ライフサイエンスコーパス: superoxide anion

1 effects of corresponding ROS, H(2)O(2), and superoxide anion.

2 es the assembly of NADPH oxidase to generate superoxide anion.

3 ntrols and was accompanied by an increase in superoxide anion.

4 at appears to be related to the formation of superoxide anion.

5 cells, utilize molecular oxygen to generate superoxide anion.

6 oluminescent probe for in vitro detection of superoxide anion.

7 e activated in response to the production of superoxide anion.

8 was decreased with a concomitant increase in superoxide anion.

9 rmed the identity of the reaction product as superoxide anion.

10 inone (DMNQ), which generates a low level of superoxide anion.

11 potential bioluminescent reporter protein of superoxide anion.

12 It also directly detoxifies superoxide anion.

13 he reaction product of nitric oxide (NO) and superoxide anion.

14 ress with enhanced endothelial production of superoxide anion.

15 major defense against ROS by detoxifying the superoxide anion.

16 ng damage mediated by detrimental actions of superoxide anion.

17 s formed in the reaction of nitric oxide and superoxide anion.

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

19 eactive oxygen species by disproportionating superoxide anion.

20 ells, indicating eNOS as a primary source of superoxide anion.

21 ir reaction with dissolved oxygen to produce superoxide anions.

22 o interfere with NADH oxidation and generate superoxide anions.

23 s low, leading to an increased production of superoxide anions.

24 medullae, suggesting increased generation of superoxide anions.

25 roxide dismutases (SOD) that act to detoxify superoxide anions.

26 a secretion by PBMC in response to exogenous superoxide anions.

27 gen peroxide, a stable dismutated product of superoxide anions.

28 ikewise is associated with the production of superoxide anions.

29 ne NADPH oxidases that produce extracellular superoxide anion, a reactive oxygen species that is read

30 Second, the formation of superoxide anion, a scavenger of nitric oxide, was also

31 Phagocyte NADPH oxidase produces superoxide anions, a precursor of reactive oxygen specie

32 It was hypothesized that a specific ROS, superoxide anion, acts as an intracellular signaling mol

33 ight provide a preorganized binding site for superoxide anion, an obligatory intermediate in the two-

34 A and protein as well as increased levels of superoxide anion and apoptotic cell death.

35 se wave velocity, measurement of circulating superoxide anion and C-reactive protein, as well as bloo

36 NADPH oxidases, leading to production of the superoxide anion and decreased availability of nitric ox

37 hagocytes are defective in the generation of superoxide anion and downstream reactive oxidant species

38 e reaction of OG with the E1o-h gave rise to superoxide anion and hydrogen peroxide (reactive oxygen

39 the data suggest the novel observation that superoxide anion and hydrogen peroxide are produced sepa

40 w cytometry that 1,6-BPQ and 3,6-BPQ produce superoxide anion and hydrogen peroxide in MCF-10A cells.

41 n of reactive oxygen species (ROS) including superoxide anion and hydrogen peroxide.

42 ric reducing antioxidant power (FRAP), ABTS, superoxide anion and hydroxyl radical scavenging tests.

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

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

45 tress as measured by increased generation of superoxide anion and increased expression of nitrotyrosi

46 significant reduction in hydrogen peroxide, superoxide anion and malondealdehyde contents under stre

47 d that DB infestation significantly increase superoxide anion and malondialdehyde production to two-f

48 dant and nitrating agent readily formed from superoxide anion and nitric oxide generated by mitochond

49 power, DPPH (2,2-diphenyl-1-picrylhydrazyl), superoxide anion and nitric oxide radical scavenging.

50 thological states in which the production of superoxide anion and NO is increased.

51 y F(2)-isoprostanes (P < 0.001) and monocyte superoxide anion and tumor necrosis factor release compa

52 inding that nicotine significantly increased superoxide anions and 3-nitrotyrosine-positive proteins,

53 lization, linked with abundant generation of superoxide anions and apoptosis.

