ライフサイエンスコーパス: superoxide

1 he Rh-TiO2 interface in a form of Rh-O-O-Ti (superoxide).

2 proatherosclerotic imbalance between NO and superoxide.

3 cing significant amounts of the free radical superoxide.

4 ion of inflammatory signaling of endothelial superoxide.

5 atalyst to the Cr(III) ground state, forming superoxide.

6 und SOD and protection against extracellular superoxide.

7 rmalities, including increased mitochondrial superoxide.

8 sphorylation of eNOS and excess Nox2-derived superoxide.

9 proatherosclerotic imbalance between NO and superoxide.

10 Superoxide abundance was elevated in ECSHIP2(Delta/+) EC

11 Importantly, exogenous superoxide addition to CB3-infected NOD.Ncf1(m1J) bone m

12 etween a Co(II)(salophen) complex, a Co(III)-superoxide adduct, and a hydrogen-bonded adduct between

13 /min/30,000 cells; P < 0.001), produced more superoxide after exposure to hyperoxia (mean +/- SEM, 89

14 hibited mitochondrial complex I, stimulating superoxide and AMPK activation, but had no effect in non

15 ic event during peripheral ischemia produces superoxide and diminishes the NO bioavailability by form

16 , enables the inner-sphere reduction of both superoxide and dioxygen.

17 Reducing glycolysis, scavenging superoxide and enforcing PKM2 tetramerization correct th

18 e mechanism of generation and involvement of superoxide and H2O2 by the deoxyribozymes is not yet def

19 ldehyde-dependent differential generation of superoxide and hydrogen peroxide by AAO4 and the inducti

20 lex IV (Cox4i2) and the subsequent mediators superoxide and hydrogen peroxide for pulmonary oxygen se

21 HUVEC oxygen consumption and superoxide and hydrogen peroxide generation were measure

22 Mitochondrial production of superoxide and hydrogen peroxide is potentially importan

23 xudate generates nanomolar concentrations of superoxide and hydrogen peroxide on irradiation with sim

24 Here we show that the ROS superoxide and hydrogen peroxide were present in dark wa

25 energy dissipation, reactive oxygen species (superoxide and hydrogen peroxide) appeared.

26 g oxidative stress (e.g., hydrogen peroxide, superoxide and hydroxyl radicals, nitric oxide, ascorbic

27 eishmania major), in which the Gzms generate superoxide and inactivate oxidative defense enzymes to k

28 nt MitoQuinone (MitoQ) reduced intracellular superoxide and inhibited cyst epithelial cell proliferat

29 d by a rapid reaction of tetramethylammonium superoxide and LiClO4 in solution, and its amorphous nat

30 of small crystallites show higher yields of superoxide and lower stability.

31 2+) overload driving increased generation of superoxide and necrotic cell death, which was rescued by

32 immune mechanisms that provoke hypoxia, and superoxide and nitric oxide formation, all of which can

33 n viewed as a reactive damaging byproduct of superoxide and nitric oxide, as a mediator of GPCR-CaMKI

34 rate a new intermediate, best described as a superoxide and nitrosyl adduct, [Cu(II)2(UN-O(-))(NO)(O2

35 Batteries based on sodium superoxide and on potassium superoxide have recently bee

36 iated redox cycle that causes high levels of superoxide and then peroxide formation, which damages DN

37 nd reductive activity toward both oxygen and superoxide, and (vi) mechanism for its transformation in

38 Levels of lipid peroxidation and of superoxide anion (O2(* horizontal line )) were higher in

39 It may derive from reaction of superoxide anion (O2(*-)) with nitric oxide (.NO) and ha

40 active site in class I b RNRs that requires superoxide anion (O2(.-) ), rather than dioxygen (O2 ),

41 SLDLPVLRW, FVPY) were found able to scavenge superoxide anion and hydroxyl radicals, organic nitro-ra

42 by disrupting electron transport, generating superoxide anion and inactivating bacterial oxidative de

43 Superoxide anion as a primary member of reactive oxygen

44 Corroboratively, we found that scavenging of superoxide anion by Mn(III) tetrakis (4-benzoic acid) po

45 Ang II increased the generation of superoxide anion from NADPH oxidase, as well as the amou

46 oll-Like receptors (TLR) induce an influx of superoxide anion in the ensuing endosomes.

