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

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

8 inery that protects from the accumulation of lipid hydroperoxides.

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

10 thiobarbituric acid-reactive substances, and lipid hydroperoxides.

11 pharmocological compound that can neutralize lipid hydroperoxides.

12 ility of emulsions and led to lower level of lipid hydroperoxides.

13 he aqueous phase and stabilizing cleavage of lipid hydroperoxides.

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

15 alyze the reduction of hydrogen peroxide and lipid hydroperoxides.

16 Os) convert polyunsaturated fatty acids into lipid hydroperoxides.

17 tathione levels, and increased production of lipid hydroperoxides.

18 erized by the iron-dependent accumulation of lipid hydroperoxides.

19 reincubated with phorbol ester or with other lipid hydroperoxides.

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

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

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

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

24 0.23% water and a high (>1,000 mmol O(2)/kg lipid hydroperoxides after 4 weeks) in gels with > 2.4%

25 Lipid oxidation was low (~30 mmol O(2)/kg lipid hydroperoxides after 6 weeks) in gels with < 0.23%

26 Lipid hydroperoxides, aldehydes, and epoxides generated

27 release these lipid-protein particles causes lipid hydroperoxide and iron accumulation and sensitizes

28 The lipid hydroperoxide and p-Anisidine values of emulsions

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

30 able to extend the lag phase to 20 days for lipid hydroperoxide and to 14 days for hexanal productio

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

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

33 onium bromide (CTAB) and the distribution of lipid hydroperoxides and antioxidants.

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

35 or their inhibition against the formation of lipid hydroperoxides and carbonyl compounds in a strippe

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

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

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

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

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

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

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

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

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

45 Our laboratory previously showed lipid hydroperoxides and oxylipin levels are elevated in

46 ective, with an inhibition of 80% and 72% in lipid hydroperoxides and TBA-RS formation after digestio

47 ss was evaluated by plasma concentrations of lipid hydroperoxides and the redox status of circulating

48 Lipid hydroperoxides and thiobarbituric acid reactive su

49 A lower accumulation of lipid hydroperoxides and volatile compounds was found in

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

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

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

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

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

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

56 Lipid hydroperoxides are reduced by glutathione peroxida

57 Oxidation of fats and oils gives rise to lipid hydroperoxides as primary oxidation products (POPs

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

59 nd critical reverse micelle concentration of lipid hydroperoxides as the two interstitial parameters

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

61 Lipid hydroperoxide breakdown to form truncated phosphol

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

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

64 iocyanate method was not suitable to measure lipid hydroperoxides by the both in auto- and photo-oxid

65 oxidase 4, an enzyme that regulates membrane lipid hydroperoxides, can mitigate sarcopenia in mice.

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

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

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

69 conditions that result in increased hepatic lipid hydroperoxide content.

70 tion period which indicates the formation of lipid hydroperoxides could be detected via this method.

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

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

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

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

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

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

77 Such lipid hydroperoxide-derived modifications could potentia

78 primarily regulated by mechanisms mediating lipid hydroperoxide detoxification.

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

80 reduced the levels of both free radicals and lipid hydroperoxides, effectively extending the lag phas

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

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

83 partial least squares regression to relevant lipid hydroperoxide formation data, which provide the si

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

85 Lipid hydroperoxide formation in liposomes (but not isol

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

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

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

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

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

91 Ferroptosis is associated with lipid hydroperoxides generated by the oxidation of polyu

92 Lipid hydroperoxides generated under oxidative stress co

93 Homolytic decomposition of lipid hydroperoxides gives rise to endogenous genotoxins

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

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

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

97 uting NaCl with KCl changed the formation of lipid hydroperoxides in emulsions by decreasing emulsifi

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

99 plays a fundamental role in the reduction of lipid hydroperoxides in membranes, and overexpression of

100 (GPx4), an enzyme that targets reduction of lipid hydroperoxides in membranes, in adult CuZn superox

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

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

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

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

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

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

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

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

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

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

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

112 4 (GPX4) prevents ferroptosis by converting lipid hydroperoxides into non-toxic lipid alcohols(3,4).

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

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

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

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

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

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

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

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

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

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

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

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

125 me at 60 degrees C and the kinetic curves of lipid hydroperoxides (LOOH) accumulation were drawn.

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

127 The concentration of total lipid hydroperoxides (LOOH) and total conjugated dienes

128 c parameters and rate constants representing lipid hydroperoxides (LOOH) formation and decomposition

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

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

131 drial hydroperoxide production (H(2)O(2) and lipid hydroperoxides (LOOHs)).

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

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

134 ion, CLs inhibited lipid oxidation products (lipid hydroperoxide, Malondialdehyde, and 4-hydroxynonen

135 erry press cake remarkably reduced levels of lipid hydroperoxides, malondialdehyde (MDA) and 4-hydrox

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

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

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

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

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

141 acological intervention designed to modulate lipid hydroperoxides might be an effective strategy to r

142 macological interventions designed to reduce lipid hydroperoxides might be effective for preventing s

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

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

145 A protective effect of salt on lipid hydroperoxides, over storage, was highlighted, mai

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

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

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

149 Lipid hydroperoxide products are generated promptly afte

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

151 in the fillets were free fatty acids (FFA), lipid hydroperoxides (PV) and thiobarbituric acid reacti

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

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

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

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

156 Lipid hydroperoxide-supported P450 oxidation has been re

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

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

159 This in turn results in the production of lipid hydroperoxides that increase membrane tension and

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

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

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

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

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

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

166 4 (GPX4) suppresses ferroptosis by reducing lipid hydroperoxides to lipid alcohols.

167 ferroptosis, converting unstable ferroptotic lipid hydroperoxides to nontoxic lipid alcohols in a tis

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

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

170 Lipid hydroperoxides undergo reductive beta-cleavage to

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

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

173 significant decrease of 46.1 % and 40.9 % in lipid hydroperoxides was attended after in vitro digesti

174 To elucidate the pathological impact of lipid hydroperoxides, we overexpressed glutathione perox

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

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

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

178 were recorded in retarding free radicals and lipid hydroperoxides when 300 ppm of GTE and 75 ppm of E

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

180 ter) significantly reduced the production of lipid hydroperoxides, which was maintained to an average

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