ライフサイエンスコーパス: F2-isoprostane

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

2 xB2), and 8-epi-PGF2 alpha, but not of other F2-isoprostanes.

3 change was detected in urinary excretion of F2-isoprostanes.

4 hydrolases have high affinity for esterified F2-isoprostanes.

5 ction by generating vasoconstrictive E2- and F2-isoprostanes.

6 ted increase in total (free plus esterified) F2-isoprostanes.

7 y, the hcb-FP could also be activated by the F2 isoprostane, 12-iso-PGF2alpha, in addition to its cog

8 specifically, by the free radical-catalyzed F2 isoprostane, 12-iso-PGF2alpha, in addition to the cyc

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

10 rometry assays for two structurally distinct F2 isoprostanes, 8-epi-PGF2alpha and IPF2alpha-I.

11 Four additional F2 isoprostanes, 8-iso-PGF2alpha, IPF2alpha-I, IPF2alpha

12 (autoantibodies to epitopes of oxidized LDL, F2-isoprostanes, 8-hydroxy-2'-deoxyguanosine), inflammat

13 genesis of acute chest syndrome and measured F2 isoprostanes, a nonenzymatically generated molecule r

14 doubled the ghost membrane concentration of F2-isoprostanes, a sensitive marker of lipid peroxidatio

15 el of inflammatory cytokines and chemokines, F2 -isoprostanes and isofuranes, markers of oxidative st

16 as biomarkers of systemic inflammation, and F2 isoprostanes and isofurans were measured as biomarker

17 ficant associations between either 8-OHdG or F2-isoprostane and blood pressure over time.

18 vention also led to significant decreases in F2-isoprostane and IL-6 concentrations.

19 ated with a non-significant decrease in mean F2-isoprostane and no effect on thiobarbituric acid reac

20 In contrast, the levels of F2-isoprostanes and atherosclerosis in the ApoE-/- mice

21 -epi PGF2alpha and IPF2alpha-I, two distinct F2-isoprostanes and markers of oxidative stress in vivo,

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

23 2) oxidative stress assessed by total plasma F2-isoprostanes, and 3) inflammation assessed by plasma

24 aconitase, increased levels of 8-oxo dG and F2-isoprostanes, and a moderate reduction in glutathione

25 F2 isoprostanes are stable, free radical-catalyzed produ

26 F2-isoprostanes are a prototype wastewater biomarker to

27 F2-isoprostanes are free radical-catalyzed products of a

28 F2-isoprostanes are produced in vivo by nonenzymatic per

29 F2-Isoprostanes are prostaglandin (PG) isomers formed in

30 F2-isoprostanes are prostaglandin F2-like compounds that

31 F2-isoprostanes are prostaglandin-like products of nonen

32 oute by which certain prostanoids, including F2 isoprostanes, are transported across plasma membranes

33 using a gas chromatography/mass spectrometry F2-isoprostane assay and compared these results with a m

34 = 0.10 [95% CI: 0.06, 0.13], p < 0.001), and F2-isoprostane (beta = 0.13 [95% CI: 0.01, 0.25], p = 0.

35 duced a 30-fold increase in the formation of F2-isoprostanes by a mechanism involving redox cycling b

36 gnificantly reduced the urinary excretion of F2-isoprostanes by approximately 80%.

37 Urinary F2-isoprostanes can also be efficiently quantified by th

38 me measures (PWV changed by +9.5% and +6.0%, F2-isoprostanes changed by -3.0% and -9.7%, and pentraxi

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

40 e genetic and CSF measures, only greater CSF F2-isoprostane concentration was significantly associate

41 In addition, F2-isoprostane concentrations were associated with incre

42 ne in absolute fat mass, body weight, plasma F2-isoprostane concentrations, and peak oxygen uptake (V

43 y concentrations of KIM-1, NGAL, 8-OHdG, and F2-isoprostane controlling for sex, age, race/ethnicity,

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

45 rs an advantage over measuring unmetabolized F2-isoprostanes, e.g. in a plasma sample, in that it can

46 e, implicating the PB-induced P450(s) in the F2-isoprostane elevation.

47 drolases play key roles in the hydrolysis of F2-isoprostanes esterified on phospholipids in vivo.

48 was assessed using cerebrospinal fluid (CSF) F2-isoprostane (F2-IsoP) concentrations correlated with

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

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

51 ic oxidation of arachidonic acid, termed the F2-isoprostanes (F2-IsoPs), provides an accurate assessm

52 cerebrospinal fluid (CSF) concentrations of F2-isoprostanes (F2-IsoPs), stable products of arachidon

53 f a tetranor-dicarboxylic acid metabolite of F2-isoprostanes (F2IP-M) by mass spectrometry in 8 patie

54 and circulating oxidative stress biomarkers (F2-isoprostanes, F3-isoprostanes, isofurans) in plasma c

55 to ghosts during resealing largely prevented F2-isoprostane formation due to extravesicular ferricyan

56 It is an abundant F2-isoprostane formed in a free radical- but not COX-dep

57 icient in PAF acetylhydrolase do not release F2-isoprostanes from esterified precursors.

58 The amounts formed exceeded levels of F2-isoprostanes generated from arachidonic acid by 3.4-f

59 rement of levels of endogenous unmetabolized F2-isoprostanes has proven to be a valuable approach to

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

61 There was a 9-fold increase in F2 isoprostanes in patients with acute chest syndrome as

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

63 CSF levels of amyloid beta, tau protein, and F2-isoprostanes in elderly individuals with major depres

64 F2-Isoprostanes in plasma and urine are generally determ

65 therosclerosis was correlated with a reduced F2-isoprostanes in the plasma and aortas in ApoE-/- mice

66 surement of levels of urinary metabolites of F2-isoprostanes in timed urine collections offers an adv

67 ogenesis and an increase in iPF2alpha-VI, an F2-isoprostane, in urine, plasma and vascular tissue.

