ライフサイエンスコーパス: nitrotyrosine

1 munohistochemistry of oxidative potential (3-nitrotyrosine).

2 well as the amount of hydrogen peroxide and nitrotyrosine.

3 ynthesis, atrial natriuretic peptide, and 3'-nitrotyrosine.

4 AbGSC90 and probed with antibodies against 3-nitrotyrosine.

5 and dysfunction and increased myocardial 3'-nitrotyrosine.

6 or neuron cultures become immunoreactive for nitrotyrosine.

7 , cyclic guanosine monophosphate (cGMP), and nitrotyrosine.

8 e brain vascular lining and colocalized with nitrotyrosine.

9 markers gp91(phox), 4-hydroxynonenal, and 3-nitrotyrosine.

10 sed expression of TNF-alpha, CD14, iNOS, and nitrotyrosine.

11 fications involving methionine sulfoxide and nitrotyrosine.

12 iodothyronine, gentisate, rosmarinate, and 3-nitrotyrosine.

13 ist 1alpha,25-dihydroxylumisterol(3) reduced nitrotyrosine 16 hours after UVR, detected by a sensitiv

14 /endoplasmic reticulum Ca(2+) ATPase (SERCA) nitrotyrosine-294,295 and cysteine-674 (C674)-SO(3)H wer

15 The presence of 3-nitrotyrosine (3-NT) adducts in Lewy bodies in Parkinson

16 n-1 receptor in the production of striatal 3-nitrotyrosine (3-NT) and l-citrulline (indirect indices

17 athione depletion, lipid peroxidation, and 3-nitrotyrosine (3-NT) formation were measured as indicato

18 of nitrosative stress is the formation of 3-Nitrotyrosine (3-NT) from Tyrosine (Tyr) by adding a nit

19 Treatment of tau with ONOO- results in 3-nitrotyrosine (3-NT) immunoreactivity and the formation

20 ygen species (ROS), nitric oxide (NO), and 3-nitrotyrosine (3-NT) in Huh7.5.1 cells.

21 3-Nitrotyrosine (3-NT) is formed by the reaction of peroxy

22 creases of 4-hydroxy-2-nonenal (4-HNE) and 3-nitrotyrosine (3-NT) protein adducts, whereas the cerebr

23 steatosis, lower NOS2 induction, and less 3-nitrotyrosine (3-NT) protein residues, indicating that r

24 he selective fluorogenic derivatization of 3-nitrotyrosine (3-NT) residues in peptides (after reducti

25 Hepatic steatosis, 3-nitrotyrosine (3-NT), 4-hydroxynonenal (4-HNE), hypoxia

26 4-HNE significantly increased the level of 3-Nitrotyrosine (3-NT), a marker of oxidative stress, in H

27 We then assessed 3-nitrotyrosine (3-NT), an indirect index of NO production

28 e free radical (A(.-)), NO metabolites and 3-nitrotyrosine (3-NT).

29 stigated the association between placental 3-nitrotyrosine (3-NTp), a biomarker of oxidative stress,

30 or increasing the impact and assessment of 3-nitrotyrosine (3-Nty) as a biomarker for early diagnosis

31 3-nitrotyrosine (3-Nty) quenches the luminescence intensit

32 Cardiac protein nitration (3-nitrotyrosine [3-NT]) and lipid peroxidation were signif

33 d pNO(2)Phe, sulfotyrosine (SO(3)Tyr), and 3-nitrotyrosine (3NO(2)Tyr) at specific sites in murine TN

34 rise in myocardial and peripheral protein-3-nitrotyrosine (3NT) and protein-carbonyl formation that

35 s as determined by antibodies specific for 3-nitrotyrosine (3NT) and via mass spectrometry (MS).

36 iseases, and it is evident by detection of 3-nitrotyrosine (3NT) in inflamed tissues.