54 c complexes are not effective in scavenging superoxide anions and are not effectively reduced by asc

55 ltered cellular redox state due to increased superoxide anions and establish a new relationship betwe

56 153), an enzyme mediating the dismutation of superoxide anions and examined the in vitro and in vivo

57 A medium resulted in increased production of superoxide anions and H(2)O(2), transduction of the PI 3

58 somes was determined against the toxicity of superoxide anions and hydroxyethyl radicals in HepG2 cel

59 n excess, iron is toxic because it generates superoxide anions and hydroxyl radicals that react readi

60 mechanisms involving increased generation of superoxide anions and suggest that hypoxia-evoked CA eff

61 ate immunity (phagocytosis and production of superoxide anion) and pathogen challenge were used to ev

62 of surface adhesion molecules, generation of superoxide anion, and appearance of reactive oxygen spec

63 ntaneous generation of hydrogen peroxide and superoxide anion, and decreased ATP, as well as subseque

64 at least four individual RONS (NO, H(2)O(2), superoxide anion, and peroxynitirte), induced apoptotic

65 denced by increased levels of monocyte IL-6, superoxide anion, and plasma CRP, sICAM, sCD40L, and nit

66 a exposed to light generated singlet oxygen, superoxide anion, and the hydroxyl radical.

67 tein kinase (MAPK) activation, generation of superoxide anion, and Toll-like receptor 4 expression wa

68 e in circulating endothelial cell sloughing, superoxide anion, and vasoconstriction in diabetic rats

69 at all 15 strains exhibit elevated levels of superoxide anions, and we show that elevated levels of r

70 Superoxide anions are proposed to generate singlet oxyge

71 Hp disrupt NADPH oxidase targeting such that superoxide anions are released into the extracellular mi

72 Reactive oxygen species (ROS), particularly superoxide anion, are well known to inhibit NO, and ther

73 Superoxide anion as a primary member of reactive oxygen

74 ocyanostilbene-2,2'-disulphonate, confirming superoxide anion as the mediating oxidant.

75 endothelial NADPH oxidase and generation of superoxide anion at the extracellular surface of the cel

76 Furthermore, the production of superoxide anion but not hydrogen peroxide increased in

77 rom peritoneal lavage fluids did not produce superoxide anion, but did produce an anti-inflammatory a

78 s of AT1R protein and measured production of superoxide anion by brain tissue under basal conditions

79 Selective removal of superoxide anion by M40401 results in inhibition of I/R

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

81 nhibitors of the extracellular production of superoxide anion by preventing the up-regulation of the

82 d the generation of NAD(P)H oxidase-mediated superoxide anions by increasing the translocation and me

83 not only generate hydrogen peroxide but also superoxide anions by transferring aldehyde-derived elect

84 d by diminished activation and intracellular superoxide anion concentration, and reduced leukocyte ad

85 genously produced hydrogen peroxide, but not superoxide anions, contributed to the formation of oxidi

86 ously that inactivation of catecholamines by superoxide anions contributes to the loss of vascular re

87 The regulator is primarily activated by superoxide anion-dependent oxidation.

88 Heterozygous manganese superoxide anion dismutase (SOD2) gene-knockout mice (SO

89 the presence of H2(18)O all suggest that the superoxide anion drives the deprotection reaction.

90 al tubules as a major site for generation of superoxide anions during diabetic nephropathy.

91 lectron transport chain in the generation of superoxide anions during IH.

92 e have hypothesized that the balance between superoxide anion efflux through inner membrane anion cha

93 a cleavage is blocked under conditions where superoxide anion formation is blocked or monocytes are t

94 Superoxide anion formation was assayed by hydroethidine

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

96 Model simulation studies showed that superoxide anion generated by dithionite reduction of mo

97 inhibited nitroblue tetrazolium reduction of superoxide anion generated in a xanthine-xanthine oxidas

98 uman Burkitt's lymphoma cells are exposed to superoxide anion, generated as a flux from xanthine and

99 ) deficiency, the catalytic component of the superoxide anion-generating NADPH oxidase complex, is ad

100 (18 +/- 12% of control, n = 4) and increased superoxide anion generation (358 +/- 37%, p = 0.003).

101 VEGF and angiogenin 1 together with reduced superoxide anion generation and an increase in MnSOD com

102 y assess the relative rates of mitochondrial superoxide anion generation in isolated islets in respon

103 this end, PMN transendothelial migration and superoxide anion generation were assessed with LAP patie

104 t aggregation, adhesion, thrombus formation, superoxide anion generation, and surface activation mark

105 PLD activation, myeloperoxidase release, and superoxide anion generation, and that PLD activation occ

106 s associated with increased NOX activity and superoxide anion generation.

