ライフサイエンスコーパス: superoxide production

1 uce inflammatory responses) did not increase superoxide production.

2 of fMLF-induced p47phox phosphorylation and superoxide production.

3 ect of BH4 treatment on vascular function or superoxide production.

4 ote mitochondrial ATP synthesis and suppress superoxide production.

5 nduced and synaptically evoked mitochondrial superoxide production.

6 ecreased effector function in the absence of superoxide production.

7 ber of mitochondria are in the state of high superoxide production.

8 ted nitric oxide release and zymosan-induced superoxide production.

9 ed p-38 mitogen-activated protein kinase and superoxide production.

10 n also affects semiquinone concentration and superoxide production.

11 e adenine dinucleotide phosphate oxidase and superoxide production.

12 pocket and might not directly participate in superoxide production.

13 uately delivered to the subcellular sites of superoxide production.

14 (Ang II) increased endothelial mitochondrial superoxide production.

15 ite a strong candidate for being a center of superoxide production.

16 sion-induced cell spreading or activation of superoxide production.

17 xidase as the primary source of NMDA-induced superoxide production.

18 plasmic enzyme NADPH oxidase in NMDA-induced superoxide production.

19 ) mice had a 40% reduction in PHOX-dependent superoxide production.

20 f the PHOX complex that results in decreased superoxide production.

21 ant activity and inhibition of NADPH oxidase superoxide production.

22 cytochrome oxidases, causing an increase in superoxide production.

23 MI-1) was a potent antagonist of Nox-derived superoxide production.

24 ity of the ligand with respect to neutrophil superoxide production.

25 inal domain of TSP2 also stimulates monocyte superoxide production.

26 Dihydroethidium (DHE) was used to detect superoxide production.

27 e, we addressed whether GTPase loss affected superoxide production.

28 ere the semiquinone is destabilized to limit superoxide production.

29 is the elusive intermediate responsible for superoxide production.

30 xpression of NADPH oxidase and intracellular superoxide production.

31 the dominant inhibitory effect of p40R57Q on superoxide production.

32 helial function, eNOS coupling, and vascular superoxide production.

33 reducing equivalents accumulate and promote superoxide production.

34 ly of the neuronal NADPH oxidase complex and superoxide production.

35 -dependent hypertension and decreased aortic superoxide production.

36 dase activation, as demonstrated by enhanced superoxide production.

37 sh a full agonist from a partial agonist for superoxide production.

38 mation was dependent on calpain activity and superoxide production.

39 It also suppressed NOS-derived superoxide production.

40 imulated human neutrophils, correlating with superoxide production.

41 s was generally in those with lower residual superoxide production.

42 DNA restores mitochondrial Ca(2+) uptake and superoxide production.

43 m with concomitant increase in mitochondrial superoxide production.

44 phorylate subunits of the oxidase leading to superoxide production.

45 on after hypoxia by decreasing mitochondrial superoxide production.

46 oupling between NMDA receptor activation and superoxide production.

47 , varying in a manner that directly mirrored superoxide production.

48 persal and cell death, likely by stimulating superoxide production.

49 ge are thus potent regulators of excitotoxic superoxide production.

50 treated rats showed reduced NADPH-stimulated superoxide production.

51 ther attenuation of NO and greatly increased superoxide production.

52 lting in bioenergetics defects and increased superoxide production.

53 ochondrial membrane potential (Deltapsi) and superoxide production.

54 pears to be a side reaction of extracellular superoxide production.

55 hox), NOX1 and -4), NAD(P)H oxidase-mediated superoxide production, 26S proteasome activity, IkappaBa

56 phox), NOX1 to -4), NAD(P)H oxidase-mediated superoxide production, 26S proteasome activity, IkappaBa

57 roglial phagocytotic activity (48 h) and the superoxide production (4 days).

58 Extracellular superoxide production, a phenomenon well established to

59 ne properties, and provide a vital source of superoxide production across many different cell types.