47 at pomegranate extract reduced mitochondrial superoxide anion levels and increased mitochondrial func

48 inum and glass were tested and the amount of superoxide anion produced by NADPH oxidase was measured

49 destalilization which leads to Ca(2+) rise, superoxide anion production, ATP drop and late NADP(H) d

50 n aqueous solutions, EBN does not react with superoxide anion radical (O2(-*)) to form EBN/(*)OOH to

51 eactive oxygen species by disproportionating superoxide anion radical to oxygen and hydrogen peroxide

52 S) to be released, including singlet oxygen, superoxide anion radicals, and hydrogen peroxide.

53 ndothelial dysfunction, which was reduced by superoxide anion scavenging.

54 luding at 37 degrees C or in the presence of superoxide anion.

55 itric oxide (NO) and NAD(P)Hoxidase produces superoxide anions (O2 (-) , quenching NO) we propose tha

56 ndogenous neuroprotectant for RGCs through a superoxide-associated mechanism.

57 s copper site, yet they can still react with superoxide at rates limited only by diffusion.

58 The RGC superoxide burst was significantly reduced by intravitre

59 tion and generation of hydrogen peroxide and superoxide, but none of them can fully explain its toxic

60 In endothelial cells, endosomal surplus of superoxide causes pro-inflammatory activation and TLR4 a

61 udes in essence a ferrous iron center, minor superoxide character of the noninnocent ligand, signific

62 We report a superoxide colloidal solution route for preparing a LBSO

63 ctroscopies indicate [3](1-) to be an end-on superoxide complex with an S = 1/2 ground state.

64 accessible triplet state for this unique bis-superoxide complex.

65 remarkably analogous to those of ferric heme superoxide complexes.

66 red to measure the dynamics of extracellular superoxide concentration.

67 Extracellular superoxide concentrations are independent of light, alga

68 The changes in superoxide content upon charge show that charge proceeds

69 ation deficiency (25%) and increased nodular superoxide content.

70 otes mitochondrial respiration, leading to a superoxide-dependent activation of mitophagy.

71 41.1 +/- 17.6% of normoxic control), reduced superoxide dismutase (60.7 +/- 6.3%), increased phosphod

72 The copper chaperone for superoxide dismutase (Ccs1) activates immature copper-zi

73 ious studies have shown that levels of Cu/Zn superoxide dismutase (CSD) are down-regulated by miR398.

74 nding site for miR398 in an isoform of Cu/Zn superoxide dismutase (CSD1) is eliminated by alternative

75 e overexpressing lung-specific extracellular superoxide dismutase (ecSOD) were exposed to HEPA-filter

76 species, in part, by deacetylating manganese superoxide dismutase (MnSOD) and mitochondrial 8-oxoguan

77 Manganese-dependent superoxide dismutase (MnSOD) expression also increased s

78 tylation and decreased activity of manganese superoxide dismutase (MnSOD).

79 H2O2 accumulation, which result from higher superoxide dismutase (SOD) activity, associated with low

80 yphenol oxidase (PPO), peroxidase (POX), and superoxide dismutase (SOD) enzymes activities were measu

81 The activity of superoxide dismutase (SOD) in Brassica rapa also display

82 Superoxide dismutase (SOD) level in the blood samples ex

83 ning differences in antioxidant capacity and superoxide dismutase (SOD) levels between phenotypes may

84 malondialdehyde (MDA) and activity of total superoxide dismutase (SOD), and its mitochondrial (Mn-SO

85 Activities of superoxide dismutase (SOD), catalase (CAT) and peroxidas

86 tly, GA + UV-A also inhibits the activity of superoxide dismutase (SOD), magnifying the imbalance of

87 uced these cytokines only when stimulated by superoxide dismutase (SOD)-1.

