ライフサイエンスコーパス: lipid peroxide

1 y reduced hepatic inflammation, fibrosis and lipid peroxides.

2 NE) is one of the most abundant and reactive lipid peroxides.

3 dase 4 (GPx4), which preferentially degrades lipid peroxides.

4 ed selenium levels result in accumulation of lipid peroxides.

5 adation, a process dependent on PUFA-derived lipid peroxides.

6 leading to the 2-3-fold increase of cellular lipid peroxides.

7 oB-lipoproteins containing potentially toxic lipid peroxides.

8 ide, superoxide anion, hydroxyl radical, and lipid peroxides.

9 cell death induced by the build-up of toxic lipid peroxides.

10 nt enzyme that reduces hydrogen peroxide and lipid peroxides.

11 s during brain ischemia is a major source of lipid peroxides.

12 tion of reactive oxygen species and membrane lipid peroxides.

13 diated partly through increased formation of lipid peroxides.

14 nted the twofold increase in oxidant-induced lipid peroxides.

15 bition was attenuated by the addition of the lipid peroxide 15-hydroperoxyeicosatertaenoic acid.

16 oxidative stress associated with circulating lipid peroxides (2-4), and in cases of severe maternal h

17 /- 9 versus 73 +/- 6 mmHg; P < 0.01), plasma lipid peroxides (2.6 +/- 0.3 versus 2.0 +/- 0.3 nM; P <

18 hApoD overexpression reduces age-associated lipid peroxide accumulation, suggesting a proximal mecha

19 ed production of reactive oxygen species and lipid peroxides, activation of nuclear factor-kappa B, a

20 piration followed by increased production of lipid peroxides and c-Jun N-terminal kinase activity.

21 ficient T cells rapidly accumulated membrane lipid peroxides and concomitantly underwent cell death d

22 ve stress that included levels of myocardial lipid peroxides and Cu/Zn superoxide dismutase.

23 ed tissue levels of oxidized glutathione and lipid peroxides and elicited small intestinal tissue inj

24 pid peroxidase, cause lethal accumulation of lipid peroxides and induce ferroptotic cell death.

25 e 4 (GPX4), which catalyzes the reduction of lipid peroxides and is a target of ferroptosis inducers,

26 um of TLR4-deficient Cr mice contained fewer lipid peroxides and less complement deposition compared

27 months of PC inhibited elevations in retinal lipid peroxides and NO levels by approximately 50%, but

28 Tissue lipid peroxides and reactive carbonyls were increased in

29 ant strains each show a greater abundance of lipid peroxides and suffer more DNA damage and more prot

30 Prx silencing revealed an abrupt increase of lipid peroxides and the generation of several oxidized p

31 In conclusion, lipid peroxides and their breakdown products are the cau

32 nocysteine-containing enzyme that dissipates lipid peroxides and thereby prevents the iron-mediated r

33 Plasma markers of lipid peroxidation (lipid peroxides and thiobarbituric acid-reactivity), pla

34 and prevented the increases in formation of lipid peroxides and tyrosine nitration as well as the in

35 ts, including reactive oxygen species (ROS), lipid peroxides, and metals.

36 levels of molecular markers of hypertrophy, lipid peroxides, and oxidized mitochondrial DNA; and the

37 lmo1, as do the plasma levels of cystatin C, lipid peroxides, and TGFbeta1, and erythrocyte levels of

38 increases in the formation of nitric oxide, lipid peroxides, and the peroxynitrite biomarker nitroty

39 We hypothesized that selenium-lipid peroxide antagonism controls the above prognostic

40 e in reactive oxygen species detoxification, lipid peroxides are elevated in soz1, but not in wild ty

41 had partially beneficial effects on retinal lipid peroxides, but the levels of an endogenous antioxi

42 Serum nitrotyrosine was measured by ELISA, lipid peroxide by spectrophotometer, and microvascular f

43 The hydrolysis of lipid peroxides by PON1 makes a major contribution to th

44 oprecipitation, SO by 2-hydroxyethidine, and lipid peroxides by thiobarbituric acid reactive substanc

45 Preeclamptic women had increased circulating lipid peroxides compared with normal pregnant women, as

46 ressing cells also showed significantly less lipid peroxide formation and decreased perturbation of t

47 e time-course curves of conjugated diene and lipid peroxide formation.