37 s for identification and quantification of 3-nitrotyrosine (3NT) post-translationally modified protei

38 enal (HNE) [a lipid peroxidation product], 3-nitrotyrosine (3NT), and protein carbonyls in the p50 (-

39 que by identifying an original FET ligand, 3-nitrotyrosine (3NY), for GluR2 (R(o) approximately 24 A;

40 of PTEN, LKB1-Ser428 phosphorylation, and 3-nitrotyrosine (a biomarker of ONOO-) were significantly

41 nonenal (a marker of lipid peroxidation) and nitrotyrosine (a marker for peroxynitrite) in wild-type

42 n in substantia nigra and colocalized with 3-nitrotyrosine, a marker for oxidative protein damage.

43 Nitrotyrosine, a marker of oxidative stress, was increas

44 Parallel increases in OS protein-bound nitrotyrosine, a post-translational modification by nitr

45 of NO synthase (iNOS) and elevated levels of nitrotyrosine, a product derived from NO.

46 er 1,25(OH)(2)D(3) altered the expression of nitrotyrosine, a product of NO, or p53 after UVR in huma

47 ulation and it can be tracked by quantifying nitrotyrosine, a stable biomarker of NO-induced reactive

48 H(2)O(2) content and nitrotyrosine abundance also increased in the kidney wit

49 superoxide production and oxidative stress (nitrotyrosine abundance), as well as with increases in m

50 injury as suggested by cell infiltration and nitrotyrosine accumulation in the lung, and a significan

51 ed by increases in 4-hydroxy-2-nonenal and 3-nitrotyrosine adduct formation.

52 bsequent reperfusion in vitro as measured by nitrotyrosine adduct formation.

53 y Fe-TMPyP pretreatment, and mitochondrial 3-nitrotyrosine adduct levels (peroxynitrite marker) were

54 (GSH) levels, and increased production of 3-nitrotyrosine adducts and protein carbonyl formation.

55 tric oxide synthase, a profound induction of nitrotyrosine adducts was observed.

56 formation (nitrite and nitrate levels and 3-nitrotyrosine adducts) increased more profoundly in FPG

57 A nitrotyrosine affinity column (NTAC) was used to prefere

58 dition, rhAPC limited the increase in lung 3-nitrotyrosine (after 24 hrs [%]: sham, 7 +/- 2; control,

59 staining for the protein nitration product 3-nitrotyrosine (all P<.001).

60 marker of endothelial function, and plasma 3-nitrotyrosine and 24-h urinary excretion rates of free 8

61 Levels of nitrotyrosine and 4-hydroxynonenal increased in Ins2(Aki

62 peptide and the oxidative stress markers 3'-nitrotyrosine and 4-hydroxynonenal.

63 ynthase levels determined by Western blot, 3-nitrotyrosine and 4-hydrpxnonenal both assayed by ELISA,

64 age was assessed by immunofluorescence for 3-nitrotyrosine and 8-hydroxydeoxyguanosine and lipid pero

65 Plasma nitrotyrosine and ADMA levels were similar in OSA and co

66 were characterized by measuring circulating nitrotyrosine and catalase activity.

67 Expression of both nitrotyrosine and cyclooxygenase-2 was 5-fold greater in

68 superoxide anion and increased expression of nitrotyrosine and gp91phox.

69 Nitrotyrosine and lipid peroxide levels (n = 102, 74 wit

70 Co-localization of nitrotyrosine and Lmo4 was particularly high in outer ha

71 ignificantly increased whereas expression of nitrotyrosine and nuclear factor-kappaB significantly de

72 s production, as evidenced by increases in 3-nitrotyrosine and PGIS nitration.

73 atory cytokine release; and the incidence of nitrotyrosine and poly(ADP)ribose in the colon.