107 nt of accurate methods for quantification of superoxide anion has attracted tremendous research atten

108 NADPH oxidase 4 (NOX4), a source of cellular superoxide anions, has multiple biological functions tha

109 ve oxygen species, including singlet oxygen, superoxide anion, hydrogen peroxide, and hydroxyl radica

110 ted lotus slices exhibited reduced browning, superoxide anion, hydrogen peroxide, electrolyte leakage

111 Reactive oxygen species (ROS), including superoxide anions, hydrogen peroxide and hydroxyl radica

112 ases, reactive species levels (nitric oxide, superoxide anion, hydroxyl radical scavenger capacity) a

113 f different ROS including hydrogen peroxide, superoxide anion, hydroxyl radical, and lipid peroxides.

114 ectroscopic evidence of the participation of superoxide anion in a related chemical model reaction th

115 cells was mediated by induction of cellular superoxide anion in cancerous but not normal cells.

116 owever, tempol decreased basal production of superoxide anion in diabetic rats.

117 ngeners increased the in vitro production of superoxide anion in head kidney macrophages.

118 d molecular pattern, activates production of superoxide anion in leukocytes without the need for phag

119 ngiotensin II increased lucigenin-detectable superoxide anion in LV tissue in a manner that was inhib

120 inished NADPH oxidase-mediated production of superoxide anion in response to bacteria by MyD88-/- pha

121 ormation of nitrotyrosine, nitric oxide, and superoxide anion in retinal vascular endothelial cells a

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

123 successfully applied to the determination of superoxide anion in the plant cell samples.

124 rin was proportional to the concentration of superoxide anion in the range from 4 to 40 000 pM with a

125 The role of superoxide anions in the development of vascular dysfunc

126 Paraquat-induced ROS production (including superoxide anions) in BV-2 cells was accompanied by tran

127 abrogated cell chemotaxis and the release of superoxide anions induced by the bacterial formylpeptide

128 potent oxidant generated by nitric oxide and superoxide anions, instigates GTPCH1 ubiquitination and

129 e capacity is reduced in conditions in which superoxide anion is increased, and this is associated wi

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

131 Attenuation of L-NAME-inhibitable superoxide anion levels by GW501516 demonstrated that ac

132 ide synthase (eNOS) expression and increased superoxide anion levels in both vessels and HPAECs.

133 IH increased superoxide anion levels in mitochondria as evidenced by

134 f proliferating fibroblasts led to increased superoxide anion levels, juxtanuclear accumulation of ub

135 MTKO tumors also exhibited higher superoxide anion levels.

136 Thus, generation of H2O2 from superoxide anion likely produced from DT-diaphorase cata

137 Furthermore, the production of superoxide anion (lucigenin chemiluminescence) was incre

138 kinase C (PKC) contributes to generation of superoxide anion (O(-)(2)) after fluid percussion brain

139 Overproduction of superoxide anion (O(2) (.-) ), the primary cellular reac

140 D2p is the primary defence of Cn against the superoxide anion (O(2) (.-)) in the mitochondria.

141 mediated host defense by producing cytotoxic superoxide anion (O(2)( )).

142 re we show that Fe(2+) induces generation of superoxide anion (O(2)()) in endosomes, reduces protein-

143 The rate of superoxide anion (O(2)(*)(-)) generation is 4 times high

144 ochrome bc(1) complex (bc(1)) also catalyzes superoxide anion (O(2)(*)) generation upon oxidation of

145 endent activity increases eNOS generation of superoxide anion (O(2)(*)) upon enzyme activation.

146 CFR simultaneously detects superoxide anion (O(2)(*-)) and caspase-3 (casp3) throug

147 We quantified myocardial superoxide anion (O(2)(-)) and peroxynitrite (ONOO(-)) a

148 A. phagocytophila rapidly inhibits the superoxide anion (O(2)(-)) generation by human neutrophi

149 me activity, and cellular NO levels, whereas superoxide anion (O(2)(-)) production was significantly

150 ed that diabetic monocytes produce increased superoxide anion (O(2)(-)), and alpha-tocopherol (AT) su

151 rved with NADH may involve the generation of superoxide anion (O(2)(-).) as they were attenuated to j

152 espiratory burst" of NADPH oxidase-dependent superoxide anion (O(2)(-*)) production that is required

153 Although the superoxide anion (O(2)(-.)) is generated during normal c

154 hate (NADPH) oxidase activity causes reduced superoxide anion (O(2)(.)) radical production leading to

155 ective effect by scavenging of mitochondrial superoxide anion (O(2)(.-)) and intramitochondrial free

156 NADPH- and NADH-stimulated superoxide anion (O(2)(.-)) generation was assessed by c

157 , which decreases NO synthesis and increases superoxide anion (O(2)(.-)) production by the enzyme.

