ライフサイエンスコーパス: isoprostane

1 (8-hydroxy-2'-deoxyguanosine [8-OHdG] and F2-isoprostane).

2 adiponectin, low-density lipoprotein, and 8-isoprostane.

3 ot only CHGB secretion but also excretion of isoprostane.

4 rkers 8-hydroxydeoxyguanosine (8-OHdG) and 8-isoprostane.

5 n significantly correlated with changes in 8-isoprostane.

6 cluding 8-hydroxydeoxyguanosine (OHdG) and 8-isoprostane.

7 , total and phosphorylated tau proteins, and isoprostanes.

8 ange was detected in urinary excretion of F2-isoprostanes.

9 antly lower plasma oxidative stress and F(2)-isoprostanes.

10 te to eight enantiomerically enriched 5-F(2)-isoprostanes.

11 rolases have high affinity for esterified F2-isoprostanes.

12 poglycemia (91.7 ng/mL) was seen for urinary isoprostanes.

13 infusion), showing higher increase in 8alpha-isoprostanes.

14 has investigated whether levels of 15-F(2t)-isoprostane (15-F(2t)-IsoP) and its metabolite 2,3-dinor

15 ne metabolite 2,3-dinor-5,6-dihydro-15-F(2t)-isoprostane (15-F(2t)-IsoP-M) compared with F(2)-isopros

16 , and urinary oxidative stress marker 15-F2t-isoprostane (15-F2t-IsoP), were evaluated using linear r

17 rations of the lipid peroxidation product F2-isoprostanes (18.5 pg/mL, interquartile range 9-22.2) co

18 us +5%), and the lipid peroxidation marker 8-isoprostane (-21% versus +1.3%) in treatment versus sham

19 ess), and augmented urinary excretion of the isoprostane 8,12-iso-iPF(2alpha)-VI (which reflects lipi

20 ies, A- and J-series prostaglandins, and the isoprostane 8-iso-prostaglandin A(2)-evoked calcium infl

21 nterested especially in the potential of the isoprostane 8-iso-prostaglandin F (8-iso-PGF2alpha), amo

22 We measured urinary excretion of the isoprostane 8-iso-prostaglandin F(2alpha), which is an i

23 tive stress in the form of increased serum 8-isoprostane (8-IP) levels, and airway inflammation in th

24 a (IL-1beta), prostaglandin E(2) (PGE(2)), 8-isoprostane (8-iso), and IL-6, and serum levels of IL-6,

25 Plasma concentrations of F(2)-isoprostane (8-iso-PGF2alpha), 9-hydroxyoctadecadieneoic

26 ylipid product 8-isoprostaglandin F(2) alpha-isoprostane (8-IsoP) were increased by OPN treatment, an

27 At baseline and 16 weeks, urinary isoprostanes (8, 12-iso-iPF(2 alpha)-VI isoform), plasma

28 eneration of both thromboxane (Tx)A2 and the isoprostane, 8, 12 -iso iPF(2alpha)-VI, are increased in

29 o plasma levels of F(2)-8alpha isoprostanes (isoprostane), 9-hydroperoxy-10,12-octadecadienoic acid (

30 terval =0.59, 30.1), and a 48% increase in 8-isoprostane (95% confidence interval =16.7, 87.0).

31 Carratelli units; P < 0.05) and plasma F(2)-isoprostanes (97.7 +/- 8.3 compared with 136.3 +/- 11.3

32 rpose of this study is to understand whether isoprostane, a biomarker of oxidative stress, is subject

33 sure results in increased generation of A(2)-isoprostane, a cyclopentenone isoprostane that blunts in

34 In addition, the cellular level of F(2)-isoprostanes, a direct indicator of oxidative stress, wa

35 tioxidants, antioxidant enzymes, and urinary isoprostanes, a marker of oxidative stress, were measure

36 Old CR-high mice developed high levels of 8-isoprostanes, AGEs, RAGE, and p66(shc), coupled with low

37 Associations between urinary isoprostanes, alphaSMA levels, and retinoids were assess

38 Phthalate metabolites and 8-isoprostane, an oxidative stress biomarker, were measure

39 8-isoprostane, an oxidized lipid created by oxidative stre

40 F(2)-isoprostanes, an arachidinate metabolite/lipid peroxidat

41 d-liquid extraction (LLE) procedure for F(2)-isoprostane analysis to use a combination of solid phase

42 Increases in urinary isoprostane and 8-hydroxydeoxyguanosine, parameters of o

43 ant associations between either 8-OHdG or F2-isoprostane and blood pressure over time.

