ライフサイエンスコーパス: lipid hydroperoxide

1 ry oxidation products (conjugated dienes and lipid hydroperoxides).

2 lular Ca2+ concentration in response to this lipid hydroperoxide.

3 ms have similar initial reactivity with this lipid hydroperoxide.

4 ne, leading to the reduction in the level of lipid hydroperoxide.

5 r results were obtained in the presence of a lipid hydroperoxide.

6 ecadienoic acid (13-HPODE) as a model of the lipid hydroperoxides.

7 ed activation of NF-kappa B and formation of lipid hydroperoxides.

8 thiobarbituric acid-reactive substances, and lipid hydroperoxides.

9 ml) at inhibiting the formation of TBARS and lipid hydroperoxides.

10 alyze the reduction of hydrogen peroxide and lipid hydroperoxides.

11 Os) convert polyunsaturated fatty acids into lipid hydroperoxides.

12 tathione levels, and increased production of lipid hydroperoxides.

13 reincubated with phorbol ester or with other lipid hydroperoxides.

14 on, have GSH peroxidase activity, and reduce lipid hydroperoxides.

15 The lipid hydroperoxide 13(S)-hydroperoxy-9Z,11E-octadecadie

16 ith heme or mangano protoporphyrin IX with a lipid hydroperoxide, 15-hydroperoxyeicosatetraenoic acid

17 n is observed during turnover with CHP and a lipid hydroperoxide, 15-hydroperoxyeicosatetraenoic acid

18 , which included omega-6 and omega-3 derived lipid hydroperoxides, 2,4-alkadienals, 2-alkenals, 4,5-e

19 The lipid hydroperoxide and p-Anisidine values of emulsions

20 Emulsified oils had lower detectable lipid hydroperoxide and p-Anisidine values than their co

21 lta) and old WT liver, including lipofuscin, lipid hydroperoxides and acrolein, as well as increased

22 emical markers of oxidative stress including lipid hydroperoxides and alkenals were significantly hig

23 yze the direct reduction of various membrane lipid hydroperoxides and by so doing could play a vital

24 nerve, dorsal root, and sympathetic ganglia lipid hydroperoxides and conjugated dienes.

25 mol GAE/ml emulsion delayed the formation of lipid hydroperoxides and headspace hexanal in the 5.0%(w

26 and HO-1 induction was largely dependent on lipid hydroperoxides and heme associated with HbLDL.

27 ess by utilizing glutathione (GSH) to reduce lipid hydroperoxides and hydrogen peroxide to their corr

28 s during germination and contained levels of lipid hydroperoxides and hydroxy fatty acids elevated up

29 ficantly related to plasma concentrations of lipid hydroperoxides and liposoluble antioxidant vitamin

30 lucose disposal and plasma concentrations of lipid hydroperoxides and liposoluble antioxidant vitamin

31 n addition, fasting plasma concentrations of lipid hydroperoxides and liposoluble antioxidant vitamin

32 two groups, which showed decreased levels of lipid hydroperoxides and MDA.

33 Lipid hydroperoxides and thiobarbituric acid reactive su

34 tive stress, including superoxide dismutase, lipid hydroperoxide, and protein carbonyl groups, and ma

35 redox-active cysteines to reduce peroxides, lipid hydroperoxides, and peroxynitrites.

36 recycling of alpha-tocopherol, reduction of lipid hydroperoxides, and reduction of ferric iron prior

37 nt status, oxidative stress index, levels of lipid hydroperoxides, and the activities of paraoxonase,

38 bile approximately 2-fold and elevated serum lipid hydroperoxides approximately 4-fold.

39 It is not known whether total circulating lipid hydroperoxides are increased in insulin-resistant

40 with linoleic acid hydroperoxide, indicating lipid hydroperoxides as the likely physiologic targets.

41 d-reactive substance, which was confirmed by lipid hydroperoxide assay.

42 thiobarbituric acid-reactive substances and lipid hydroperoxides, but was unaccompanied by PG G/H S-

43 de, singlet oxygen by cholesterol assay, and lipid hydroperoxides by iodometric assay.

44 d pressure (r = 0.44, P: = 0.008) and plasma lipid hydroperoxide concentrations (r = 0.42, P: = 0.01)

45 By contrast, plasma lipid hydroperoxide concentrations were similar in both

46 First, the plasma lipid hydroperoxide content was reduced significantly, a

47 conditions that result in increased hepatic lipid hydroperoxide content.