74 al nerve, as well as 4-hydroxynonenal adduct nitrotyrosine and poly(ADP-ribose) accumulation and 12/1

75 activity in the sciatic nerve and increased nitrotyrosine and poly(ADP-ribose) immunofluorescence in

76 tochemical detection of 4-hydroxynonenal and nitrotyrosine and quantitative analysis of malondialdehy

77 ormation of the ion pair associate between 3-nitrotyrosine and the optical sensor binuclear Pt-2-pyra

78 in vivo administration of statin increased 3-nitrotyrosine and the phosphorylation of AMPK and ACC in

79 ease the oxidative productions of protein (3-nitrotyrosine) and lipid (malondialdehyde) and increase

80 , increased inducible nitric oxide synthase, nitrotyrosine, and cyclooxygenase-2 expression, c-Met ac

81 ROS, nitrotyrosine, and gelatinase (MMP-2 and MMP-9) zymogen

82 (P)H oxidase activity, protein expression of nitrotyrosine, and hydrogen peroxide production were inc

83 720 decreased the levels of malondialdehyde, nitrotyrosine, and inducible nitric oxide synthase expre

84 malondialdehyde, 4-hydroxynonenal adducts, 3-nitrotyrosine, and inducible nitric oxide synthase in th

85 ch also expressed high levels of basal VEGF, nitrotyrosine, and membrane-type (MT1) matrix metallopro

86 odified DNA, electron transport complex III, nitrotyrosine, and mitochondrial superoxide dismutase we

87 oxal-derived advanced glycation end product, nitrotyrosine, and nitrite/nitrate accumulation in the p

88 Plasma levels of 3-chlorotyrosine, 3-nitrotyrosine, and o,o'-dityrosine were markedly elevate

89 sine oxidation products (3-chlorotyrosine, 3-nitrotyrosine, and o,o'-dityrosine) were quantified by t

90 n, and vascular endothelial growth factor, 3-nitrotyrosine, and poly(adenosine diphosphate ribose) ex

91 stochemical staining for ICAM-1, P-selectin, nitrotyrosine, and poly(ADP)ribose showed a positive sta

92 tissue vascular endothelial growth factor, 3-nitrotyrosine, and poly(ribose) expression were attenuat

93 BAY 11-7082 or BBG also down-regulated iNOS, nitrotyrosine, and poly-ADP-ribosyl polymerase expressio

94 lso induced increases in lipid peroxidation, nitrotyrosine, and the pro-apoptotic p75(NTR) receptor i

95 s in the liver, such as 4-hydroxynonenal and nitrotyrosine, and was inhibited by the administration o

96 The utility of this assay for nitrotyrosine as a clinically translatable biomarker was

97 tudy, we applied a proteomic approach, using nitrotyrosine as a marker, to evaluate the oxidation of

98 t time, the site-specific incorporation of 3-nitrotyrosine at different regions of alpha-syn using na

99 ee and HDL-bound forms, apoA-I harboring a 3-nitrotyrosine at position 166 apoA-I (NO2-Tyr(166)-apoA-

100 Nitrotyrosine at position 33 or 56 stimulates a toxic ga

101 spectrometry (LC-MS/MS) method to measure 3-nitrotyrosine at very low (picomolar) levels.

102 age products 3-chlorotyrosine (Cl-Tyr) and 3-nitrotyrosine, both of which increased with disease dura

103 reased in HF (-20%) and inversely related to nitrotyrosine-bound ceruloplasmin (r, -0.305; P=0.003).

104 (n=35), serum FeOxI, FeOxII, ceruloplasmin, nitrotyrosine-bound ceruloplasmin, B-type natriuretic pe

105 ein (CRP), and the oxidative damage marker 3-nitrotyrosine (BSA-3NT) on a silicon nitride substrate.

106 ut further increases in p53 or reductions of nitrotyrosine by 1,25(OH)(2)D(3) are unlikely to contrib

107 er Nox2, alpha-SMA, phosphorylated Smad3 and nitrotyrosine by immunoblot analyses.