44 ated genetic covariance (pleiotropy) for the isoprostane and CHGB traits (rho(G) = 0.27), and therefo

45 Because the isoprostane and Chromogranin B (CHGB) traits shared rho(

46 Plasma levels of 8-isoprostane and CRP were significantly elevated in acute

47 Increased urinary excretion of isoprostane and decreased antioxidant production is an i

48 Moreover, the H67D brain had increased isoprostane and decreased glutathione, indicating elevat

49 A newly established route to 15-F(2t)-isoprostane and ent-15-epi-F(2t)-isoprostane has allowed

50 tion also led to significant decreases in F2-isoprostane and IL-6 concentrations.

51 white blood cell count), oxidative stress (8-isoprostane and total carbonyl content), and endothelial

52 f inflammatory cytokines and chemokines, F2 -isoprostanes and isofuranes, markers of oxidative stress

53 biomarkers of systemic inflammation, and F2 isoprostanes and isofurans were measured as biomarkers o

54 F(2)-isoprostanes and malondialdehyde were lower in the GSTM1

55 tions of the lipid peroxidation biomarkers 8-isoprostanes and malondialdehyde.

56 VAT was more highly associated with urinary isoprostanes and monocyte chemoattractant protein-1 (SAT

57 cant total oxidative stress measured by F(2)-isoprostanes and neuronal stress evaluated by F(4)-neuro

58 y accentuated the effect of dialysis on F(2)-isoprostanes and P-selectin.

59 erbated neutrophil influx, accumulation of 8-isoprostanes and protein carbonyls, and increased expres

60 ificant and progressive reduction of urinary isoprostanes and serum Nox2, along with inhibition of pl

61 , left atrial diameter and levels of urinary isoprostanes and serum sNOX2-dp and hs-CRP were signific

62 Urinary isoprostanes and serum sNOX2-dp levels were inversely co

63 We report a potential synthetic route to the isoprostanes and the neuroprostanes that could allow rea

64 biting platelet Nox2 and ultimately platelet isoprostanes and thromboxane A(2).

65 ne/oxidized glutathione and reduced plasma 8-isoprostanes and tissue RAGE and p66(shc) levels compare

66 d state (including nitric oxide metabolites, isoprostanes) and autoantibodies to oxidized low-density

67 ntrations of biomarkers of oxidative stress (isoprostanes) and inflammation (prostaglandins and throm

68 age to proteins (3-nitrotyrosine), lipids (8-isoprostane), and nucleic acid (8-oxoguanine).

69 thrombin complex); "oxidative stress" (urine isoprostane); and "tissue hypoxia" (lactate) at 0, 6, 24

70 Cysteine, cystine (CySS), glutathione, isoprostane, and isofuran were measured, and participant

71 were assessed in relation to airway IL-13, 8-isoprostane, and malondialdehyde concentrations.

72 stress, 8-OH deoxyguanosine (8-OHdG) and F2-isoprostane, and measures of renal function and blood pr

73 Higher platelet recruitment, platelet isoprostane, and NOX2 activation was found in diabetic v

74 vels to 16 oral organisms, serum levels of 8-isoprostane, and periodontal status.

75 oxidative stress assessed by total plasma F2-isoprostanes, and 3) inflammation assessed by plasma pen

76 tress, as assessed by serum Nox2 and urinary isoprostanes, and platelet activation, as assessed by pl

77 loperoxidase, oxidized LDL, lipoprotein (a), isoprostanes, and small, dense LDL.