88 responsive MRI contrast agent and a mimic of superoxide dismutase (SOD).

89 regulation of antioxidant enzymes, including superoxide dismutase (SOD).

90 mutase (Ccs1) activates immature copper-zinc superoxide dismutase (Sod1) by delivering copper and fac

91 nano-formulation (nanozyme) for copper/Zinc superoxide dismutase (SOD1) by polyion condensation with

92 Mutations in superoxide dismutase (SOD1) cause amyotrophic lateral sc

93 s and differences among apo-, Zn-, and Cu,Zn-superoxide dismutase (SOD1) dimers.

94 YFP throughout the brain and spinal cord of superoxide dismutase (SOD1) G93A transgenic mice.

95 Previously, we found that human Cu, Zn-superoxide dismutase (SOD1) is S-acylated (palmitoylated

96 Cu/Zn superoxide dismutase (SOD1) reduction prolongs survival

97 Ubiquitous expression of mutant Cu/Zn-superoxide dismutase (SOD1) selectively affects motor ne

98 Delivery of copper-zinc superoxide dismutase (SOD1), an efficient ROS scavenger,

99 We focused on Cu-Zn superoxide dismutase (SOD1), which protects cells from o

100 also reported for ALS-linked forms of Cu, Zn superoxide dismutase (SOD1).

101 /aP2 is the upregulation of the antioxidants superoxide dismutase (SOD2), catalase, methionine sulfox

102 ownregulation of ROS-producing extracellular superoxide dismutase (SOD3) in thyroid cancer cell lines

103 (glxK), valine-pyruvate transaminase (avtA), superoxide dismutase (sodB), and 2 hypothetical proteins

104 ssion of the G985R and G93A mutated forms of superoxide dismutase 1 (linked to familial amyotrophic l

105 e enhanced by expression of a mutant form of superoxide dismutase 1 (SOD1 G93A) that causes astrocyte

106 ouse model expressing a mutant form of human superoxide dismutase 1 (SOD1(G93A) ).

107 Mutant superoxide dismutase 1 (SOD1(G93A)) expression in astroc

108 Using a mouse model of ALS expressing mutant superoxide dismutase 1 (SOD1(G93A)), we show that motor

109 uired for copper-dependent activation of the superoxide dismutase 1 (SOD1) during spore germination.

110 shown that ALS-associated mutations in Cu/Zn superoxide dismutase 1 (SOD1) impair axonal transport of

111 rew-like structure of a cytotoxic segment of superoxide dismutase 1 (SOD1) in its oligomeric state.

112 e find that injection of oligomers of mutant superoxide dismutase 1 (SOD1) into the cytoplasm of inve

113 asked if decreasing metabolism in the mutant superoxide dismutase 1 (SOD1) mouse model of ALS (G93A S

114 Here we show that, in vitro, mutant superoxide dismutase 1 (SOD1) mouse oligodendrocytes ind

115 ally bind and neutralize misfolded and toxic superoxide dismutase 1 (SOD1) mutant proteins may find a

116 Superoxide dismutase 1 (SOD1) mutations account for up t

117 as abrogated by transgenic overexpression of superoxide dismutase 1 (SOD1) or an SOD1 mimetic.

118 ophic lateral sclerosis-associated cytosolic superoxide dismutase 1 (SOD1) protein between motor neur

119 Notably, G85R is a mutant version of Cu/Zn superoxide dismutase 1 (SOD1) that is unable to reach na

120 signal sequence lacking cytoplasmic protein, superoxide dismutase 1 (SOD1), and its mutant form linke

121 uppressed by oligomers of mutant human Cu/Zn superoxide dismutase 1 (SOD1), which are associated with

122 croglial phenotypes in preclinical stages of superoxide dismutase 1 (SOD1)-mutant-mediated disease.

123 nly caused by mutations in the gene encoding superoxide dismutase 1 (SOD1).