48 n level, left ventricle myocardial levels of lipid hydroperoxides, cytochrome-c, and mitochondrial ac

49 We have now determined that vit C induces lipid hydroperoxide decomposition to the DNA-reactive bi

50 t 4-oxo-2-nonenal is also a major product of lipid hydroperoxide decomposition.

51 adducts can only arise from the reaction of lipid hydroperoxide-derived 4-oxo-2(E)-nonenal with DNA.

52 ve established that 4-hydroxy-2-nonenal is a lipid hydroperoxide-derived aldehydic bifunctional elect

53 e-type adduct may be a useful marker for the lipid hydroperoxide-derived modification of biomolecules

54 Such lipid hydroperoxide-derived modifications could potentia

55 and in transgenic mice that overexpress the lipid hydroperoxide-detoxifying enzyme glutathione perox

56 ase-4 (GPx4), which specifically metabolizes lipid hydroperoxides, fell in TNFalpha-stimulated cells

57 preterm infants did not result in detectable lipid hydroperoxide formation (</=10 nM cholesteryl este

58 ic littermate controls, by itself stimulated lipid hydroperoxide formation in artery wall cells and i

59 Lipid hydroperoxide formation in liposomes (but not isol

60 At 37 degrees C, the rate of lipid hydroperoxide formation increased with decreasing

61 Therefore, inhibition of COX-2-mediated lipid hydroperoxide formation offers a potential therape

62 n the lipid environment, we hypothesize that lipid hydroperoxides formed within the mitochondrial lip

63 d-induced monocyte chemotaxis, and scavenged lipid hydroperoxides from low density lipoprotein.

64 Our results demonstrate that ROS and lipid hydroperoxides function as not-yet-recognized unco

65 Lipid hydroperoxides generated under oxidative stress co

66 Homolytic decomposition of lipid hydroperoxides gives rise to endogenous genotoxins

67 els of mitochondrial superoxide and cellular lipid hydroperoxides, had reduced activities of superoxi

68 the peroxidative chain initiation potency of lipid hydroperoxides has been developed, which involves

69 formation of genotoxic LPO products from the lipid hydroperoxide, hydroperoxy octadecadienoic acid.

70 pase-8 activity in both models and decreased lipid hydroperoxides in MCD mice.

71 ized that SCP-2-facilitated translocation of lipid hydroperoxides in oxidatively stressed cells might

72 In contrast, the ability to inactivate lipid hydroperoxides in oxidized low-density lipoprotein

73 ty lipoprotein (HDL) is the major carrier of lipid hydroperoxides in plasma, but it is not yet establ

74 s are resistant to the fibrogenic effects of lipid hydroperoxides in primary culture.

75 amin C-mediated formation of genotoxins from lipid hydroperoxides in the absence of transition metal

76 showed that the total amount of extractable lipid hydroperoxides in the ahpC mutant cells is approxi

77 id treatment, there is a marked elevation of lipid hydroperoxides in the coq3 mutant as compared with

78 Similarly, the increase in levels of lipid hydroperoxides in the midbrain and striatum of par

79 ntly reported to induce the decomposition of lipid hydroperoxides independent of metal interactions,

80 pose that cellular lipid peroxyl radicals or lipid hydroperoxides induce an apoptotic signaling casca

81 ptosis in endothelial cells, suggesting that lipid hydroperoxides induce apoptosis.

82 injury via translocation of ChOOHs and other lipid hydroperoxides is readily apparent from these find

83 Direct treatment of proteins with various lipid hydroperoxides led to a slight increase in the for

84 eliorate the transient imbalance between the lipid hydroperoxide level and antioxidant status related

85 cholesterol domains correlated directly with lipid hydroperoxide levels and was inhibited by treatmen

86 (MDA) levels of fresh eggs but reduced their lipid hydroperoxide levels compared to controls.

87 ipolysis but attenuated protein carbonyl and lipid hydroperoxide levels in 3T3-L1 cells.