78 hormone, sex hormone-binding globulin, F(2)-isoprostanes, and thiobarbituric acid-reactive substance

79 inhibition of platelet recruitment, platelet isoprostanes, and thromboxane A(2), and increased vasodi

80 s assessed by platelet recruitment, platelet isoprostanes, and thromboxane A(2), platelet Nox2, Rac1,

81 ity, glucose uptake, plasma concentration of isoprostanes, and total antioxidant capacity were unaffe

82 toxicity-associated parameters, i.e., Hsp70, isoprostanes, and total nitrates from HIV-1-infected cel

83 Serum 8-isoprostane, another marker of oxidative stress, showed

84 F2-isoprostanes are a prototype wastewater biomarker to stu

85 The F(2)-isoprostanes are products of free-radical-induced oxidat

86 If F(2)-isoprostanes are specific markers of oxidative stress, t

87 F(2)-isoprostanes are stereo- and regioisomers of prostagland

88 F(2)-isoprostanes are useful biomarkers of oxidative status i

89 ng a gas chromatography/mass spectrometry F2-isoprostane assay and compared these results with a matc

90 For 8-isoprostane, associations with nearly all phthalates wer

91 .10 [95% CI: 0.06, 0.13], p < 0.001), and F2-isoprostane (beta = 0.13 [95% CI: 0.01, 0.25], p = 0.04)

92 oprostanes, the precursors of J(2)- and A(2)-isoprostanes, both at base line and following ozone expo

93 ndidate pathway) effects indicated that F(2)-isoprostanes, but not IL-6 or PAI-1, partially mediate t

94 We evaluated plasma levels of 8-isoprostane, C-reactive protein (CRP) and total matrix m

95 measures (PWV changed by +9.5% and +6.0%, F2-isoprostanes changed by -3.0% and -9.7%, and pentraxin-3

96 animals have a higher capacity to release F2-isoprostanes compared with nontransgenic littermates.

97 Women with an 8-isoprostane concentration >or=75th percentile at enrollm

98 ress early in pregnancy, as measured by an 8-isoprostane concentration >or=75th percentile, were at a

99 lop preeclampsia compared to women with an 8-isoprostane concentration <75th percentile (38.2% versus

100 te/severe periodontal disease, an elevated 8-isoprostane concentration (>or=75th percentile) did not

101 ecies generation, measured by plasma F2alpha isoprostane concentration (systemic) and dihydroethidium

102 enetic and CSF measures, only greater CSF F2-isoprostane concentration was significantly associated w

103 amin D was inversely associated with urinary isoprostane concentration, an indicator of oxidative str

104 ed by periodontal disease and the level of 8-isoprostane concentration.

105 ntervention, fasting and postmeal TRLs and 8-isoprostane concentrations in 24-h urine samples were me

106 Maternal blood was assayed for 8-isoprostane concentrations using an enzyme-linked immuno

107 In addition, F2-isoprostane concentrations were associated with increase

108 or marine LCn3s on plasma TRLs and urinary 8-isoprostane concentrations, a biomarker of oxidative str

109 in absolute fat mass, body weight, plasma F2-isoprostane concentrations, and peak oxygen uptake (VO2

110 oncentrations of KIM-1, NGAL, 8-OHdG, and F2-isoprostane controlling for sex, age, race/ethnicity, gl

111 PB-mediated increases in liver and plasma F2-isoprostanes could be ablated by 1-aminobenztriazole, im

112 igands for the TxA(2) receptor (TP), such as isoprostanes, could still induce a proatherogenic vascul

113 Furthermore, we determined that A(2)-isoprostane covalently modified the active Cys(179) doma

114 um and 3-nitrotyrosin staining and urinary 8-isoprostane/creatinine assay.

115 The concentrations of urinary 8-isoprostane decreased significantly with the polyphenol-

116 implicating the PB-induced P450(s) in the F2-isoprostane elevation.

117 Isoprostane excretion also aggregated with systemic hype

118 sia was increased 5-fold with higher urinary isoprostane excretion and decreased 3-fold with higher t

119 Isoprostane excretion is substantially heritable and sha

120 rostane marks oxidative stress, and elevated isoprostane excretion might be involved in cardiovascula

121 Isoprostane excretion was inversely correlated with tota

122 Urinary isoprostane excretion was substantially heritable (h(2)

123 nificant trends for an association of higher isoprostane excretion with increased consumption of ener

124 +84A) associated with plasma CHGB as well as isoprostane excretion.