124 c slice cultures from a mutant form of human superoxide dismutase 1 (SOD1G93A) mouse model of ALS all

125 rimary astrocytes isolated from mutant human superoxide dismutase 1-overexpressing mice as well as hu

126 ncreased reactive oxygen species and reduced superoxide dismutase 2 (SOD2) activity.

127 deacetylase activity of sirtuin 3 to inhibit superoxide dismutase 2 (SOD2) activity.

128 f the increased acetylation of mitochondrial superoxide dismutase 2 (SOD2) and isocitrate dehydrogena

129 y of a key mitochondrial antioxidant enzyme, superoxide dismutase 2 (SOD2) because of hyperacetylatio

130 heat shock protein 70 (hsp70) interacts with superoxide dismutase 2 (SOD2) in the cytosol after synth

131 Ectopic expression of superoxide dismutase 2 (SOD2) reduced ROS and preserved

132 was associated with a reduced ratio of mROS/superoxide dismutase 2.

133 ariable analysis with higher MMP-2 and lower superoxide dismutase 3 gene expression, independent of a

134 inase-2 (MMP-2), MMP-14, endoglin (ENG), and superoxide dismutase 3 in ascending aorta samples from 5

135 Superoxide dismutase activity in human blood plasma mirr

136 The superoxide dismutase activity was relatively insensitive

137 Furthermore, the synthetic superoxide dismutase and catalase mimetic EUK-134 also a

138 ing, which restored NO production, increased superoxide dismutase and catalase, and suppressed NADPH

139 oxidase, dynamin related protein, manganese superoxide dismutase and Lon protease, respectively, wer

140 se through higher activities of antioxidant (superoxide dismutase and peroxidase) and defense enzymes

141 s such as mitochondrial manganese-containing superoxide dismutase and peroxiredoxin 5 were only upreg

142 ulation of GR and up-regulation of manganese superoxide dismutase and reduced glutathione levels.

143 f 215 amino acids, and has an iron/manganese superoxide dismutase domain.

144 e that IL-27 is able to induce extracellular superoxide dismutase during differentiation of monocytes

145 r-cGMP also activated catalase and manganese superoxide dismutase expression, indicating that this pa

146 Since the linking of mutations in the Cu,Zn superoxide dismutase gene (sod1) to amyotrophic lateral

147 ut NRAMP2 can functionally replace cytosolic superoxide dismutase in yeast, indicating that the pool

148 ortantly, treatment with the small-molecule, superoxide dismutase mimetic (GC4419; 0.25 mumol/L) sign

149 the addition of 4-hydroxy-TEMPO (TEMPOL), a superoxide dismutase mimic that reacts with superoxide,

150 surprisingly high abundance of extracellular superoxide dismutase produced by Synechococcus and a dyn

151 quired to deliver the metal ion to the Cu/Zn superoxide dismutase SodCII.

152 eductase, catalase, ascorbate peroxidase and superoxide dismutase together with xanthophyll cycle and

153 ize, number, and mRNA levels of catalase and superoxide dismutase were increased, whereas those of ni

154 ogenase E1 component, biotin carboxylase and superoxide dismutase were related to energy and carbon m

155 ties of catalase, glutathione peroxidase and superoxide dismutase were significantly lower in PSE-ind

156 complexes, not antioxidant enzymes (e.g., Mn superoxide dismutase), govern IR survival.

157 gates of biomolecules, e.g., of enzyme Cu/Zn-superoxide dismutase, abnormal aggregation of which is l

158 in substrate proteins such as cyclophilin D, superoxide dismutase, and PEPCK1 were not deacetylated.