158 idase and could provide high local levels of superoxide anion (O(2)), that when dismutated would gene

159 maintain the steady-state concentrations of superoxide anion (O(2)*-) and hydrogen peroxide (H(2)O(2

160 tive (reduced) oxygen species (ROS), such as superoxide anion (O-2.) and/or hydrogen peroxide (H2O2).

161 (eNOS) and increases enzymatic production of superoxide anions (O(2)()).

162 Cerebral ischemia and reperfusion increase superoxide anions (O(2)(*-)) in brain mitochondria.

163 e of this study was to determine the role of superoxide anions (O(2)(-)) in mononuclear phagocyte-ind

164 diated tissue injury involves the release of superoxide anions (O(2)(-)), the present study examined

165 HUVECs to high glucose (30 mmol/l) increased superoxide anions (O(2).(-)) and prostacyclin synthase n

166 e latter are trapped by O2, thus forming the superoxide anion O2*-.

167 Efforts to understand how a lipophobic superoxide anion (O2 (-)) can be detoxified by cytoplasm

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

169 ed inhibition, indicating the involvement of superoxide anion (O2(*-)) in the inactivation process.

170 Production of superoxide anion (O2(*-)) was detected by its selective

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

172 5-Epi-LXA4 (0.1-100 nM) inhibited neutrophil superoxide anion (O2(-)) generation in a concentration-

173 decreased, eNOS becomes uncoupled to produce superoxide anion (O2(-)) instead of NO, which contribute

174 H2O2 and superoxide anion (O2(-)) production were significantly b

175 The mediator of the restrictive signal is superoxide anion (O2(-)) released by membrane NAD(P)H ox

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

177 Therefore, we have examined the effect of superoxide anion (O2) on IP3R-mediated Ca(2+) signaling.

178 The rate of superoxide anion (O2*) generation, measured by the chemi

179 nd that arsenic induced the formation of the superoxide anion (O2*) in SVEC4-10 cells.

180 ory activity by modulating the generation of superoxide anion (O2*).

181 XO) from ischemic tissues increases vascular superoxide anion (O2*-) generation.

182 n in MCF-7 cells increased the generation of superoxide anion (O2*-) in anthracycline-treated cell ex

183 thelial function by modulating levels of the superoxide anion (O2*-) in the extracellular space.

184 on by modulating the levels of extracellular superoxide anion (O2*-) in the vasculature.

185 It catalyses the transformation of the superoxide anion (O2*-) into hydrogen peroxide.

186 cholesterol decreased NO (*NO) and increased superoxide anion (O2*-) production and increased ATP-bin

187 o induce NAD(P)H oxidase to produce vascular superoxide anion (O2*-) production, which has been impli

188 oxide synthase (eNOS) activity, which allows superoxide anion (O2*-)) to be generated rather than nit

189 es the reactive oxygen species intermediate, superoxide anion (O2*-).

190 here was an increase in lucigenin-detectable superoxide anion (O2-) in cardiac tissues from nNOS-/- c

191 We hypothesized that in states in which superoxide anion (O2-) is increased, especially in the m

192 thromboxane prostanoid receptors (TP-Rs), or superoxide anion (O2-) mediates enhanced contractions of

193 Overproduction of superoxide anion (O2-) rather contributes to various car

194 ROS-generating systems for hydroxyl radical, superoxide anion (O2-), and H2O2.

195 thelial generation of nitric oxide (*NO) and superoxide anion (O2-).

196 oxygen, partially reducing this molecule to superoxide anion (O2-*).

197 as NoxA1ds) potently inhibited Nox1-derived superoxide anion (O2.-) production in a reconstituted No

198 Previous treatment with superoxide anion (O2.-) scavenger prevented sensory LTF.

199 ct of donor-ion charge on reduction of O2 to superoxide anion (O2.-), is obtained using an isostructu

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

201 and increased vascular NADPH oxidase-derived superoxide anions (O2 (-)).