125 Plasma 8-isoprostane F(2)alpha and insulin concentrations did not

126 ls of lipid peroxidation product (total 8,12-isoprostane F(2alpha)-VI), despite marked elevations in

127 Here we describe F(2)-isoprostane (F(2)-IsoP) and F(4)-neuroprostane (F(4)-NP)

128 Urinary isoprostanes (F(2)-IsoPs and 15-F(2t)-IsoP-M) were measu

129 rostane (15-F(2t)-IsoP-M) compared with F(2)-isoprostanes (F(2)-IsoPs) as an oxidative stress biomark

130 Measurement of F(2)-isoprostanes (F(2)-IsoPs) has been independently verifie

131 However, when F(2)-isoprostanes (F(2)-IsoPs) were measured in tissues and u

132 MeHg caused a significant increase in F(2)-isoprostanes (F(2)-IsoPs), lipid peroxidation biomarkers

133 ative stress (plasma malondialdehyde, 22%; 8-isoprostane-F(2alpha), 12%; P < 0.0005) and lower inflam

134 assessed using cerebrospinal fluid (CSF) F2-isoprostane (F2-IsoP) concentrations correlated with age

135 The F2-isoprostanes (F2-IsoP) are a series of prostaglandin (PG

136 To assess oxidative stress, we monitored F2-Isoprostanes (F2-IsoPs) and protein carbonyls (PC), prod

137 oxidation of arachidonic acid, termed the F2-isoprostanes (F2-IsoPs), provides an accurate assessment

138 s from these cells enhanced the release of 8-isoprostane-F2-alpha in the conditioned medium six- to s

139 ll-characterized oxidative stress markers, 8-isoprostane-F2-alpha, total nitrates as an indicator for

140 Urinary excretion of 8-isoprostane F2alpha (8-iso-PGF2alpha) was used as an ind

141 Plasma 8-isoprostane F2alpha analysis revealed opposing effects o

142 These data show differential postprandial 8-isoprostane F2alpha responses to high-fat meals containi

143 ce diet, the geometric mean (+/-SD) plasma 8-isoprostane F2alpha-III concentration was 176 +/- 85 pmo

144 moral pulse wave velocity (PWV) and plasma 8-isoprostane F2alpha-III concentrations.

145 Isoprostane F2alpha-VI, a specific marker of oxidative s

146 Urinary Clara Cell 16 (CC16) and 15-isoprostane F2t (8-iso-PGF2alpha) levels were used to as

147 m as a hydration biomarker and to measure 15-isoprostane F2t (F2-Iso) and 8-hydroxydeoxyguanosine (8-

148 circulating oxidative stress biomarkers (F2-isoprostanes, F3-isoprostanes, isofurans) in plasma coll

149 rostaglandin D2, cysteinyl leukotrienes, and isoprostanes following the challenge.

150 scle biopsy for gene expression, and urinary isoprostanes for global oxidative stress.

151 asurement, and proteomic markers and urinary isoprostanes for oxidative measures, together with endot

152 ) altered prostacyclin (PGI(2)) and enhanced isoprostane formation.

153 variation results in oxidative stress, with isoprostane formation.

154 ent in PAF acetylhydrolase do not release F2-isoprostanes from esterified precursors.

155 to 15-F(2t)-isoprostane and ent-15-epi-F(2t)-isoprostane has allowed for the selective preparation of

156 Isomers of prostaglandin F(2alpha), the F(2)-isoprostanes, have emerged as sensitive indices of lipid

157 However, the rate of esterified F2-isoprostane hydrolysis is much slower compared with the

158 termined whether the TXAR was activated by 8-isoprostane in SSc endothelial cells (ECs) and whether t

159 pha, or C-reactive protein in plasma or of 8-isoprostane in urine.

160 in isolated mouse heart mitochondria and F2-isoprostanes in brains and hearts of mice.

161 panying elevations in MDA in liver, and F(2)-isoprostanes in cortex.

162 levels of amyloid beta, tau protein, and F2-isoprostanes in elderly individuals with major depressiv

163 fluorescence in rat muscles and urinary F(2)-isoprostanes in humans, demonstrating oxidative stress.

164 en endogenous reproductive hormones and F(2)-isoprostanes in the BioCycle Study.

165 o ozone by regulating the generation of A(2)-isoprostanes in the lung.

166 yclopentenone-containing molecules termed J3-isoprostanes in vitro and in vivo and were shown to indu

167 g oxidative injury, as measured by plasma F2-isoprostanes, in adult patients with severe sepsis and d

168 To determine whether isoprostanes increase Abeta production, we delivered iso

169 actor (PAF), prostaglandin E2 (PGE2), and F2-isoprostane increased 2.5, 5.2, and 36 times, respective

170 he percent of the total effect mediated by 8-isoprostane increased from 47% to 60% with inclusion of

171 whereas addition of vitamin E, by reducing 8-isoprostane, increased tube formation.