60 F MDMs demonstrate a nearly 60% reduction in superoxide production after PMA stimulation compared wit

61 shed NO production and elevated eNOS-derived superoxide production, along with a concomitant reductio

62 potential changed the relationships between superoxide production and b(566) reduction and between b

63 Diabetes-induced superoxide production and cardiac fibrosis were partiall

64 In neuron cultures, postischemic superoxide production and cell death were completely pre

65 aling axis and was associated with increased superoxide production and cell death.

66 iodonium chloride), enzymes responsible for superoxide production and cell differentiation in fungi.

67 Superoxide production and content of the oxidative stres

68 In murine stroke, neuronal superoxide production and death were decreased by the gl

69 f mfpr1 resulted in abrogation of neutrophil superoxide production and degranulation in response to f

70 keletal rearrangement, and ultimately induce superoxide production and degranulation.

71 cytoskeleton prevents Pseudomonas-initiated superoxide production and DNA release.

72 es showed a pH-dependent correlation between superoxide production and enhanced sperm motility.

73 e, safinamide potently suppressed microglial superoxide production and enhanced the production of the

74 ctron donor for reperfusion-induced neuronal superoxide production and establish a previously unrecog

75 ion of mitoribosomes, elevated mitochondrial superoxide production and eventual loss of OXPHOS comple

76 nt spatial-temporal changes in mitochondrial superoxide production and execution of programmed cell d

77 these changes, we independently manipulated superoxide production and GSH metabolism during reperfus

78 8 with SB203580 or JNK with SP600125 reduced superoxide production and improved shear stress-induced

79 sistance and deletion of Nox2 showed reduced superoxide production and improved vascular function.

80 ; (v) the engulfed Hb-Hp aggregates activate superoxide production and induce intracellular oxidative

81 esis that ET(A) receptor blockade attenuates superoxide production and inflammation in the kidney of

82 d nitric oxide production and dampened renal superoxide production and inflammatory cell infiltration

83 BMPs can stimulate superoxide production and inflammatory responses in endo

84 erations in transcripts involved in heme and superoxide production and insulin signaling.

85 ominant inhibitory effect on agonist-induced superoxide production and membrane translocation of p47(

86 l biogenesis and activation of AMPK enhances superoxide production and mitochondrial function while r

87 It also increased mitochondrial superoxide production and mitochondrial permeability tra

88 on of the p47(phox) subunit blocked neuronal superoxide production and negated the deleterious effect

89 Moreover, the degree of superoxide production and neuronal death increased with

90 Superoxide production and neuronal death were also block

91 Superoxide production and neuronal death were blocked by

92 In cultured neurons, NMDA-induced superoxide production and neuronal death were prevented

93 re in high glucose conditions led to reduced superoxide production and NOX4 expression.

94 s in total and mitochondria-derived arterial superoxide production and oxidative stress (nitrotyrosin

95 PBM inhibited diabetes-induced superoxide production and preserved MnSOD expression in

96 Fenofibrate significantly reduced superoxide production and protein oxidation in the ische

97 trophil adhesion and migration, and augments superoxide production and proteolytic enzyme degranulati

98 minant-negative transcript that can modulate superoxide production and provides an example of genetic

99 These mechanisms limit superoxide production and short circuiting of the Q-cycl

100 the cell membrane potentiate haem-associated superoxide production and subsequent oxidative damage.

101 f NGB attenuated ocular hypertension-induced superoxide production and the associated decrease in ATP

102 These results establish a link between superoxide production and trans-sulfuration pathway sele

103 AICAR treatment induced superoxide production and was linked with glomerular mat

104 I activity, impaired respiration, increased superoxide production, and a reduction in membrane poten

105 kinase (Hck), and induced cellular adhesion, superoxide production, and degranulation of eosinophils.

106 s of neutrophils, including phagocytosis and superoxide production, and did not inhibit neutrophils f

107 ity to chemoattractant stimulation, elevated superoxide production, and enhanced neutrophil recruitme

108 proliferation, migration, monocyte adhesion, superoxide production, and gene expression assays.