108 the expression of nuclear factor-kappaB and nitrotyrosine by immunofluorescence in freshly harvested

109 % higher VECPE of NAD(P)H oxidase-p47(phox), nitrotyrosine, catalase, and the cytosolic antioxidant C

110 [CAMs], monocyte chemoattractant protein 1, nitrotyrosine, CD40 ligand [CD40L], and monocyte functio

111 ed postischemic induction of phospho-Drp1, 3-nitrotyrosine, cleaved caspase-3, and LC-3 II/I, indicat

112 At 24 hrs, pulmonary 3-nitrotyrosine concentrations were negatively correlated

113 eric forms of cyt c positively stained for 3-nitrotyrosine confirming the reactivity of NO toward tyr

114 ological fluids when either nitrotyrosine or nitrotyrosine-containing peptides were added exogenously

115 the proteomic characterization of specific 3-nitrotyrosine-containing sequences of nitrated target pr

116 se and neurogenic locus notch homolog, two 3-nitrotyrosine-containing sequences were identified, i.e.

117 ion, as indicated by augmented lung tissue 3-nitrotyrosine content (30 +/- 3 vs. 216 +/- 8 nM; p < .0

118 yeloperoxidase with apoA-I and reduced the 3-nitrotyrosine content of apoA-I.

119 3-Nitrotyrosine content was decreased: 0.04 vs. 0.12 mol%

120 2.9 vs. 1.9 mol% (P < 0.05), respectively; 3-nitrotyrosine content was higher: 0.10 vs. 0.03 mol% (P

121 ratio (r = -.882; p < .001) and myocardial 3-nitrotyrosine content with stroke volume indexes (r = -.

122 contain cysteines or methionines proximal to nitrotyrosines, contrary to suggestions that these amino

123 HCV-induced ROS and nuclear nitrotyrosine could be decreased with small interfering

124 gnificantly increased, whereas expression of nitrotyrosine, cyclooxygenase-2, and inducible NOS signi

125 stological evaluation, immunohistochemistry (nitrotyrosine, cystathionine gamma-lyase, activated casp

126 In PC12 cells, 3-nitrotyrosine decreases intracellular dopamine levels an

127 rk synergistically to form lipid radical and nitrotyrosine early in the skin inflammation caused by L

128 Specific immunoglobulins that recognize 3-nitrotyrosine epitopes were identified in human lesions,

129 els of circulating immunoglobulins against 3-nitrotyrosine epitopes were quantified in patients with

130 ilation was inversely related to arterial EC nitrotyrosine expression (r=-0.62, P=0.01; n=22).

131 EC samples of older men and correlated with nitrotyrosine expression (r=0.51, P<0.05 n=16).

132 MP concentration, proBNP-108 expression, and nitrotyrosine expression, a measure of nitrosative/oxida

133 analysis was performed for PKG activity and nitrotyrosine expression.

134 e stress markers xanthine oxidoreductase and nitrotyrosine, findings that could also be evidenced in

135 tracheal rhSOD decreased the enhanced lung 3-nitrotyrosine fluorescence observed with iNO therapy.

136 rine and KCl, lung isoprostane levels, and 3-nitrotyrosine fluorescent intensity were measured.

137 ctron microscopy demonstrated an increased 3-nitrotyrosine formation (ONOO(-)-specific protein nitrat

138 s of respiratory NADH dehydrogenases prevent nitrotyrosine formation and abrogate the cytotoxicity of

139 Furthermore, hyperoxia decreased cardiac 3-nitrotyrosine formation and increased inducible nitric o

140 ease occurred, as well as significantly more nitrotyrosine formation at all ages studied.

141 highly reactive peroxynitrite, as shown by 3-nitrotyrosine formation in diseased liver.

142 Interestingly, nitrotyrosine formation in LPS-treated skin was also sup

143 3-Nitrotyrosine formation in proteins is considered a hall

144 aconitase activity without affecting protein nitrotyrosine formation in the hearts.

145 gens; therefore, resistance of ALR islets to nitrotyrosine formation may, in part, explain why ALR mi

146 oxide (NO) and utilized nitrite to promote 3-nitrotyrosine formation on IDO.