48 of peroxynitrite or other peroxides such as lipid peroxides formed at inflammatory sites might overw

49 systems, by accelerated selective uptake of lipid peroxides from HDL and by antioxidant molecules.

50 s of paraoxonase 1, which are most active in lipid peroxide hydrolysis, as revealed by meta-analysis

51 s the capacity to retard the accumulation of lipid peroxides in LDL under oxidizing conditions in vit

52 st the hypothesis that increased circulating lipid peroxides in preeclamptic women activate vascular

53 rape juices promoted significant decrease of lipid peroxides in serum and TBARS levels in plasma.

54 The lipid peroxides in the membrane were detected by fluores

55 h a reaction of methylselenol with PKC-bound lipid peroxides in the membrane.

56 min E) significantly abrogated H(2)O(2)- and lipid peroxide-induced 2',7'-dichlorofluorescein fluores

57 stellate cells strongly resist oxidant- and lipid peroxide-induced collagen synthesis in primary cul

58 Mito-Q and MitoVit-E inhibited H(2)O(2)- and lipid peroxide-induced inactivation of complex I and aco

59 ioxidant activity measurements (antiradical, lipid peroxide inhibition, H2O2 and NO scavenging) were

60 lease of eight different glycohydrolases and lipid peroxides into serum were determined and compared

61 The twofold increase in vitreous lipid peroxide level in diabetic rabbits was completely

62 Oxidized LDL with a lipid peroxide level of 80-100 nmol/mg of LDL protein an

63 Nitrotyrosine and lipid peroxide levels (n = 102, 74 with OSA) were higher

64 ter 2 to 3 hours' postischemia and the serum lipid peroxide levels followed the same pattern.

65 The effect of AG on rabbit vitreous lipid peroxide levels was also determined.

66 ractility with enhancing urinary and cardiac lipid peroxide levels, compared to wild type and TRPC3-d

67 nt both fluorescence decay and generation of lipid peroxides (LOOH) when peroxidation was initiated b

68 tment decreases nitric oxide (NO) by 27% and lipid peroxide (LPO) by 18% as compared to injury, which

69 Oxidative stress was estimated by measuring lipid peroxides (measured as thiobarbituric acid reactiv

70 rosis and ones involved in detoxification of lipid peroxide-mediated oxidative stress to be different

71 n contrast, no detectable changes (P>.05) in lipid peroxide occurred within 2h except for samples wit

72 The levels of lipid peroxide, oxidatively modified DNA, electron trans

73 Concentrations of lipid peroxides precardiopulmonary bypass were similar t

74 bituric acid reactive substances (TBARs) for lipid peroxide products and by colorimetric assay for hy

75 ipid peroxidation, and the concentrations of lipid peroxide products in the wild-type mice were lower

76 omarkers examined, in which the formation of lipid peroxides, protein carbonyls and DNA oxidised prod

77 ither tertiary butyl hydroperoxide, TBOOH (a lipid peroxide prototype) (T cells), or H2O2 (H cells).

78 lenge with another type of peroxide, TBHP, a lipid peroxide prototype.

79 e than 2-fold elevation of the intracellular lipid peroxides, resulting in apoptosis.

80 urated fatty acids and lower accumulation of lipid peroxides than did wild-type seeds.

81 cantly less vitamin E and significantly more lipid peroxides than do livers of wild-type mice.

82 T1D and produces proinflammatory lipids and lipid peroxides that exacerbate beta-cell dysfunction an

83 karyotic cells where it reduces hydrogen and lipid peroxides to alcohols.

84 Reduction of pre-existing lipid peroxides using ebselen delayed HbLDL kinetics and

85 LV myocardial lipid peroxides were greater (CIH, 1,258+/-703; HC 715+/

86 Lipid peroxides were increased in both septic patients (

87 The lipid peroxides were localized exclusively in the photor

88 gh levels of SO were higher (+44%); those of lipid peroxides were similar, and their reduction by alp

89 injury (e.g. chemokine transcript levels and lipid peroxides) were disproportionately increased in th

90 zyme catalyzes the reduction of hydrogen and lipid peroxides, which limits the availability of these

91 ckout animals may be due to the formation of lipid peroxides, which serve as substrates for GPX-1.

92 ium, a cofactor of peroxidases that detoxify lipid peroxides, would inhibit atherosclerosis more effe