Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:1.6.99.6 (NADPH oxidase)
10,295 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Nitric oxide (NO) and hydrogen peroxide (H2O2) function as signalling molecules in plants under abiotic and biotic stresses. Calluses from Populus euphratica, which show salt tolerance, were used to study the interaction of NO and H2O2 in plant adaptation to salt resistance. The nitric oxide synthase (NOS) activity was identified in the calluses, and this activity was induced under 150 mM NaCl treatment. Under 150 mM NaCl treatment, the sodium (Na) percentage decreased, but the potassium (K) percentage and the K/Na ratio increased in P. euphratica calluses. Application of glucose/glucose oxidase (G/GO, a H2O2 donor) and sodium nitroprusside (SNP, a NO donor) revealed that both H2O2 and NO resulted in increased K/Na ratio in a concentration-dependent manner. Diphenylene iodonium (DPI, an NADPH oxidase inhibitor) counteracted H2O2 and NO effect by increasing the Na percentage, decreasing the K percentage and K/Na ratio. NG-monomethyl-L-Arg monoacetate (NMMA, an NO synthase inhibitor) and 2-phenyl-4,4,5,5-tetramethyl-imidazoline-1-oxyl-3-oxyde (PTIO, a specific NO scavenger) only reversed NO effect, but did not block H2O2 effect. The increased activity of plasma membrane (PM) H+ -ATPase caused by salt stress was reversed by treatment with DPI and NMMA. Exogenous H2O2 increased the activity of PM H+ -ATPase, but the effect could not be diminished by NMMA and PTIO. The NO-induced increase of PM H+ -ATPase can be reversed by NMMA and PTIO, but not by DPI. Western blot analysis demonstrated that NO and H2O2 stimulated the expression of PM H+ -ATPase in P. euphratica calluses. These results indicate that NO and H2O2 served as intermediate molecules in inducing salt resistance in the calluses from P. euphratica under slat stress by increasing the K/Na ratio, which was dependent on the increased PM H+ -ATPase activity.
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PMID:Involvement of hydrogen peroxide and nitric oxide in salt resistance in the calluses from Populus euphratica. 1754 50

H(2)O(2), plasma membrane H(+)-ATPase (PM H(+)-ATPase) and salicylic acid (SA) play important roles in sensing external stimulation and activating defense responses in plants. However, it remains uncertain whether they are involved and interrelated in response to heat acclimation. Experiments were performed by pharmacological methods, and the relationship and the connection between endogenous H(2)O(2), free SA and PM H(+)-ATPase were investigated in pea plants (Pisum sativum L.) during heat acclimation. The results showed that an accumulation peaks of H(2)O(2), free SA and PM H(+)-ATPase, were detected during heat acclimation at 37 degrees C for 2 h and H(2)O(2) burst appeared before SA accumulation that followed by increase of PM H(+)-ATPase activity (Fig.1). Pretreatments with either scavengers of active oxygen species (dimethyl sulfoxide and ascorbic acid) or antioxidant (reduced glutathione) inhibited the increases in both H(2)O(2) and free SA contents as a part of heat acclimation (Fig.2). Additionally, changes in activity of plasma membrane NADPH oxidase paralleled with H(2)O(2) level during heat acclimation (Figs.1 and 3), implicating that H(2)O(2) might be generated by plasma membrane NADPH oxidase. Moreover, pretreatments with either diphenylene iodonium (DPI), a suicide substrate inhibitor of plasma membrane NADPH oxidase, or dimethylthiourea (DMTU), a quencher of H(2)O(2), could block the increase in free SA content and activity of plasma membrane NADPH oxidase as a part of heat acclimation (Fig.4). According to the assay described above, it is suggested that both H(2)O(2) and PM H(+)-ATPase participate in SA signaling that leads to the development of thermotolerance in pea plant, and H(2)O(2) functions upstream and PM H(+)-ATPase functions downstream of the SA signal. Also, the regulation mechanism of PM H(+)-ATPase activity was investigated, which showed that during heat acclimation, increase of PM H(+)-ATPase activity was independent of PM H(+)-ATPase amount and the enzyme activity may be modulated at post-translational level that may involve in reversible protein phosphorylation (Fig.5).
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PMID:[Changes in H2O2 and salicylic acid contents as well as plasma membrane H+-ATPase activity and their relations in pea leaves during thermotolerance induction]. 1796 46