159 lly, S.PEPS and S.EPS significantly improved superoxide dismutase, catalase and glutathione peroxidas

160 L-6, IL-10, TNF-alpha) and oxidative stress (superoxide dismutase, catalase, glutathione peroxidase,

161 ns, namely Ras-related nuclear, p53, PEPCK1, superoxide dismutase, cyclophilin D, and Hsp10, and anal

162 stigated dimeric beta-lactoglobulin, dimeric superoxide dismutase, dimeric and tetrameric concanavali

163 r alpha (TNF-alpha), CXCL10, CCL5, IL-6, and superoxide dismutase, in human macrophages infected with

164 adaptive or stress proteins (e.g. manganese superoxide dismutase, mitochondrial KATP channels and pe

165 thetase, alanine aminotransferase, catalase, superoxide dismutase, ornithine decarboxylase, glutamate

166 Here, we show superoxide dismutase-1 (SOD-1), an enzyme that converts

167 This article investigates how the rate of superoxide dismutase-1 (SOD1) fibrillization is affected

168 The acylation of lysine residues in superoxide dismutase-1 (SOD1) has been previously shown

169 ))ATSM enhanced the association of DJ-1 with superoxide dismutase-1 (SOD1), paralleled by significant

170 disease, as has been shown for mutations in superoxide dismutase-1 (SOD1).

171 es, reactive oxidative species scavenging by superoxide dismutase-1 and superoxide dismutase-2.

172 d to neuronal and vascular oxidative stress (superoxide dismutase-2), neuroinflammation (astroglial a

173 synthase and enhanced lung concentrations of superoxide dismutase-2, thereby reducing lung tissue rea

174 ies scavenging by superoxide dismutase-1 and superoxide dismutase-2.

175 is could be partially inhibited by Tempol (a superoxide dismutase-mimetic agent) and by glyburide (an

176 e scavenger, with a rate constant similar to superoxide dismutase.

177 of toxic superoxide to hydrogen peroxide by superoxide dismutase.

178 , which was exaggerated in the presence of a superoxide dismutase/catalase mimetic.

179 -oxidant systems that include iron-dependent superoxide dismutases (SODs) in mitochondria and glycoso

180 The copper-containing superoxide dismutases (SODs) represent a large family of

181 arbon fixation, oxidative stress protection (superoxide dismutases) and iron and nitrogen metabolism

182 ormation and directed the recombination of a superoxide/dithranyl radical pair.

183 of exogenous superoxide via the paramagnetic superoxide donor potassium dioxide or superoxide-suffici

184 porphyrin (MnTMPyP), an antioxidant, reduced superoxide formation in UNx-mice and prevented the elong

185 to measure the release rate of drug-induced superoxides from C2C12 cells through a porous membrane.

186 ein described that allows for solution phase superoxide generated via the reduction of dioxygen in ne

187 tension and the cellular distribution of the superoxide generating NADPH oxidase (NOX) in AVP-express

188 Although F. nucleatum vincentii also reduced superoxide generation (25%), the impact was not as stron

189 lymorphum significantly blocked fMLP-induced superoxide generation (P <0.001).

190 Two of three subspecies blocked neutrophil superoxide generation in response to a secondary stimulu

191 Superoxide generation rates captured from monolayer myob

192 Superoxide generation was measured by cytochrome C reduc

193 ts of angiotensin II (Ang II) by attenuating superoxide generation, apoptosis, proliferation and incr

194 tial lipid-dependent decrease in the rate of superoxide generation, modulate H2O2 emission as a funct

195 Angiotensin II and phorbol ester increased superoxide/H2O2 generation in PMVECs, AMs, and isolated

196 based on sodium superoxide and on potassium superoxide have recently been reported.

197 We found that cobalamin scavenged superoxide in neuronal cells in vitro treated with the r

198 To get insight into the role of phagocytic superoxide in the onset of diabetic complications, we us

199 ated inflammatory signaling by intracellular superoxide in vitro and in animal models, although total

200 Our SEIRAS studies show that the superoxide induced ring opening reaction of PC is determ

201 HPV could be inhibited by mitochondrial superoxide inhibitors proving the functional relevance o

202 o form pools of hydroperoxide, peroxide, and superoxide intermediates.