109 High fat feeding increased Nox2 expression, superoxide production, and impaired insulin signaling in

110 mitochondrial membrane potential, increased superoxide production, and increased expression of a glu

111 inhibited nitric oxide production, promoted superoxide production, and increased vascular cell adhes

112 (OXPHOS) efficiency, increased mitochondrial superoxide production, and mtDNA depletion as well as ab

113 reduced ischemia-induced zinc translocation, superoxide production, and neuron death.

114 ice also had significantly less leukostasis, superoxide production, and nuclear factor-kappaB (NF-kap

115 s suppressed fMLP-stimulated Rac activation, superoxide production, and PI3-kinase activation in diff

116 lial NO synthase, increased endothelial cell superoxide production, and prevented the increase in NO

117 uced TNF-alpha-stimulated p65 translocation, superoxide production, and proinflammatory gene expressi

118 proliferation, migration, monocyte adhesion, superoxide production, and proinflammatory gene expressi

119 activity, restore physiologic mitochondrial superoxide production, and promote organ healing.

120 flux through the enzyme, different rates of superoxide production are attained when the enzyme is di

121 In addition, HHcy accelerated HG-induced superoxide production as determined by dihydroethidium a

122 om Rap1a-/- mice had reduced fMLP-stimulated superoxide production as well as a weaker initial respon

123 yphal morphology and size, and mitochondrial superoxide production as well as development.

124 Acute infusion of ascorbic acid to inhibit superoxide production associated with a nonsignificant t

125 e mouse neutrophil chemotaxis at 1-10 nM and superoxide production at 10-100 nM, similar to the poten

126 Thus, superoxide production at Q(o) depends on the reduction s

127 ve force of the reaction rate, and simulates superoxide production at the Qo-site.

128 e p40(phox) or PI3 kinase activity, although superoxide production before and after phagosome sealing

129 eficiency, BCNU exposure further exacerbates superoxide production, BH4 oxidation, and eNOS activity.

130 /gp91(phox) protein expression, decreased NO/superoxide production, blocked peroxynitrite formation,

131 The effects of hyperglycemia on superoxide production, blood-brain barrier disruption, i

132 ctase inhibition abolished the difference in superoxide production but did not affect myocardial func

133 nd primes leukocytes for marginalization and superoxide production but not for transmigration.

134 on of Mn(II) oxidation by NADH oxidase-based superoxide production by a common marine bacterium (Rose

135 Superoxide production by a model bacterium within the ub

136 Phagocyte superoxide production by a multicomponent NADPH oxidase

137 Superoxide production by brain mitochondria isolated fro

138 In addition, indirect measurements of superoxide production by cells and isolated mitochondria

139 mational changes and NADPH oxidase-dependent superoxide production by cells.

140 on the mechanisms of energy transduction and superoxide production by complex I, discusses contempora

141 se electron transport and rotenone-sensitive superoxide production by complex I.

142 ndependent of NQO1 inhibition, that cellular superoxide production by dicoumarol does not seem linked

143 astica-van Gieson-stained slides, and intima superoxide production by dihydroethidium fluorescence.

144 tor in regulating the balance between NO and superoxide production by endothelial NOS (eNOS coupling)

145 ey role for Trp-447 in determining NO versus superoxide production by eNOS, by effects on BH4-depende

146 ts clarify the maximum rate and mechanism of superoxide production by mGPDH.

147 Superoxide production by NADPH oxidase is a requisite ev

148 rglycemia is mediated through an increase in superoxide production by NADPH oxidase.

149 Here, we evaluated superoxide production by neuronal nicotinamide adenine d

150 studies, apocynin was administered to block superoxide production by nicotinamide adenine dinucleoti

151 h inhibition of Nf-kappaB, and inhibition of superoxide production by phagocytes.

152 inflammation, we suggest that the decreased superoxide production by PHOX in p66Shc-deficient mice c

153 sion studies, we found that H(2)O(2)-induced superoxide production by primary sperm cells was mediate

154 inflammation, results from loss of phagocyte superoxide production by recessive mutations in any 1 of

155 ermatozoa motility, was required for optimal superoxide production by spermatozoa.