172 the TXAR pathway results in a blockade of 8-isoprostane-induced ROCK activation and restoration of V

173 ROCK activity and 8-isoprostane-induced ROCK activation were significantly h

174 e), lipid peroxidation (4-hydroxy-2-nonenal, isoprostane), inflammation (interleukin-6) and iron stat

175 c surgery and whether oxidative stress (F(2)-isoprostanes), inflammation (IL-6), or antifibrinolysis

176 l human bronchial epithelial cells that A(2)-isoprostane inhibited ozone-induced NF-kappaB activation

177 establishing the biochemical basis for A(2)-isoprostane inhibition of NF-kappaB.

178 anes increase Abeta production, we delivered isoprostane iPF(2alpha)-III into the brains of Tg2576 mi

179 12/15LO-/-/ApoE-/- mice, the amount of brain isoprostane iPF2alpha-VI, a marker of lipid peroxidation

180 Isoprostanes (iPs) are prostaglandin (PG) isomers genera

181 ed neuroprostanes and are more abundant than isoprostanes (iPs) in brain.

182 as a crucial role in angiogenesis and that 8-isoprostane is not just a by-product of oxidative stress

183 ective approach for the synthesis of all-syn isoprostanes is reported.

184 ative stress biomarkers (F2-isoprostanes, F3-isoprostanes, isofurans) in plasma collected before, dur

185 ne (Cys), cystine (CySS), glutathione (GSH), isoprostane (IsoP), and isofuran (IsoF) were determined.

186 in relation to plasma levels of F(2)-8alpha isoprostanes (isoprostane), 9-hydroperoxy-10,12-octadeca

187 Structurally similar compounds, the isoprostanes (IsoPs), are generated from the free radica

188 staglandin (PG) F2-like compounds, termed F2-isoprostanes (IsoPs), are produced in vivo and in vitro

189 landin J(2)-like compounds, termed A(2)/J(2)-isoprostanes (IsoPs), are produced in vivo by the free r

190 y prostaglandin F2-like compounds, termed F2-isoprostanes (IsoPs), are produced in vivo by the free r

191 Cyclopentenone isoprostanes (IsoPs), highly reactive structural isomers

192 dation markers, malondialdehyde (MDA) and F2-isoprostanes (IsoPs).

193 alpha, vascular cell adhesion molecule-1, 8-isoprostane, leptin, circulating AGEs and receptor for A

194 P = 0.9), HOMA (3.2 vs. 3.2; P = 0.6), or F2-isoprostane levels (1,332 vs. 1,190 pmmol/L; P = 0.6) be

195 ated rats had increased plasma and urinary 8-isoprostane levels (a marker of oxidative stress) and in

196 Increased urinary and plasma F2-isoprostane levels are associated with a number of human

197 F2-isoprostane levels before asthma onset were not differen

198 ges in 25-(OH)-vitamin D, PTH, FGF-23, of F2-isoprostane levels between efavirenz and PI use or betwe

199 s in serum protein, GPx, aconitase, TAS, and isoprostane levels compared with control subjects.

200 Isoprostane levels decreased 6.80% (95% confidence inter

201 F(2)-Isoprostane levels had an independent positive associati

202 e was a significant reduction in plasma F(2)-isoprostane levels immediately after PPCI (2878+/-1461 v

203 was an age-dependent increase in the cardiac isoprostane levels in Hfe-deficient mice, indicating ele

204 8-Isoprostane levels in sputum supernatants were inversely

205 Overall mean (+/- SE) brain tissue F2-isoprostane levels increased significantly to 370 +/- 60

206 ted with urinary KIM-1, NGAL, 8-OHdG, and F2-isoprostane levels over time.