147 droxy guanosine levels), nitrosative stress (nitrotyrosine formation), and apoptosis of retinal endot

148 tive/nitrative stress (lipid peroxidation, 3-nitrotyrosine formation, and expression of reactive oxyg

149 Ang II promotes a rapid increase in 3-nitrotyrosine formation, and uric acid attenuates Ang II

150 spinal cord including general tissue damage, nitrotyrosine formation, lipid peroxidation, activation

151 s neuronal loss was accompanied by increased nitrotyrosine formation, nitrosylated alpha-synuclein, a

152 requires molecular O2 and coincides with the nitrotyrosine formation, the oxidation of [4Fe-4S] clust

153 Ischemia also increased 3-nitrotyrosine formation, which was significantly reduced

154 by increased striatal protein carbonyl and 3-nitrotyrosine formation.

155 modifications through NO(2) production and 3-nitrotyrosine formation.

156 tochondrial respiratory capacity and lower 3-nitrotyrosine formation.

157 c oxide synthase as well as the formation of nitrotyrosine groups and a subsequent reduction in myeli

158 Similarly, nitrotyrosine immunoblots of whole brain homogenates sho

159 Sciatic nerve nitrotyrosine immunofluorescence and the number of poly(

160 e stained for oxidative damage markers using nitrotyrosine immunohistochemistry.

161 axonal mitochondrial transport and increased nitrotyrosine immunoreactivity in axonal mitochondria, s

162 GSH diminished the nitrotyrosine immunoreactivity of peroxynitrite-treated

163 or 24 h reduced KGDHC activity and increased nitrotyrosine immunoreactivity.

164 duced subunit immunoreactivity and increased nitrotyrosine immunoreactivity.

165 us ONOO- increased proteasome activity and 3-nitrotyrosine in 26S proteasome.

166 The levels of protein-bound nitrotyrosine in atrial tissue increased from 16 +/- 1 t

167 not only free amino acid but also protein 3-nitrotyrosine in biological fluids.

168 line prevented the ADMA-mediated increase in nitrotyrosine in HBECs in cells from asthmatics and cont

169 inally, concentrations of ortho-tyrosine and nitrotyrosine in knockout endothelial cells were markedl

170 d circulating immunoglobulins that recognize nitrotyrosine in LA-apoA-I(-/-) as compared with the LA

171 of PGHS-1 was confirmed by the absence of 3-nitrotyrosine in lesions from ApoE(-/-)iNOS(-/-) mice.

172 ol, significantly increased superoxide and 3-nitrotyrosine in PGI(2) synthase (PGIS).

173 Nitrotyrosine in position 33, but not in any of the othe

174 Detection of 3-nitrotyrosine in the asthmatic lung confirms the presenc

175 and IK1 protein, superoxide (O(2)(-)), and 3-nitrotyrosine in the endothelium of SMAs.

176 oxygen had increased immunopositivity for 3-nitrotyrosine in the hippocampus and increased lipid per

177 s associated with a diminished generation of nitrotyrosine in the plaques.

178 ioning of macrophages induced formation of 3-nitrotyrosine in the PP2Ac associated with VCP/p97, a re

179 PKC)-alpha, PKC-beta, protein oxidation, and nitrotyrosine in the skeletal muscle were significantly

180 xygen species and the peroxynitrite marker 3-nitrotyrosine in wild-type mice but not in nox2 nulls.