To provide an insight into the mechanism of interspecific interactions mediated by allelochemicals, cucumber and figleaf gourd seedlings were compared on their response to cinnamic acid, an autotoxin from root exudates of cucumber. Reactive oxygen species metabolism and plasma membrane H(+)-ATPase activity were examined in roots upon exposure to cinnamic acid. This exposure resulted in significant increases in activities of NADPH oxidase, superoxide dismutase, guaiacol peroxidase, and catalase, as well as in O(2)(.-) production and H(2)O(2) content, in cucumber roots but not in figleaf gourd roots. Notably, the cucumber roots produced significant amount of reactive oxygen species (ROS) immediately after cinnamic acid treatment, consequently increasing membrane peroxidation, decreasing membrane H(+)-ATPase activity, and losing root viability. By contrast, no such changes were observed in figleaf gourd roots. All these results indicated that there was an interspecies difference in the recognition of allelochemicals, which induced oxidative stress accompanied by root cell death in cucumber, an autotoxic plant, but not in figleaf gourd, a cucumber relative.
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PMID:Physiological basis of different allelopathic reactions of cucumber and figleaf gourd plants to cinnamic acid. 1796 43

In Arabidopsis thaliana cells, fusicoccin (FC) treatment induced an early and marked increase in the extracellular H(2)O(2) level. It also increased the huge hypo-osmotic stress-induced oxidative wave and, in addition, prevented the H(2)O(2) peak drop. These effects were apparently not linked to changes in either cytoplasmic pH or cytoplasmic free calcium concentration, since they occurred independently of the activity state of the plasma membrane (PM) H(+)-ATPase and neither influx nor efflux of (45)Ca(2+) was modified by FC. In the presence of diphenylene iodonium (DPI), inhibiting the PM NADPH oxidase presumably responsible for reactive oxygen species (ROS) production, no apoplastic H(2)O(2) development was detected either with or without FC. However, no increase in DPI-sensitive ferricyanide reduction, but rather a gradual decrease, occurred with FC. These results suggested that the H(2)O(2) increase observed with FC was not due to a overproduction of ROS but, more probably, to a reduced capability of FC-treated cells to degrade the H(2)O(2) formed. This view, at first supported by the finding that FC-treated cells failed to break down exogenously supplied H(2)O(2), was clearly confirmed by a series of measurements on exogenous catalase activity, tested in cell-free media of FC-treated samples. This assay, in fact, allowed ascertainment and partial characterization of an as yet unidentified factor increasingly accumulating in the incubation medium of FC-treated cells, behaving as a non-competitive catalase inhibitor and able to reduce markedly the cell's capability for H(2)O(2) scavenging.
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PMID:Inhibition of catalase activity as an early response of Arabidopsis thaliana cultured cells to the phytotoxin fusicoccin. 1803 36

We have previously implicated reactive oxygen species oxygen (ROS) as a critical signal transducer in the upregulation of Na,K-ATPase by low K+ in MDCK cells, but how ROS mediate this process has not been well defined. We reported here that both of hydrogen peroxide (H2O2) and superoxide anion (O2*(-)) were rapidly produced at the early stage of low K+-treated MDCK cells. Further analysis revealed that NADP/NADPH oxidase-derived H2O2 was specifically involved in low K+-induced Na,K-ATPase alpha1 gene transcription as well as alpha1 and beta1 subunits expressions. Exogenous H2O2 even mimicked the stimulatory effect of low K+ on Na,K-ATPase alpha1 gene transcription. Low K+ triggered a H2O2-dependent ERK1/2 phosphorylation in MDCK cells, nonetheless, this ERK1/2 activation did not finally lead to the upregulation of Na,K-ATPase. Similar to previous findings that Na,K-ATPase beta1 gene transcription was mediated by Sp1, Na,K-ATPase alpha1 gene transcription in low K+-treated MDCK cells was also closely relevant to Sp1 participation, as confirmed by siRNA as well as PCR mutagenesis technologies. Furthermore, Sp1 activation was dependent on H2O2 generation triggered by low K+. Taken together, the data described in this study outlines an essential role of H2O2 and Sp1 in mediating the upregulation of Na,K-ATPase in MDCK cells by low external K+.
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PMID:Requirement of hydrogen peroxide and Sp1 in the stimulation of Na,K-ATPase by low potassium in MDCK epithelial cells. 1815 51