68 cing oxidative injury, as measured by plasma F2-isoprostanes, in adult patients with severe sepsis an

69 g factor (PAF), prostaglandin E2 (PGE2), and F2-isoprostane increased 2.5, 5.2, and 36 times, respect

70 odel of rhabdomyolysis, urinary excretion of F2-isoprostanes increased by 7.3-fold compared with cont

71 eveloped by use of mass spectrometry for the F2 isoprostanes iPF2alpha-III and iPF2alpha-VI and arach

72 F2-isoprostanes (iPs) are prostaglandin isomers formed b

73 ve shown that 8-epi-PGF2 alpha, unlike other F2-isoprostanes, is a minor product of the prostaglandin

74 he N + WSH group had lower concentrations of F2-isoprostanes isomers (differences ranging from -0.16

75 We measured four F2-isoprostanes isomers (iPF(2alpha)-III; 2,3-dinor-iPF(

76 prostaglandin (PG) F2-like compounds, termed F2-isoprostanes (IsoPs), are produced in vivo and in vit

77 tory prostaglandin F2-like compounds, termed F2-isoprostanes (IsoPs), are produced in vivo by the fre

78 Measurement of F2-isoprostanes (IsoPs), prostaglandin F2-like compounds

79 oxidation markers, malondialdehyde (MDA) and F2-isoprostanes (IsoPs).

80 Urinary F2 isoprostane levels are elevated in patients after tre

81 7; 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)

82 Increased urinary and plasma F2-isoprostane levels are associated with a number of hu

83 F2-isoprostane levels before asthma onset were not diffe

84 hanges in 25-(OH)-vitamin D, PTH, FGF-23, of F2-isoprostane levels between efavirenz and PI use or be

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

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

87 F2-isoprostane levels peaked on day 1 after injury and w

88 Although F2-isoprostane levels were approximately three-fold lowe

89 oxidant reserve, glutathione, protein-thiol, F2-isoprostane levels were assessed by bivariate and mul

90 However, F2-isoprostane levels were not different between those i

91 line mean arterial, venous, and brain tissue F2-isoprostane levels were not significantly different w

92 three-fold increases in venous and arterial F2-isoprostane levels, which peaked between 15 and 30 mi

93 emic lipid peroxidation determined by plasma F2-isoprostane levels.

94 riched in the brain, led to the formation of F2-isoprostane-like compounds, which we term F4-neuropro

95 Measurement of F2-isoprostanes may offer a sensitive, specific, and non

96 an increase in hepatic 4-hydroxynonenal and F2-isoprostanes (measured by gas chromatography-mass spe

97 This study shows that F2-isoprostane measurement could be used to assess oxida

98 (biomarkers of Alzheimer disease) as well as F2-isoprostanes (measures of free radical injury).

99 oxidative stress, measured by generation of F2 isoprostanes, occurs during acute chest syndrome and

100 F2-Isoprostanes on study day 3, the primary outcome, did

101 no significant effect on plasma hsCRP, IL-6, F2 isoprostane, or isofuran concentrations and did not i

102 Although vitamins C and E tended to reduce F2-isoprostanes (p = 0.065), they failed to alter oxidiz

103 Baseline urinary F2-isoprostanes, plasma concentrations of antioxidant mi

104 nt injury to the kidney and the formation of F2-isoprostanes, potent renal vasoconstrictors formed du

105 PAF, PGE2, and F2 isoprostane produced dose-dependent reductions in ton

106 8-epi PGF2alpha and IPF2alpha-I are F2-isoprostanes produced in humans which circulate in pl

107 bolite in humans of one of the more abundant F2-isoprostanes produced, 8-iso-prostaglandin F2alpha (8

108 tive prostaglandin F2-like compounds, termed F2-isoprostanes, produced in vivo in humans by the non-c

109 sessed by measurements of protein thiols and F2-isoprostane, respectively, in ventricular cerebrospin

110 Urinary F2-isoprostanes, secondary end products of lipid peroxid

111 eterm infants contains high levels of AA and F2-isoprostanes, stable lipid peroxidation end products.

112 es marked increase in free radical-catalyzed F2-isoprostanes suggests that radicals might be formed d

113 Urinary excretion of the 2 F2 isoprostanes was significantly increased in hyperchol

114 hod for the measurement of esterified plasma F2-isoprostanes was developed by replacing these steps w

115 An increase in F2-isoprostanes was discernible at 16.5 microM cisplatin

116 F2 isoprostanes were measured by gas chromatography/mass

117 Plasma levels of F2 isoprostanes were not significantly increased after p

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

119 ha, protein-associated carbonyl content, and F2-isoprostanes were assessed at 1 week pretransplantati

120 With this procedure, esterified plasma F2-isoprostanes were found to be 8.3-fold higher in an e

121 Pentafluorobenzyl esters of F2-isoprostanes were prepared and purified by HPLC, sily

122 However, F2-isoprostanes were significantly reduced on study day

123 stress markers plasma protein carbonyls and F2-isoprostanes, were significantly elevated in ESRD pat

124 rs an increased production of PAF, PGE2, and F2-isoprostane, which are responsible for reducing LES t

125 Plasma F2-isoprostanes, which are formed in concert with isoket