181 h is shown by mass spectrometry to recognize nitrotyrosines in the calcium signaling protein calmodul

182 oped recombinant apoA-I with site-specific 3-nitrotyrosine incorporation only at position 166 using a

183 PGHS-2 was also found in lesions, but 3-nitrotyrosine incorporation was not detected.

184 y with the immunohistochemical expression of nitrotyrosine, indicative of nitrative stress, was found

185 3-Nitrotyrosine induced loss of tyrosine hydroxylase-posit

186 chial artery (1.25+/-0.12 versus 0.61+/-0.11 nitrotyrosine intensity/human umbilical vein EC [HUVEC]

187 In NT2 cells, incorporation of 3-nitrotyrosine into alpha-tubulin induces a progressive,

188 In both cell lines, 3-nitrotyrosine is a substrate for tyrosine tubulin ligase

189 he young (adult) heart 1 molar equivalent of nitrotyrosine is distributed over at least five tyrosine

190 Herein, we show that extracellular 3-nitrotyrosine is transported via the l-aromatic amino ac

191 e NADPH oxidase p22phox genotypes and plasma nitrotyrosine level (P = 0.06), as well as between the c

192 Tissue superoxide and nitrotyrosine levels and myeloperoxidase activity change

193 Measurement of nitrotyrosine levels in biological fluids can serve as a

194 in the hind paw, and reduced superoxide and nitrotyrosine levels in epineurial arterioles.

195 We measured SERCA2a levels and nitrotyrosine levels in tissue from normal and failing h

196 onstrated by quantifying both free and total nitrotyrosine levels in various biological fluids, inclu

197 th non-LPS controls; however, frontal cortex nitrotyrosine levels only increased in the BDL + LPS rat

198 in a clinical setting, the quantification of nitrotyrosine levels should provide support for NOS-driv

199 Hippocampal 3-nitrotyrosine levels were determined by immunohistochemi

200 VEGF and nitrotyrosine levels were higher in cerebral microvessel

201 Nitrotyrosine levels were higher in diabetic patients, i

202 Genotype-associated increases in nitrotyrosine levels were observed.

203 e activity and the intestinal superoxide and nitrotyrosine levels were reduced, whereas the plasma ni

204 Xanthine oxidoreductase and nitrotyrosine levels were reduced.

205 lular adhesion molecule (sICAM), sCD40L, and nitrotyrosine levels were significantly elevated in type

206 and, asymmetric dimethylarginine (ADMA), and nitrotyrosine levels, as well as 2 iterations of 60-seco

207 de anion, and plasma CRP, sICAM, sCD40L, and nitrotyrosine levels.

208 ein oxidation markers, including chloro- and nitrotyrosine, linking oxidative modification to the red

209 ng levels of oxidative damage to proteins (3-nitrotyrosine), lipids (8-isoprostane), and nucleic acid

210 interleukin-1beta, protein carbonyl, higher nitrotyrosine, malondialdehyde, and Fas/Fas ligand than

211 speckle tracking; and (4) interleukin-1beta, nitrotyrosine, malondialdehyde, protein carbonyl, and Fa

212 ogenase, protein carbonyl (marker of ROS), 3-nitrotyrosine (marker of RNS), poly(adenosine diphosphat

213 antibodies specific for 4-hydroxynonenal and nitrotyrosine, markers of lipid peroxidation, and reacti

214 to PN and identified the major metabolite, 3-nitrotyrosine-methionine-sulfoxide (NSO)-MENK, using liq

215 roducts (protein carbonyls, lipid aldehydes, nitrotyrosine), mitochondrial function, and cardiac cont

216 That iNOS-derived NO is essential for 3-nitrotyrosine modification of PGHS-1 was confirmed by th

217 tified the active site residue Tyr385 as a 3-nitrotyrosine modification site in purified PGHS-1 expos

218 tently, immunohistochemistry showed enhanced nitrotyrosine modifications in tissues of mice infected

219 Increased abundance of nitrotyrosine modifications of proteins have been docume

220 C-reactive protein, E-selectin, nitrotyrosine, monocyte superoxide, and cytokines were e

221 ponsiveness to the specific peptide, whereas nitrotyrosine-negative CD8(+) T cells responded normally

222 3-Nitrotyrosine (NO(2)Y, pK(a) 7.1) has been incorporated

223 onary parenchymal inflammation, and tissue 3-nitrotyrosine (NO2 Y) were increased to a greater extent

224 omonas aeruginosa azurins that incorporate 3-nitrotyrosine (NO2YOH) between Ru(2,2'-bipyridine)2(imid

225 f NO with O2- were non-toxic, did not form 3-nitrotyrosine, nor did they elicit any signal transducti

226 hyperalgesia was associated with increased 3-nitrotyrosine (NT), a PN biomarker, in the RVM.