We investigated if extracellular signal-regulated kinases (ERK) and oxidative stress are involved in the pathogenesis of arterial hypertension induced by chronic leptin administration in the rat. Leptin was administered at a dose of 0.25 mg/kg twice daily s.c. for 4 or 8 days. Blood pressure (BP) was higher in leptin-treated than in control animals from the third day of the experiment. The superoxide dismutase (SOD) mimetic, tempol, normalized BP in leptin-treated rats on days 6, 7 and 8, whereas the ERK inhibitor, PD98059, exerted a hypotensive effect on days 3 through 6. Leptin increased ERK phosphorylation level in renal and aortic tissues more markedly after 4 than after 8 days of treatment. In addition, leptin reduced urinary Na(+) excretion and increased renal Na(+),K(+)-ATPase activity, and these effects were abolished on days 4 and 8 by PD98059 and tempol, respectively. The levels of NO metabolites and cGMP were reduced in animals receiving leptin for 8 days. Markers of oxidative stress (H(2)O(2) and lipid peroxidation products) were elevated to a greater extent after 4 than after 8 days of leptin treatment. In contrast, nitrotyrosine, a marker of protein nitration by peroxynitrite, was higher in animals receiving leptin for 8 days. NADPH oxidase inhibitor, apocynin, prevented leptin's effect on BP, ERK, Na(+),K(+)-ATPase/Na(+) excretion and NO formation at all time points. SOD activity was reduced, whereas glutathione peroxidase (GPx) activity was increased in the group treated with leptin for 8 days. These data indicate that: (1) ERK, activated by oxidative stress, is involved only in the early phase of leptin-induced BP elevation, (2) the later phase of leptin-induced hypertension is characterized by excessive NO inactivation by superoxide, (3) the time-dependent shift from ERK to O(2)(-)-NO dependent mechanism may be associated with reduced SOD/GPx ratio, which favors formation of O(2)(-) instead of H(2)O(2).
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PMID:Role of extracellular signal-regulated kinases (ERK) in leptin-induced hypertension. 1820 59

Coupling factor 6 (CF6), a component of ATP synthase, suppresses the generation of prostacyclin and nitric oxide (NO). Platelet endothelial cell adhesion molecule-1 (PECAM-1) is involved in shear-induced NO production. To investigate the linkage between the actions of CF6 and PECAM-1, we examined the effects of CF6 on PECAM-1 expression and shear-mediated NO release, comparatively with those of angiotensin II (AngII). Treatment of human umbilical vein endothelial cells (HUVEC) and aortic endothelial cells (HAEC) with CF6 at 10(-7)M or AngII at 10(-7)M for 24h suppressed PECAM-1 gene and protein expression. CF6 or AngII activated c-Src at 15 min in HUVEC, and blockade of c-Src with PP1, its specific inhibitor, restored them. Efrapeptin, an inhibitor of ATPase, attenuated CF6-induced suppression of PECAM-1 gene expression by blockade of acidification, whereas superoxide dismutase or apocinin, an inhibitor of NADPH oxidase, blocked AngII-induced suppression of PECAM-1. Exposure of the cells to shear stress at 25 dynes/cm(2) for 30 min enhanced phosphorylation of eNOS at Ser(1177) and NO release. Pretreatment with CF6 or AngII for 24h attenuated them in HUVEC and HAEC. These suggest that CF6 downregulates PECAM-1 expression via c-Src activation and attenuates shear-induced NO release presumably by suppressing eNOS phosphorylation.
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PMID:Coupling factor 6 downregulates platelet endothelial cell adhesion molecule-1 via c-Src activation and acts as a proatherogenic molecule. 1824 11

We examined the role of epidermal growth factor (EGF) receptor in the pathogenesis of leptin-induced hypertension in the rat. Leptin, administered in increasing doses (0.1-0.5 mg/kg/day) for 10 days, increased phosphorylation levels of non-receptor tyrosine kinase, c-Src, EGF receptor and extracellular signal-regulated kinases (ERK) in aorta and kidney, which was accompanied by the increase in plasma concentration and urinary excretion of isoprostanes and H2O2. Blood pressure and renal Na+,K+-ATPase activity were higher, whereas urinary sodium excretion was lower in animals receiving leptin. The effects of leptin on renal Na+,K+-ATPase, natriuresis and blood pressure were abolished by NADPH oxidase inhibitor, apocynin, Src kinase inhibitor, PP2, EGF receptor inhibitor, AG1478, protein farnesyltransferase inhibitor, manumycin A, and ERK inhibitor, PD98059. In contrast, inhibitors of insulin-like growth factor-1 and platelet-derived growth factor receptors, AG1024 and AG1295, respectively, only slightly reduced ERK phosphorylation and had no effect on blood pressure in rats receiving leptin. These data indicate that: (1) experimental hyperleptinemia is associated with oxidative stress and c-Src-dependent transactivation of the EGF receptor, which stimulates ERK in vascular wall and the kidney, (2) overactivity of EGF receptor-ERK pathway contributes to leptin-induced hypertension by stimulating renal Na+,K+-ATPase and reducing sodium excretion, (3) inhibitors of c-Src, EGF receptor and ERK may be considered as a novel therapy for hypertension associated with hyperleptinemia, e.g. in patients with obesity and metabolic syndrome.
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PMID:Transactivation of epidermal growth factor receptor in vascular and renal systems in rats with experimental hyperleptinemia: role in leptin-induced hypertension. 1828 56