207 F2-isoprostane levels peaked on day 1 after injury and were

208 Although F2-isoprostane levels were approximately three-fold lower i

209 dant reserve, glutathione, protein-thiol, F2-isoprostane levels were assessed by bivariate and multip

210 Liver F(2) -isoprostane levels were elevated, and copper/zinc and ma

211 In contrast, isoprostane levels were higher in the major depression g

212 et serum and tissue AGEs as well as plasma 8-isoprostane levels were lower in AGER1-tg mice than in w

213 hrine- and KCl-induced contractions and lung isoprostane levels were significantly increased by 100%

214 ated the inverse association of high serum 8-isoprostane levels, a marker for oxidative stress, with

215 neration PAs to norepinephrine and KCl, lung isoprostane levels, and 3-nitrotyrosine fluorescent inte

216 Platelet recruitment, isoprostane levels, and NOX2 activation showed a paralle

217 Valsartan increased F(2)-isoprostane levels, and ramipril suggested a similar tre

218 ratios, alpha myosin heavy chain and cardiac isoprostane levels, suggesting that iron overload promot

219 ree-fold increases in venous and arterial F2-isoprostane levels, which peaked between 15 and 30 mins

220 superoxide dismutase (SOD) activity and F(2)-isoprostane levels.

221 Oxidative stress was assessed by plasma F(2)-isoprostane levels.

222 e increased PA contraction response and lung isoprostane levels.

223 n or irbesartan plus lipoic acid decreased 8-isoprostane levels.

224 c lipid peroxidation determined by plasma F2-isoprostane levels.

225 I was supported by similar increases in F(2)-isoprostanes levels in the cerebral cortex from term inf

226 Urinary isoprostanes levels were inversely correlated with serum

227 ased serum LZ levels and decreased AGE and 8-isoprostanes levels, although hyperlipidemia remained si

228 thma and was associated with higher airway 8-isoprostane, malondialdehyde, and IL-13 concentrations.

229 F(2)-isoprostanes, malondialdehyde, C-reactive protein, serum

230 tive stress (LDL oxidizability, urinary F(2)-isoprostanes, malondialdehyde, or protein carbonyls in n

231 kines linked to asthmatic inflammation, F(2)-isoprostanes (markers of oxidative stress), and IgE were

232 Isoprostanes, markers of in vivo oxidative stress, are e

233 Isoprostane marks oxidative stress, and elevated isopros

234 dition to being markers of oxidative stress, isoprostanes may have pathogenic functions.

235 This study shows that F2-isoprostane measurement could be used to assess oxidant

236 omarkers of Alzheimer disease) as well as F2-isoprostanes (measures of free radical injury).

237 is limited literature on the contributors to isoprostane metabolite 2,3-dinor-5,6-dihydro-15-F(2t)-is

238 Weight, blood pressure, glucose, F(2)-isoprostanes, NOX2 (NADPH oxidase 2), and PKC (protein k

239 ession (Kv1.5) and current (I(Kur)) and F(2)-isoprostanes, NOX2, and PKC-alpha/delta expression and a

240 inhibition of platelet recruitment, platelet isoprostanes, Nox2, Rac1, p47(phox), and protein kinase

241 F2-Isoprostanes on study day 3, the primary outcome, did no

242 significant effect on plasma hsCRP, IL-6, F2 isoprostane, or isofuran concentrations and did not impr

243 patients, oxidative stress-mediated platelet isoprostane overproduction is associated with enhanced p

244 tes/nitrites (nitric oxide production) and 8-isoprostane (oxidative stress).

245 2)-isoprostane (P=0.04), intraoperative F(2)-isoprostane (P=0.003), and intraoperative PAI-1 (P=0.04)

246 Baseline F(2)-isoprostane (P=0.04), intraoperative F(2)-isoprostane (P

247 mentation significantly reduced urinary F(2)-isoprostanes (P < 0.001) and monocyte superoxide anion a

248 tent (P < 0.05) and 30% reduction in urinary isoprostanes (P = 0.01) were also observed.

249 n; P=0.006 for men), interleukin-6 (P=0.01), isoprostanes (P=0.0002), and monocyte chemoattractant pr

250 d a specific, highly reactive product of the isoprostane pathway of lipid peroxidation, E2-isoketal,

251 Baseline urinary F2-isoprostanes, plasma concentrations of antioxidant micro

252 Isoprostanes, produced in vivo by non-enzymatic free-rad

253 llular peroxidation and in the levels of the isoprostane product, 8-epi-PGF(2alpha).

254 high mt CYP2E1 showed higher levels of F(2)-isoprostane production.