227 protein adducts, superoxide dismutase (SOD), nitrotyrosine (NT), and inducible nitric oxide synthase

228 ssion, with peak levels of autoantibodies to nitrotyrosine (NT)-modified enolase, Ro, alpha-actin, an

229 ucible nitric oxide synthase (iNOS), NO, and nitrotyrosine (NT).

230 ydroxynonenal [4-HNE]-modified proteins, and nitrotyrosine [NT]).

231 Nitrotyrosine (NY), Akt and p38 activity, p85 nitration,

232 with myocardial oxidative stress markers 3'-nitrotyrosine or 4-hydroxynonenal expression (P<0.05).

233 recovery from biological fluids when either nitrotyrosine or nitrotyrosine-containing peptides were

234 imately three tyrosine residues converted to nitrotyrosine out of the total four tyrosine residues in

235 < 0.05) and were concomitant with increased nitrotyrosine (P < 0.05) and reduced expression of brown

236 ial and pulmonary tissue concentrations of 3-nitrotyrosine (p = .041 and p = .042 vs. controls, respe

237 e (P<0.0001), monomethylarginine (P=0.0003), nitrotyrosine (P<0.0001), and bromotyrosine (P<0.0001) a

238 Salsalate reduced nitrotyrosine (P=0.06) and expression of NADPH oxidase p

239 group displayed higher protein carbonyls, 3-nitrotyrosine, PAR, lactate dehydrogenase and proteins i

240 unaltered and nitric oxide metabolites and 3-nitrotyrosine peptide levels remained unchanged in Cu- c

241 Intracellular levels of 133 micromol of 3-nitrotyrosine per mole of tyrosine did not alter NT2 via

242 Postincubation with MDSCs, only nitrotyrosine-positive CD8(+) T cells demonstrated profo

243 nificantly increased superoxide anions and 3-nitrotyrosine-positive proteins, exogenous peroxynitrite

244 osine, 4-hydroxynonenal protein adducts, and nitrotyrosine, primarily in the LP epithelium, suggestin

245 vating reactive oxygen species, increasing 3-nitrotyrosine production by microglia, and reducing the

246 y involves spectrophotometric detection of 3-nitrotyrosine production from 3-nitrophosphotyrosine con

247 ar effect as NBO treatment on NO(x)(-) and 3-nitrotyrosine production, and when combined with NBO, no

248 logic role of iNOS was assessed by detecting nitrotyrosine products and apoptosis.

249 nducible nitric oxide synthase, and higher 3-nitrotyrosine protein adducts were found in livers of ac

250 Abundance of nitrotyrosine (quantitative immunofluorescence), an oxid

251 fat was positively associated with VECPE of nitrotyrosine (r(part) = 0.36, P = 0.003), a marker of p

252 ity and specificity, this assay showed great nitrotyrosine recovery from biological fluids when eithe

253 In contrast, reduction of nitrotyrosine remained in keratinocytes treated with 1,2

254 rage significantly induced oxidative stress (nitrotyrosine), renal tubular damage, and cell death.

255 d 2alpha, heat shock protein 70, presence of nitrotyrosine residues, and lipid peroxidation.

256 tric oxide detection, and immunoblotting for nitrotyrosine, respectively.

257 eshly isolated renal tubules produced strong nitrotyrosine signals but failed to alter membrane funct

258 resulted in the identification of 31 unique nitrotyrosine sites within 29 different proteins.

