ライフサイエンスコーパス: hydroxynonenal

1 n-3/5) and for a lipid peroxidation product (hydroxynonenal).

2 (e.g., acrolein), and endogenous ligands (4-hydroxynonenal).

3 mediated by the lipid peroxidation product 4-hydroxynonenal.

4 e latter manifested by increased levels of 4-hydroxynonenal.

5 tochemical staining of 3-nitrotyrosine and 4-hydroxynonenal.

6 ative stress defined by immunostaining for 4-hydroxynonenal.

7 y superoxide but did not block activation by hydroxynonenal.

8 ted by the presence of the toxic aldehyde, 4-hydroxynonenal.

9 adducts of the lipid peroxidation product 4-hydroxynonenal.

10 pression correlated with the generation of 4-hydroxynonenal.

11 id oxidation products 4-hydroxyhexenal and 4-hydroxynonenal.

12 aturated 4-hydroxyacids (C(4) to C(11)) or 4-hydroxynonenal.

13 ed levels of a lipid peroxidation product, 4-hydroxynonenal.

14 dative stress markers 3'-nitrotyrosine and 4-hydroxynonenal.

15 ongeners of the lipid peroxidation product 4-hydroxynonenal.

16 The lipid peroxidation product 4-hydroxynonenal (1 mumol/L), an endogenous reactive oxyge

17 xic incubation increased oxidative stress (4-hydroxynonenal, 141.1 +/- 17.6% of normoxic control), re

18 ously occurring alkenyl aldehydes (EC(50): 4-hydroxynonenal 19.9 microM, 4-oxo-nonenal 1.9 microM, 4-

19 ation products such as malondialdehyde and 4-hydroxynonenal-2-nonenal.

20 4-Hydroxynonenal (4-HNE or HNE) is a main endogenous produ

21 4-Hydroxynonenal (4-HNE) and 4-hydroxyhexenal (4-HHE) are

22 Levels of protein modification by 4-hydroxynonenal (4-HNE) and 4-hydroxyhexenal (4-HHE), whi

23 y with plasma lipid peroxidation products, 4-hydroxynonenal (4-HNE) and 8-isoprostane F2alpha, and ne

24 turated alkanals and unsaturated alkenals, 4-hydroxynonenal (4-HNE) and trans-2-nonenal (nonenal), wa

25 ed increase in the lipid oxidation product 4-hydroxynonenal (4-HNE) as well as increased expression o

26 amount of oxidized glutathione (GSSG) and 4-hydroxynonenal (4-HNE) in airway-lining fluid.

27 Previously, we have shown that 4-hydroxynonenal (4-HNE) induces Fas-mediated apoptosis in

28 Modification of Abeta by 4-hydroxynonenal (4-HNE) initially increases the hydrophob

29 4-Hydroxynonenal (4-HNE) is a cytotoxic alpha,beta-unsatur

30 The lipid peroxidation product 4-hydroxynonenal (4-HNE) is a signaling mediator with wide

31 4-Hydroxynonenal (4-HNE) is one of the most abundant and r

32 e production of reactive aldehydes such as 4-hydroxynonenal (4-HNE) is proposed to be an important fa

33 ole limpet hemocyanin modified in vitro by 4-hydroxynonenal (4-HNE) or acetaldehyde as immunogens.

34 ctive oxygen species (ROS), as assessed by 4-hydroxynonenal (4-HNE) staining, were elevated in tongue

35 asured by the lipid peroxidation byproduct 4-hydroxynonenal (4-HNE) throughout the carotid wall in th

36 ribution of the lipid peroxidation product 4-hydroxynonenal (4-HNE) to the observations made in vivo.

37 PAR inhibition minimized the production of 4-hydroxynonenal (4-HNE), a marker of oxidative stress, in

38 Because 4-hydroxynonenal (4-HNE), a product of lipid peroxidation

39 It is predicted to scavenge 4-hydroxynonenal (4-HNE), a toxic product of lipid oxidati

40 damage biomarkers, malondialdehyde (MDA), 4-hydroxynonenal (4-HNE), aconitase-2 and 8-hydroxydeoxygu

41 high glutathione-conjugating activity for 4-hydroxynonenal (4-HNE), an electrophilic aldehyde derive

42 eins, and ameliorated apoptosis induced by 4-hydroxynonenal (4-HNE), an oxidative stressor.

43 4-Hydroxynonenal (4-HNE), formed as a consequence of oxida

44 In human renal biopsies, staining of 4-hydroxynonenal (4-HNE), glucose-regulated protein 78 (Gr

45 Hepatic steatosis, 3-nitrotyrosine (3-NT), 4-hydroxynonenal (4-HNE), hypoxia inducible factor alpha (

46 ogically relevant lipid-derived aldehydes, 4-hydroxynonenal (4-HNE), malondialdehyde (MDA), glyoxal (

47 on end products, malondialdehyde (MDA) and 4-hydroxynonenal (4-HNE), showed a one-fold elevation with

48 (IgG) against malonyldialdehyde (MDA) and 4-hydroxynonenal (4-HNE)-derived antigens as well as with

49 s analyzed by immunohistochemistry against 4-hydroxynonenal (4-HNE)-modified proteins.

50 hat regulate the cellular concentration of 4-hydroxynonenal (4-HNE).

51 g activity toward its preferred substrate, 4-hydroxynonenal (4-HNE).