88 xidant status, oxidative stress index (OSI), lipid hydroperoxide levels, paraoxonase, arylesterase, a

89 ine had lower plasma troponin and myocardial lipid hydroperoxides levels (vs. controls, both p<0.05,

90 arameters like TBA value, carbonyl value and lipid hydroperoxides (LHPODs) exhibited significant nega

91 e of this study was to delineate the role of lipid hydroperoxide (LOOH) -induced redox shifts in inte

92 esigned to determine the predictive value of lipid hydroperoxide (LOOH) levels for adverse cardiovasc

93 Whether SCP-2 can also facilitate lipid hydroperoxide (LOOH) transfer between membranes an

94 centration of the ascorbate radical (A(*-)), lipid hydroperoxides (LOOH) and increased susceptibility

95 oral D-4F significantly reduced lipoprotein lipid hydroperoxides (LOOH), except for pre-beta HDL fra

96 rm an amphipathic helix, reduced lipoprotein lipid hydroperoxides (LOOH), increased paraoxonase activ

97 and phagocytic cells may accumulate membrane lipid hydroperoxides (LOOHs), including cholesterol- and

98 and also examined serum lipid peroxidation (lipid hydroperoxides, LPH and 4-hydroxy-2-nonenal, 4-HNE

99 inactivation of PDGF and other cytokines by lipid hydroperoxides may occur in such processes as vasc

100 This suggested that vitamin C increased lipid hydroperoxide-mediated 4-oxo-2(E)-nonenal formatio

101 are still no specific markers of endogenous lipid hydroperoxide-mediated DNA damage.

102 he presence of substrate, the CYP3A-mediated lipid hydroperoxide metabolism is inhibited along with t

103 We report that arachidonic acid lipid hydroperoxide metabolites of 5-, 12-, 15-lipoxygen

104 study were to estimate the structure of the lipid hydroperoxide-modified lysine residue and to prove

105 nti-HEL antibody, the presence of HEL in the lipid hydroperoxide-modified proteins and oxidized LDL w

106 ncreased a-cv(D) and net output of A(.-) and lipid hydroperoxides (P < 0.05 vs. sea level, SL) that c

107 Z,11Z,13E-eicosatetraenoic acid is the major lipid hydroperoxide produced endogenously by cyclooxygen

108 ly blocked the increases in free radical and lipid hydroperoxide production caused by ethanol.

109 tion, iron-oxidizing antioxidant protection, lipid hydroperoxides, protein carbonyls, and plasma thio

110 al lineC groups and an increased aldehyde-to-lipid hydroperoxide ratio.

111 Peptides that sequester lipoprotein lipid hydroperoxides release a series of high-density li

112 sue factor pathway activity, suggesting that lipid hydroperoxides, some of which exist in atheroscler

113 tic decomposition of polyunsaturated omega-3 lipid hydroperoxides such as 13(S)-hydroperoxyoctadecadi

114 Lipid hydroperoxide-supported P450 oxidation has been re

115 oxyl radicals obtained by Fe(II) cleavage of lipid hydroperoxides that are formed.

116 or 6 h resulted in a significant increase in lipid hydroperoxides that coincided wih an increase in i

117 f hydroxyl radical leads to the formation of lipid hydroperoxides that produce a family of alpha,beta

118 lysine, named HEL, in protein exposed to the lipid hydroperoxide, the antibody to the synthetic hexan

119 a results in the time-dependent formation of lipid hydroperoxides through an unknown, ascorbate-sensi

120 he formation of oxygen-containing defects by lipid hydroperoxides through photo-oxidation.

121 t5) rapidly oxidize while reducing the toxic lipid hydroperoxide to a nonreactive lipid hydroxide, wh

122 erized by the iron-dependent accumulation of lipid hydroperoxides to lethal levels.

123 facilitated rapid decomposition of preformed lipid hydroperoxides to secondary lipid oxidation produc

124 The reaction of lipid hydroperoxide toward the lysine moiety was investi

125 Lipid hydroperoxides undergo reductive beta-cleavage to

126 lysin/granulysin, HIV Tat protein, H(2)O(2), lipid hydroperoxides, vitamin K, ubiquinone, juglone, ni

127 sis was employed to show that a 5-LO-derived lipid hydroperoxide was responsible for endogenous DNA-a

128 when iron was added to plasma devoid of AA, lipid hydroperoxides were formed immediately, whereas en

129 I; myocardial lactate) and oxidative stress (lipid hydroperoxides) were measured by enzyme-linked imm

130 Primary oxidation products (lipid hydroperoxides) were measured with a ferrous oxida

131 effects of oxidative stress are mediated by lipid hydroperoxides, which are efficiently metabolized

132 anti-human LDL antibody, as well as reducing lipid hydroperoxides with ebselen, resulted in inhibitio