ライフサイエンスコーパス: F2-isoprostane

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

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

3 hydrolases have high affinity for esterified F2-isoprostanes.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

21 F2 isoprostanes are stable, free radical-catalyzed produ

22 F2-isoprostanes are a prototype wastewater biomarker to

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

24 F2-isoprostanes are produced in vivo by nonenzymatic per

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

26 F2-isoprostanes are prostaglandin F2-like compounds that

27 F2-isoprostanes are prostaglandin-like products of nonen

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

56 F2-Isoprostanes in plasma and urine are generally determ

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

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

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

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

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

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

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

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

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

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

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

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

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

70 Urinary F2 isoprostane levels are elevated in patients after tre

71 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)

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

73 F2-isoprostane levels before asthma onset were not diffe

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

95 8-epi PGF2alpha and IPF2alpha-I are F2-isoprostanes produced in humans which circulate in pl

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

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

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

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

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

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

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

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

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

105 F2 isoprostanes were measured by gas chromatography/mass

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

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

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

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

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

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

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

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

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