156 Furthermore, pyruvate suppressed superoxide production by submitochondrial particles, and

157 ial permeability transition pore stimulating superoxide production by the ETC.

158 phenylene iodonium-sensitive NADPH-dependent superoxide production by the liver following I/R.

159 ranulation responses but a profound block in superoxide production by the phagocyte oxidase.

160 s known to be associated with high levels of superoxide production by the sperm mitochondria; however

161 To better define the activation of superoxide production by this multisubunit enzyme comple

162 tly attenuated the effect of low K intake on superoxide production, c-Jun phosphorylation, c-Src expr

163 Diabetes mellitus increased superoxide production, canonical Wnt antagonist expressi

164 tivity to selenite and resulted in increased superoxide production, caspase-9 activation, and apoptos

165 This increased superoxide production causes the activation of 5 major p

166 Furthermore, an increase in superoxide production combined with an increase in p22ph

167 e decreased expression of SOD2 and increased superoxide production correlate with RPE apoptosis induc

168 Although this enhanced superoxide production correlates with effects due to the

169 ocal microscopy, revealed that Abeta-induced superoxide production could be blunted by MitoQ, but not

170 Viability, superoxide production, cytotoxic RNA transfection effici

171 Brain death leads to increased superoxide production, decreased GPx activity, decreased

172 is the sole superoxide producer, the rate of superoxide production depends on the concentrations of g

173 otein levels in aorta and increased panmural superoxide production (dihydroethidium staining).

174 by molecular modeling, to explain decreased superoxide production during alpha-tocopherol deficiency

175 In contrast, superoxide production during forward electron transport

176 e during reverse electron transport, its low superoxide production during forward electron transport

177 es in coordinating directional migration and superoxide production during neutrophil responses to che

178 showed a substantial defect in intracellular superoxide production during phagocytosis, whereas extra

179 portant role for NADPH oxidase (NOX)-derived superoxide production during T1D pathogenesis, as NOX-de

180 le to Hb autoxidation and to hypoxia-induced superoxide production enhanced the hypoxia-induced respo

181 increased glucose consumption, mitochondrial superoxide production, ERK and JNK phosphorylation, tyro

182 valents in activated microglia, GSH, trigger superoxide production, favor the reorganization of lipid

183 s responded to NMDA with a rapid increase in superoxide production, followed by neuronal death.

184 We report that superoxide production following CB3 infection may exacer

185 Superoxide production from antimycin-inhibited complex I

186 Superoxide production from atrial samples was measured b

187 de over time, OSS time-dependently increased superoxide production from endothelial cells.

188 The concept that excess superoxide production from mitochondria is the driving,

189 nergy-conserving NADH oxidation with minimal superoxide production from the nucleotide-free site.

190 semiquinone in the Q-binding site, the rapid superoxide production from this site during reverse elec

191 hypertension in intact animals by increasing superoxide production from vascular nicotinamide adenine

192 In each case, superoxide production had a similar bell-shaped relation

193 In support of this, superoxide production has also been found for native AO

194 Despite significant reduction in superoxide production, Hv1(-/-) mice are able to clear s

195 showed that estrogen decreases mitochondrial superoxide production in a receptor-mediated manner, as

196 t Crb restricts Rac1-NADPH oxidase-dependent superoxide production in epithelia and photoreceptor cel

197 attenuation of NADPH oxidase activation and superoxide production in hippocampal CA1 pyramidal neuro

198 effects on endothelial function and vascular superoxide production in human atherosclerosis, by preve

199 ent transcripts on protein translocation and superoxide production in human leukemia cells (HL-60) an

200 ing, endothelium-dependent vasodilation, and superoxide production in human vessels, whereas plasma b

201 ing and contractile performance and controls superoxide production in isolated cardiomyocytes.