202 production of proinflammatory cytokines and superoxide anions (O2-).

203 body's defence against microbes: it produces superoxide anions (O2-, precursors to bactericidal react

204 ater molecules on the nucleophilicity of the superoxide anion, O2(*-), has been investigated in detai

205 PH oxidase helps kill pathogens by producing superoxide anion, O2-.

206 ein kinase (MAPK) in mediating the effect of superoxide anions on PTK expression and ROMK (Kir 1.1) c

207 ogen peroxide, ozone, hydroxyl radicals, and superoxide anions), only H2O2 and ozone were found to be

208 ces concomitantly enhanced the production of superoxide anion, only the fungicidal activity of collag

209 tration of superoxide dismutase (to scavenge superoxide anions) or L-N(G)-nitroarginine methyl ester

210 Hydrogen peroxide, superoxide anion, oxidized lipid, and oxidized protein l

211 All three extracts scavenged superoxide anion, peroxynitrite anion, and peroxyl radic

212 gmented the production of hydrogen peroxide, superoxide anion, peroxynitrite, and nitric oxide.

213 It is concluded that superoxide anions play a key role in suppressing K secre

214 te (NADPH) oxidase generates vast amounts of superoxide anion, precursor to bactericidal reactive oxy

215 ide dismutase mimetic, a potent scavenger of superoxide anions, prevented IH-induced c-fos, AP-1 and

216 ctron paramagnetic resonance spectroscopy of superoxide anion produced by macrophages.

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

218 product, plays an important role in removing superoxide anions produced inside mitochondria.

219 42 and in the Rho GTPase-dependent functions superoxide anion production and actin polymerization.

220 veolin-1, whereas it significantly increased superoxide anion production and activated extracellular

221 man monocytes and in COSphox cells increased superoxide anion production and depletion of PAT1 by spe

222 Furthermore, IL-6 time dependently increased superoxide anion production and ONOO- formation; the lat

223 G6PD deficiency may reduce vascular superoxide anion production by limiting production of th

224 e's effects on chemotaxis, phagocytosis, and superoxide anion production by phagocytes.

225 Superoxide anion production by the neutrophil NADPH oxid

226 Superoxide anion production by the phagocyte NADPH oxida

227 als are transduced to allow the induction of superoxide anion production in human monocytes.

228 n, as well as increased TNF-alpha, IL-6, and superoxide anion production in inflammatory MC subsets.

229 uthern and Western blotting and by measuring superoxide anion production in membrane fractions in the

230 ication of NMDA and kainate did not increase superoxide anion production in nondiabetic or diabetic r

231 NADPH-dependent superoxide anion production in the rostral ventrolateral

232 Superoxide anion production induced by 500 mg/dl dextros

233 In addition, we measured superoxide anion production under basal conditions, duri

234 dinucleotide phosphate oxidase activity and superoxide anion production via downregulation of Rac1.

235 G6PD may therefore affect superoxide anion production via vascular NADPH oxidase,

236 Superoxide anion production was measured with an ethidiu

237 el regulator of NADPH oxidase activation and superoxide anion production, a key phagocyte function.

238 amily kinases, small GTPase Rac2, neutrophil superoxide anion production, and for Listeria monocytoge

239 2 resulted in increased Ca(2+) mobilization, superoxide anion production, and GTPase activity in neut

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

241 ophore, phorbol ester, or H(2)O(2) exhibited superoxide anion production, which was blocked by additi

242 s (PMNs), as shown by the stimulation of PMN superoxide anion production.

243 ceptor internalization, GTPase activity, and superoxide anion production.

244 y a glucose-driven increase in mitochondrial superoxide anion production.

245 ubstrate for oxidation by O2, leading to the superoxide anion radical (in d) and the radical (in b).

246 as superoxide dismutase (SOD), which removes superoxide anion radical (O(2)(-)) and prevents the prod

247 pecies, hydrogen peroxide (H(2)O(2)) and the superoxide anion radical (O(2)(.-)), are key redox signa

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

249 d redox-active agents (nitric oxide (NO) and superoxide anion radical (O2*).