203 dismutase-1 (SOD-1), an enzyme that converts superoxide into less toxic hydrogen peroxide and oxygen,

204 Superoxide ion (O2(*-)) is of great significance as a ra

205 , not only does the nramp2 mutant accumulate superoxide ions, but NRAMP2 can functionally replace cyt

206 oxygen movement, and ultimately, emission of superoxide ions.

207 .g., m-CPBA), peroxides (e.g., H2O2) or even superoxide is a popular choice for accessing well-charac

208 This superoxide is ready to react with the CO adsorbed on TiO

209 resulted in no significant changes in NO and superoxide levels in response to LSS but significantly r

210 rve transection in Long-Evans rats increased superoxide levels in RGCs.

211 endogenous reactive oxygen species (ROS) and superoxide levels, as well as increased membrane potenti

212 ours of slow BD induction at which increased superoxide levels, decreased glutathione peroxidase (GPx

213 vely active AMPK downregulated mitochondrial superoxide, lowered levels of dynamin-related protein (D

214 Within corals, superoxide may contribute to pathogen resistance but als

215 At 4 hours after slow BD induction, superoxide, MDA, and plasma creatinine levels increased

216 sed, it does not bind in these crystals as a superoxide mimic.

217 selective electron transfer to form Cr(III) superoxide moieties.

218 lso increased TNFalpha, TNFRI, mitochondrial superoxide (mtO2(.-)), and pCREB in the ipsilateral SCDH

219 Na-O2 batteries can be cycled forming sodium superoxide (NaO2 ) as the sole discharge product with im

220 el SEM studies that image crystalline sodium superoxide (NaO2) on the carbon cathode.

221 The initial reaction product, sodium superoxide (NaO2), is not present in a measurable quanti

222 TRX scavenged superoxide, nitric oxide and also other model stable rad

223 Aerobic metabolism also generates superoxide (O2()) and hydrogen peroxide (H2O2) as bona f

224 resonance alter relative yields of cellular superoxide (O2(*-)) and hydrogen peroxide (H2O2) ROS pro

225 ited reaction of exogenous NO and endogenous superoxide (O2(*-)) produced in the electron transport c

226 by ROS, such as hydrogen peroxide (H2 O2 ), superoxide (O2(-) ), and peroxynitrite (ONOO(-) ).

227 n provide an estimate of the initial rate of superoxide (O2(-)) formation.

228 Each deoxyribozyme generates both superoxide (O2(-*) or HOO(*)) and hydrogen peroxide (H2O

229 The reactive oxygen species superoxide (O2(.-)) is both beneficial and detrimental t

230 Conversely, adding either superoxide or H2O2 from the outset strongly enhances cat

231 RNAi of p47phox had no effects on superoxide or NO production in response to OSS but signi

232 m cations can be tuned to give either sodium superoxide or sodium peroxide discharge products at the

233 ring voltage was poised at a value at which superoxide oxidation ensued yielded bell-shaped ring cur

234 (ROS/RNS; nitroxidative species), including superoxide, peroxynitrite, and hydrogen peroxide.

235 The photo-generated superoxide plays an important role in Fe(III) reduction

236 tion of NO, which in combination with excess superoxide produced during Rtp801 activation, contribute

237 nflammatory signaling mediated by endogenous superoxide produced in the endothelial endosomes in resp

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

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

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

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

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

243 We report that superoxide production following CB3 infection may exacer

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

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

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

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

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

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

250 lting in bioenergetics defects and increased superoxide production.

251 ote mitochondrial ATP synthesis and suppress superoxide production.

252 gulate platelet CD36 signaling by increasing superoxide radical anion and hydrogen peroxide through a

253 athway requiring Src kinases, NADPH oxidase, superoxide radical anion, and hydrogen peroxide.

254 , in addition to being a potential source of superoxide radical, CBS constitutes a previously unrecog

255 Superoxide radicals (O2( *-)) and their protonated form

256 (NO) in combination with singlet oxygen and superoxide radicals (O2(*-)) as reactive oxygen species

257 ns is exposed to a range of stresses such as superoxide radicals and cationic fluxes.