202 Dihydroethidium (DHE) was used to detect superoxide production in isolated retinal arterioles.

203 elenite treatment resulted in high levels of superoxide production in LNCaP cells but only low levels

204 use carotid arteries significantly increased superoxide production in medial VSMCs and enhanced neoin

205 hese results indicate that lack of leukocyte superoxide production in mice with chronic hyperglycemia

206 ate comparable with the other major sites of superoxide production in mitochondria, the superoxide-pr

207 The accumulation of Zn caused increased superoxide production in N. caerulescens, but inoculatio

208 ced p47(phox) phosphorylation and diminished superoxide production in neutrophils.

209 phagocytosis in monocytes and stimulation of superoxide production in neutrophils.

210 aining how l-arginine decreases the level of superoxide production in nNOSox (without BH4 but with l-

211 r basal conditions, angiotensin II increased superoxide production in nondiabetics and diabetics, and

212 G. bethesdensis stimulated superoxide production in normal monocytes, but to a less

213 Superoxide production in ovarian, lung, colon, breast, a

214 us expression of p40(phox) markedly enhanced superoxide production in phorbol 12-myristate 13-acetate

215 ting, eNOS becomes "uncoupled," resulting in superoxide production in place of NO.

216 hypoxia, increased Hb autoxidation augments superoxide production in RBCs.

217 p67(phox) protein expression, and subsequent superoxide production in response to TNF-alpha.

218 ng showed that CRP produced TEMPOL-sensitive superoxide production in the arteriolar endothelium.

219 lows rapid agonist-induced redistribution of superoxide production in the cell.

220 R-dependent phagocytosis was associated with superoxide production in the early FCP and restricted ph

221 tor responses to acetylcholine, and vascular superoxide production in the presence and absence of the

222 ll-free assay system where p47SH3AB enhanced superoxide production in the presence of a p67phox (1-21

223 glomerular damage index, and NADPH-dependent superoxide production in the renal cortex from Asm(+/+)

224 y degeneration, proinflammatory changes, and superoxide production in the retina and allodynia were i

225 JCI, my colleagues and I revealed a role for superoxide production in the vascular dysfunction associ

226 d microglia in injured WT, whereas increased superoxide production in vessels and nuclear factor (NF)

227 Atrial superoxide production increased significantly after repe

228 NG-nitro-l-arginine methyl ester-inhibitable superoxide production, increased the eNOS dimer:monomer

229 on of AT1R mRNA, c-Jun mRNA, c-fos mRNA, and superoxide production induced by Ang II.

230 In mouse brain, superoxide production induced by NMDA injections or isch

231 inal cells, 30-mM glucose exposure increased superoxide production, inflammatory biomarker expression

232 nt embryos, demonstrating that limitation of superoxide production is a crucial function of Crb and t

233 -induced activation loop phosphorylation and superoxide production is also established in the differe

234 key role in host defense; however, excessive superoxide production is believed to participate to infl

235 the rate-limiting step for both Q-cycle and superoxide production is essentially identical, consiste

236 Since superoxide production is one of the first indicators of

237 ent studies showed that phagocytosis-induced superoxide production is stimulated by p40(phox) and its

238 th extensive NMDAR activation, the resulting superoxide production leads to neuronal death.

239 s 30% slower than at 510 nm, indicating that superoxide production may be overestimated at 510 nm by

240 uce superoxide, this microbial extracellular superoxide production may play a central role in the cyc

241 E2-EA, inhibits leukotriene B4 biosynthesis, superoxide production, migration, and antimicrobial pept

242 Greater superoxide production, mitochondrial injury, and oligode

243 erved differential activation of endothelial superoxide production, NF-kappaB activation, and reducti

244 at IL-27 is able to enhance the potential of superoxide production not only during differentiation bu

245 We also asked: 3) if substantial superoxide production occurs during and after HI, thinki

246 , and the strong dependence of both modes of superoxide production on DeltapH.

247 esults support a two-site model of complex I superoxide production; one site in equilibrium with the

248 icantly less leukostasis (P < 0.005) but not superoxide production or NF- kappaB expression.