255 d iron, markers of lipid peroxidation-8alpha-isoprostanes, protein oxidation-advanced oxidized protei

256 Only within the highest 8-isoprostane quartile was periodontitis (pocket depth) as

257 actant protein-1 (SAT versus VAT comparison: isoprostanes, R2 0.07 versus 0.10, P=0.002; monocyte che

258 prostaglandins, leukotrienes, thromboxanes, isoprostanes, resolvins, hydroxides, hydroperoxides, com

259 sed by measurements of protein thiols and F2-isoprostane, respectively, in ventricular cerebrospinal

260 Urinary F2-isoprostanes, secondary end products of lipid peroxidati

261 Urinary isoprostanes, serum and tissue retinoid concentrations w

262 Both baseline and allergen-induced F(2)-isoprostanes significantly decreased, providing biochemi

263 ntercellular adhesion molecule 1 (sICAM1), 8-isoprostane, soluble glycoprotein 130 (sGP130), IL-6 sol

264 F(2)-isoprostanes, specific markers of oxidant stress, and se

265 logical effects have been attributed to this isoprostane, suggesting that it could be an active facto

266 AKI after adjustment for the effect of F(2)-isoprostanes, suggesting that obesity may affect AKI via

267 ercury were not associated with increases in isoprostane, TBARS, 9-HODE, or 13-HODE levels.

268 ration of A(2)-isoprostane, a cyclopentenone isoprostane that blunts inflammation.

269 greater lung tissue levels of D(2)- and E(2)-isoprostanes, the precursors of J(2)- and A(2)-isoprosta

270 y used to attach the appropriately protected isoprostanes to the corresponding lysophospholipids.

271 ly heritable (h(2) = 65.8 +/- 4.3%), and the isoprostane trait aggregated with multiple traits (CHGB,

272 probe the role of heredity in generating the isoprostane trait.

273 at a specific candidate locus contributes to isoprostane variability.

274 Elevated 8-isoprostane was observed in plasma and conditioned media

275 8alpha-isoprostanes was also higher in patients at baseline (8.

276 Urinary excretion of isoprostanes was not significantly different between cas

277 A library of eight 5-F(2)-isoprostanes was prepared through a ring-opening metathe

278 In E-LES, levels of PAF, PGE2, and F2-isoprostane were 4, 6, and 40 times, respectively, highe

279 exposure, and 8-hydroxydeoxyguanosine and 8-isoprostane were also measured in urine as markers of ox

280 In contrast, levels of F(2)-isoprostane were comparable in both groups.

281 levels of 8-hydroxy-2'-deoxyguanosine and 8-isoprostane were examined in the context of measures of

282 , high-sensitivity C-reactive protein, and 8-isoprostane were measured.

283 roinflammatory cytokine messenger RNA, and 8-isoprostane were measured.

284 nterleukin-6, plasminogen activator-1, and 8-isoprostane were measured.

285 of plasma 8-hydroxy-2'-deoxyguanosine and 8-isoprostane were significantly higher in subjects with i

286 protein-associated carbonyl content, and F2-isoprostanes were assessed at 1 week pretransplantation

287 tric oxide products, hydrogen peroxide and 8-isoprostanes were generally elevated and related to lowe

288 ormance, LDL oxidizability, and urinary F(2)-isoprostanes were measured at the end of each dietary ph

289 ols, ascorbic acid, uric acid, and F(2alpha)-isoprostanes were measured in blood samples collected on

290 d adhesion to endothelium), and urinary F(2)-isoprostanes were measured.

291 However, among overweight women, levels of isoprostanes were positively associated with breast canc

292 However, F2-isoprostanes were significantly reduced on study day 2 i

293 id not change significantly, and plasma F(2)-isoprostanes were unaffected by dietary period.

294 ress markers plasma protein carbonyls and F2-isoprostanes, were significantly elevated in ESRD patien

295 ces production of bioactive lipids (TXA2 and isoprostanes) which act through the thromboxane receptor

296 an increased production of PAF, PGE2, and F2-isoprostane, which are responsible for reducing LES tone

297 r in T2DM patients aspirin enhances platelet isoprostanes, which are eicosanoids with proaggregating

298 Plasma F2-isoprostanes, which are formed in concert with isoketals

299 erved for MBP and MiBP (49-50% increase in 8-isoprostane with an interquartile range increase in meta

300 alate metabolites and all preterm birth by 8-isoprostane, with the greatest estimated proportion medi