250 In turn, the ability to generate superoxide anion radical and hydrogen peroxide by ozone-

251 previously shown that redox agents including superoxide anion radical and nitrogen dioxide can react

252 oxide is not the dissolved oxygen but rather superoxide anion radical generated from the reaction of

253 generate quinone, and during this process a superoxide anion radical may be produced.

254 ensor, further support that nitric oxide and superoxide anion radical quickly react resulting in near

255 hat mulberry polyphenolics may act as potent superoxide anion radical scavengers and reducing agents.

256 ing power (0.03-38.45 muM ascorbic acid) and superoxide anion radical scavenging activity (16.53-62.8

257 According to DPPH, hydroxyl radical and superoxide anion radical scavenging activity assays, the

258 All activities except superoxide anion radical scavenging activity increased a

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

260 a oxidative injury of complexes I and II and superoxide anion radical-induced hydroxyl radical produc

261 tronic properties, photocatalytic ability in superoxide anion radical-mediated coupling of (arylmethy

262 est scavenging activity was observed for the superoxide anion radical.

263 resence of NADH, indicating the formation of superoxide anion radical.

264 omplexes of manganese (Mn) that can scavenge superoxide anion radicals and provide a backup for super

265 PD-E were found to inhibit the production of superoxide anion radicals by reducing xanthine oxidase a

266 a nonheme iron metalloenzyme that detoxifies superoxide anion radicals O(2)(*-) in some microorganism

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

268 ant plants also generated elevated levels of superoxide anion radicals, H2O2, and carbonylated protei

269 Monocyte superoxide anion release was significantly increased in

270 vascular cell adhesion molecule and monocyte superoxide anion release, and interleukin-1 release in T

271 ein (CRP), LDL oxidation, monocyte function (superoxide anion release, cytokine release, and adhesion

272 r agents (e.g., iron cations, cyanide anion, superoxide anion) released, and as affected by the state

273 an increase in the stimulated production of superoxide anion replicating the phenotype of LAgP PMNs.

274 Inhibition of nanosheet-induced superoxide anion restored the suppression of CSC and EMT

275 While administration of a superoxide anion scavenger during IH did not prevent neu

276 y treatment with a HIF-1alpha inhibitor or a superoxide anion scavenger.

277 dical scavenging ability, reducing activity, superoxide anion scavenging ability, linoleic acid and p

278 erric reducing antioxidant power (FRAP), the superoxide anion scavenging activity assay (SA), and cor

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

280 against peroxyl radicals, hydroxyl radicals, superoxide anion, singlet oxygen, and peroxynitrite were

281 n both oxygen uptake and the accumulation of superoxide anion spin adducts.

282 essened by decreasing either nitric oxide or superoxide anion, suggesting that ONOO(-) was responsibl

283 d T497A/S1179D eNOS generated 2-3 times more superoxide anion than WT eNOS, and both basal and stimul

284 oreductase) is generally thought to generate superoxide anion that participates in cell signaling and

285 ion of coelenterazine under the oxidation of superoxide anion, the lower the amount aequorin regenera

286 The rapid reaction with a second superoxide anion through radical-radical coupling may ex

287 e for reaction with molecular oxygen to form superoxide anion, thus decreasing bc(1) activity.

288 Antioxidants confirmed the superoxide anion to be the primary species responsible f

289 ygen species by catalyzing the conversion of superoxide anion to hydrogen peroxide and molecular oxyg

290 ymes that catalyze the disproportionation of superoxide anion to oxygen and hydrogen peroxide to guar

291 positioned for electrostatic guidance of the superoxide anion to the narrow active site channel.

292 metabolism and, together with production of superoxide anions via quinone reduction under high oxyge

293 in kinase C (PKC) activity and production of superoxide anion were increased in the cerebral arteries

294 ally oxidized to fluorescent ethidium by the superoxide anion, whereas mice lacking UCP2 exhibited in

295 in both cases correlated with resistance to superoxide anion, whereas only LHCBM1 is also involved i

296 hibition of the dextrose-induced increase in superoxide anions, whereas inhibition of endothelin expr

297 produces reactive oxygen species, including superoxide anions, which cause DNA damage unless removed

298 ochondrial damage can lead to the release of superoxide anions, which then react with nitric oxide to

299 se mimetic, which has been shown to scavenge superoxide anion with highly specific and enhanced catal

300 iation with reduced myocardial generation of superoxide anion (WT versus DDAH-I, 465.7+/-79.8 versus