249 It is widely held that NMDA-induced superoxide production originates from the mitochondria,

250 icytes and increases in both leukostasis and superoxide production (P < 0.006).

251 state of cytochrome b(566), suggesting that superoxide production peaks at intermediate Q-reduction

252 mGPDH-specific superoxide production plateaus at a rate comparable with

253 Decreasing superoxide production prevented the effects of ketamine

254 ted growth in proportion to CGD PMN residual superoxide production, providing a potential method to i

255 rst, which corresponds to an increase in the superoxide production rate by 9 +/- 3 attomoles/cell/s.

256 sign of being overreducible, and the maximum superoxide production rate correlates with mGPDH activit

257 el is capable of explaining both kinetic and superoxide production rate data.

258 uations to more periodic oscillations as the superoxide production rate increases.

259 However, the superoxide production rate was not uniquely related to t

260 increased oxidized biopterins, NOS-dependent superoxide production, reduced NO production, and dephos

261 udes genes involved in phagosome maturation, superoxide production, response to vitamin D, macrophage

262 s investigated by using artificial enzymatic superoxide production revealing a sensitivity of 2235AM(

263 ADPH oxidase activity was blocked to prevent superoxide production showed preservation of neuronal GS

264 As the number of mitochondria in the high-superoxide-production state increases, short-lived or ab

265 When the number of mitochondria in the high-superoxide-production state reaches a critical number, r

266 burst in electron transport chain-dependent superoxide production that is coincident with a modest i

267 constriction is mediated via TRPA1-dependent superoxide production that stimulates alpha2C-adrenocept

268 TNF-alpha stimulation of PMNs resulted in superoxide production that was dependent on CD11b/CD18-m

269 ow that by eliminating macrophage and T cell superoxide production through the NADPH oxidase (NOX), T

270 The increased superoxide production, together with the increased iron

271 This is significant because superoxide production underlies the role of human PRODH

272 , and its binding of PtdIns (3)P potentiates superoxide production upon agonist stimulation.

273 Transient extracellular superoxide production upon stimulation was successfully

274 ys an important role in phagocytosis-induced superoxide production via a phox homology (PX) domain th

275 ctivity rather than assembly, and stimulates superoxide production via a PI3P signal that increases a

276 Restoration of mitochondrial function and superoxide production via activation of AMPK has now bee

277 To confirm whether the defect in superoxide production was a direct consequence of p66Shc

278 Superoxide production was also blocked by inhibiting the

279 Increased superoxide production was associated with increased expr

280 were seen of 58, 86, or 92%, and NOS-derived superoxide production was greatly increased.

281 Finally, superoxide production was higher in brain tissue from di

282 Superoxide production was localized near nectary pores a

283 Superoxide production was measured by the ethidium metho

284 revealed that a MPP(+)-mediated increase in superoxide production was reduced in MAC1(-/-) neuron-gl

285 Here, we report that superoxide production was reduced in the kidneys of a st

286 Mitochondrial superoxide production was shown to be the source of JNK-

287 eNOS-derived superoxide production was significantly elevated in W447

288 Aortic superoxide production was significantly increased in Nox

289 NADPH oxidase-dependent superoxide production was significantly increased in ves

290 s in which TRPM2 was depleted, mitochondrial superoxide production was significantly increased, parti

291 moattractant-induced transwell migration and superoxide production were also augmented.

292 tion, association with the cytoskeleton, and superoxide production were examined in transgenic COS-7

293 droethidine-based detection of intracellular superoxide production were used.

294 ate 3 oxygen consumption rates and decreased superoxide production, whereas the opposite is seen in o

295 noelaidic acid are associated with increased superoxide production, whereas Transvaccenic acid (which

296 We also measured superoxide production, which has been hypothesized to be

297 Reduction of mitochondrial superoxide production with rotenone was sufficient to re

298 nzyme can also catalyze substantial rates of superoxide production, with deleterious physiological co

299 Superoxide flashes are transient bursts of superoxide production within the mitochondrial matrix th

300 creased mitochondrial oxygen consumption and superoxide production without altering cellular ATP leve