259 obed for tyrosine nitration using monoclonal nitrotyrosine-specific Abs in a murine model of LPS-indu

260 a critical step toward the production of a 3-nitrotyrosine-specific protease useful for proteomic app

261 d aortic macrophage recruitment and vascular nitrotyrosine staining (which reflects local oxidative s

262 ncy promoted aortic thickening with enhanced nitrotyrosine staining and an increase in cardiac HSP70

263 (4) 3-o-Nitrotyrosine staining and dihydroethidium oxidation in

264 enhanced responsiveness to phenylephrine and nitrotyrosine staining and reduced sensitivity to endoth

265 There was enhanced nitrotyrosine staining in infected Arg2(-/-) versus WT m

266 was confirmed with positive 8-oxoguanine and nitrotyrosine staining in peripheral leukocytes.

267 ellular capillaries increased threefold, and nitrotyrosine staining increased 1.5-fold, in the retina

268 Arterial nitrotyrosine staining indicated that increased levels o

269 The 3-nitrotyrosine staining intensity was not different.

270 luorescence increased in injured MNs, as did nitrotyrosine staining of MNs.

271 aled increases in nonnuclear p53 expression, nitrotyrosine staining, and apoptosis in aortic EC locat

272 yocardial oxidative stress, as assessed by 3-nitrotyrosine staining, reduced expression of the adhesi

273 ration was not detected in PWMI lesions by 3-nitrotyrosine staining.

274 ric oxide synthase expression, and increased nitrotyrosine staining.

275 Levels of 3-nitrotyrosine strongly correlated with levels of 3-chlor

276 The denitrase activity converts nitrotyrosines to their native tyrosine structure withou

277 epidermal peroxynitrite (ONOO(-)) levels via nitrotyrosine together with high nitrated p53 levels.

278 d significant increases in oxidative stress (nitrotyrosine, urinary 8-hydroxy-2-deoxy-guanosine) and

279 significant increase in C-reactive protein, nitrotyrosine, vascular cell adhesion molecule and monoc

280 ting immunoglobulins against protein-bound 3-nitrotyrosine was documented in patients with CAD (3.75+

281 Nitrotyrosine was generated in NOD and C3H/HeJ islets bu

282 n and content of the oxidative stress marker nitrotyrosine was higher in MCAs from Eln(+/-) compared

283 However, immunohistochemistry showed that nitrotyrosine was increased in the tumor relative to non

284 Serum nitrotyrosine was measured by ELISA, lipid peroxide by s

285 uction in oxidative stress markers including nitrotyrosine was seen in the injured GPxTg group relati

286 e significantly lower, whereas expression of nitrotyrosine was significantly greater in OSA patients

287 f inducible nitric oxide synthase (iNOS) and nitrotyrosine were also upregulated in the infracted sid

288 Glial activation and nitrotyrosine were assessed by immunohistochemistry.

289 M lipid peroxidation, protein carbonyls, and nitrotyrosine were attenuated by CR, levels of PMRS enzy

290 tric oxide synthase (iNOS), gp91-phox, and 3-nitrotyrosine were detected in ischemic wounds, indicati

291 Lipid peroxidation and nitrotyrosine were determined using MDA assay, immunoflu

292 ugh higher levels of the inflammatory marker nitrotyrosine were found in Gstp(-/-)/Tg.AC mice.

293 matory markers chemokine CCL2, NF-kappaB and nitrotyrosine were localized in the perivascular areas o

294 NO(x)(-) (nitrite plus nitrate) and 3-nitrotyrosine were measured in the ischemic cortex.

295 ucible NOS) and markers of oxidative stress (nitrotyrosine) were quantified by immunofluorescence in

296 -mediated damage, including 8-oxoguanine and nitrotyrosine, were present both in the distal colon and

297 Intrastriatal injection of 3-nitrotyrosine, which is a biomarker for nitrating oxidan

298 the peroxynitrite to avoid the formation of nitrotyrosine, which is formed from the reaction between

299 that selectively hydrolyzes peptides after 3-nitrotyrosine while effectively discriminating against s

300 Indeed, increasing levels of nitrotyrosine within MCC tumors were associated with low