The phagocyte NADPH oxidase (NOX2) is critical for the bactericidal activity of phagocytic cells and plays a major role in innate immunity. We showed recently that NOX2 activity in mouse dendritic cells (DCs) prevents acidification of phagosomes, promoting antigen cross-presentation. In order to investigate the role of NOX2 in the regulation of the phagosomal pH in human DCs, we analyzed the production of reactive oxygen species (ROS) and the phagosomal/endosomal pH in monocyte-derived DCs and macrophages (M(diameter)s) from healthy donors or patients with chronic granulomatous disease (CGD). As expected, we found that human M(diameter)s acidify their phagosomes more efficiently than human DCs. Accordingly, the expression of the vacuolar proton ATPase (V-H(+)-ATPase) was higher in M(diameter)s than in DCs. Phagosomal ROS production, however, was also higher in M(diameter)s than in DCs, due to higher levels of gp91phox expression and recruitment to phagosomes. In contrast, in the absence of active NOX2, the phagosomal and endosomal pH decreased. Both in the presence of a NOX2 inhibitor and in DCs derived from patients with CGD, the cross-presentation of 2 model tumor antigens was impaired. We conclude that NOX2 activity participates in the regulation of the phagosomal and endosomal pH in human DCs, and is required for efficient antigen cross-presentation.
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PMID:NADPH oxidase controls phagosomal pH and antigen cross-presentation in human dendritic cells. 1902 53

Previously, we have demonstrated that leptin increases blood pressure (BP) in the rats through two oxidative stress-dependent mechanisms: stimulation of extracellular signal-regulated kinases (ERK) by H(2)O(2) and scavenging of nitric oxide (NO) by superoxide (O(2-.)). Herein, we examined if renal glutathione system and antioxidant enzymes determine the mechanism of prohypertensive effect of leptin. Leptin administered at 0.5 mg/kg/day for 4 or 8 days increased BP and renal Na(+),K(+)-ATPase activity and reduced fractional sodium excretion; these effects were prevented by NADPH oxidase inhibitor, apocynin. Superoxide scavenger, tempol, abolished the effect of leptin on BP and renal Na(+) pump in rats receiving leptin for 8 days, whereas ERK inhibitor, PD98059, was effective in animals treated with leptin for 4 days. Leptin administered for 4 days decreased glutathione (GSH) and increased glutathione disulfide (GSSG) in the kidney. In animals receiving leptin for 8 days GSH returned to normal level, which was accompanied by up-regulation of gamma-glutamylcysteine synthetase (gamma-GCS), a rate-limiting enzyme of the GSH biosynthetic pathway. In addition, superoxide dismutase (SOD) activity was decreased, whereas glutathione peroxidase (GPx) was increased in rats receiving leptin for 8 days. Cotreatment with gamma-GCS inhibitor, buthionine sulfoximine (BSO), accelerated, whereas GSH precursor, N-acetylcysteine (NAC), attenuated leptin-induced changes in gamma-GCS, SOD, and GPx. In addition, coadministration of BSO changed the mechanism of BP elevation from H(2)O(2)-ERK to (O(2-.))-NO dependent in animals receiving leptin for 4 days, whereas NAC had the opposite effect in rats treated with leptin for 8 days. These results suggest that initial change in GSH redox status induces decrease in SOD/GPx ratio, which results in greater amount of (O)2-.)) versus H(2)O(2) in later phase of leptin treatment, thus shifting the mechanism of BP elevation from H(2)O(2)-ERK to (O(2-.))-NO dependent.
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PMID:Renal antioxidant enzymes and glutathione redox status in leptin-induced hypertension. 1869 Apr 14


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