher ATP/ADP, ATP/AMP ratios and lower NADP+/NADPH, NAD+/NADH ratios in rabbit reticulocytes when compared to mature cells |