258 reactions with PFOA showed that hydroxyl and superoxide radicals, which are typically the primary pla

259 ction via photosynthesis and the disposal of superoxide radicals.

260 mitochondrial stressors, leading to elevated superoxide release and reduced mitochondrial glutathione

261 hibitors proving the functional relevance of superoxide release for HPV.

262 Hypoxia-induced mitochondrial superoxide release has been suggested as a critical step

263 e primary oxygen sensor and the mechanism of superoxide release in acute hypoxia, as well as its rele

264 ionyl-leucyl phenylalanine (fMLF)-stimulated superoxide release to an extent similar to that of cells

265 Minimal superoxide release was observed by direct bacterial chal

266 Hypoxia-induced superoxide release which was detected by electron spin r

267 agmentation, mitigated mitochondrial-derived superoxide release, improved endothelial-dependent vasod

268 olarization, which can promote mitochondrial superoxide release, was detected during acute hypoxia in

269 superoxide dismutase mimic that reacts with superoxide, rescued the growth of C. jejuni cultured in

270 hological effects of external vs. endogenous superoxide, respectively.

271 eosinophils with catalase (an extracellular superoxide scavenger) or NSC 23766 (a Rac GTPase inhibit

272 Infusion of tiron, a superoxide scavenger, attenuated the exaggerated pressor

273 the effects of ROS on the EPR, we infused a superoxide scavenger, tiron, into the superficial epigas

274 h unknown mechanisms and that it is a potent superoxide scavenger, we tested whether cobalamin, a vit

275 n B12 (cobalamin) was recently shown to be a superoxide scavenger, with a rate constant similar to su

276 The device displays a considerably improved superoxide sensitivity of 7.29nAnM(-)(1)cm(-)(2) and a l

277 han any similar enzyme-based electrochemical superoxide sensor and is attributed to the facile diffus

278 in mediating the photo-induced formation of superoxide species from oxygen.

279 Third, the superoxide species reduces the Diels-Alder cycloadduct r

280 y photo-induced formation of highly reactive superoxide species.

281 phosphate metabolism, metal homeostasis, and superoxide stress resistance presented in this study hig

282 ion and produces the male-specific paraquat (superoxide) stress adaptation.

283 eas males but not females adapt to paraquat (superoxide) stress.

284 gnetic superoxide donor potassium dioxide or superoxide-sufficient dendritic cells.

285 eptor lead to oxidative species (most likely superoxide) that in turn oxidize VMAT2.

286 ty to catalyze the production of deleterious superoxide, the formation of Cu(I)-glutathione complexes

287 the importance of the end-on coordination of superoxide to Cu for HAA along the triplet spin surface;

288 stem II complex) and biodegradation of toxic superoxide to hydrogen peroxide by superoxide dismutase.

289 chondria, autonomously adjusts mitochondrial superoxide to levels suitable to maintain stem cell-like

290 ces have been explained by solution-mediated superoxide transport, the underlying nature of this mech

291 Small molecule and enzymatic superoxide traps suppressed formation of the oxygenation

292 is were rescued by the addition of exogenous superoxide via the paramagnetic superoxide donor potassi

293 s Nox2 NADPH oxidase-dependent generation of superoxide, whereas insulin-stimulated and shear stress-

294 perpolarization and release of mitochondrial superoxide which, after conversion to hydrogen peroxide,

295 oxidase (NOX2) to generate large amounts of superoxide, which acts as a precursor of hydrogen peroxi

296 we report that in human AML, NOX2 generates superoxide, which stimulates bone marrow stromal cells (

297 to RGC axons causes a burst of intracellular superoxide, which then signals RGC apoptosis.

298 in response to LSS but significantly reduced superoxide while increasing NO in response to OSS.

299 reduction occurring via Fe(III) reduction by superoxide while the rest of the Fe(III) reduction occur

300 re, we hypothesized that loss of NOX-derived superoxide would dampen diabetogenic antiviral macrophag