52 with 7-ketocholesterol (7-KC, 5-20 muM) or 4-hydroxynonenal (4-HNE, 5-40 muM) for up to 24 hours.

53 stress (8-hydroxydeoxyguanosine [8-OHdG], 4-hydroxynonenal [4-HNE]-modified proteins, and nitrotyros

54 show that electrophilic aldehydes such as 4-hydroxynonenal (4HNE) and acrolein, generated as a resul

55 ipid peroxidation cytotoxicity mediated by 4-hydroxynonenal (4HNE) as well as the retina in vivo from

56 One such alkenal, 4-hydroxynonenal (4HNE), activates TRPA1 in cultured senso

57 y against the lipid peroxidation byproduct 4-hydroxynonenal (4HNE), is important for resistance again

58 4-Hydroxynonenal (4HNE; an indicator of oxidative stress)

59 required for the measurement; the K(H) for 4-hydroxynonenal, a marker for oxidative stress, is measur

60 ratio of n-6/n-3 fatty acids and levels of 4-hydroxynonenal, a marker of lipid peroxidation.

61 4-Hydroxynonenal, a reactive chemical produced endogenousl

62 nol-fed mice, treatment with rhTrx reduced 4-hydroxynonenal adduct accumulation, inflammatory cytokin

63 /-) and Ppara(-/-) silencing on steatosis, 4-hydroxynonenal adduct formation, oxidative stress, serum

64 tivity in the peripheral nerve, as well as 4-hydroxynonenal adduct nitrotyrosine and poly(ADP-ribose)

65 C3aR(-/-)C5aR(-/-) mice immunized with 4-hydroxynonenal-adducted protein developed severe retinal

66 , iron deposition, oxidative end products (4-hydroxynonenal adducts and 8-hydroxydeoxyguanosine), and

67 n urine, mutant huntingtin aggregates, and 4-hydroxynonenal adducts in muscle and skin tissues were a

68 cals in bile assessed by spin trapping and 4-hydroxynonenal adducts measured by immunohistochemistry

69 an immunoblot analysis, malondialdehyde and hydroxynonenal adducts were observed in chondrocyte-matr

70 a significant increase of malondialdehyde, 4-hydroxynonenal adducts, 3-nitrotyrosine, and inducible n

71 o detect the presence of malondialdehyde and hydroxynonenal adducts.

72 e toxicity of tert-butyl hydroperoxide and 4-hydroxynonenal, against free radical damage arising from

73 pecific inhibitor of the Na+/K+-ATPase) or 4-hydroxynonenal (an aldehydic product of lipid peroxidati

74 in the accumulation of protein adducts of 4-hydroxynonenal, an index of oxidative stress.

75 -type p53 TK-6 lymphoblastoid cell line to 4-hydroxynonenal, an unsaturated aldehyde involved in lipi

76 ected by the lipid peroxidation byproducts 4-hydroxynonenal and 4-hydroxyhexenal (HHE).

77 The aldehydes 4-hydroxynonenal and 4-hydroxyhexenal were more toxic to n

78 ive stress, HbG increased iron deposition, 4-hydroxynonenal and 8-hydroxydeoxyguanosine immunoreactiv

79 y-products of lipid peroxidation including 4-hydroxynonenal and acrolein can interact with DNA bases

80 stress, assessed by an increase in hepatic 4-hydroxynonenal and F2-isoprostanes (measured by gas chro

81 ne concentrations, and placental levels of 4-hydroxynonenal and heat shock protein 70 were increased

82 sessed by immunohistochemical detection of 4-hydroxynonenal and nitrotyrosine and quantitative analys

83 f toxic end products in the liver, such as 4-hydroxynonenal and nitrotyrosine, and was inhibited by t

84 re performed using antibodies specific for 4-hydroxynonenal and nitrotyrosine, markers of lipid perox

85 particular GSTs provide protection include 4-hydroxynonenal and ortho-quinones, with possible links t

86 of the chemical mechanism of formation of 4-hydroxynonenal and related aldehydes has advanced much l

87 We find that hydroxynonenal and structurally related compounds (such

88 Excretion of iPF2a-VI, as well as 4-hydroxynonenal and the iPF2a-III metabolite, 2,3-dinor-5

89 reases in a biomarker of oxidative stress (4-hydroxynonenal) and increased proteolytic activity (20S

90 stress (Nox2, HIF-1alpha, hydrogen peroxide, hydroxynonenal), and fibrogenesis (alpha-smooth muscle a

91 ated the increased ROS markers gp91(phox), 4-hydroxynonenal, and 3-nitrotyrosine.

92 o detectable differences in malonaldehyde, 4-hydroxynonenal, and erythrocyte-reduced glutathione occu

93 Plasma concentrations of malonaldehyde, 4-hydroxynonenal, and erythrocyte-reduced glutathione were

94 o oxidative stressors, including arsenite, 4-hydroxynonenal, and methylglyoxal, led to decreased GSIS

95 e also reduced reactive oxygen species and 4-hydroxynonenal, and mitigated oxidative DNA damage.

96 sors (menadione, tert-butyl hydroperoxide, 4-hydroxynonenal, and peroxynitrite) for human adult retin

97 y liver superoxide expression (P = 0.002), 4-hydroxynonenal, and plasma (ox)CoQ9 (P < 0.001) levels,

98 aldehyde (anti-MDA) protein adducts and to 4-hydroxynonenal (anti-HNE) protein adducts, MDA/HNE prote

99 4-Hydroxynonenal appears inactive at concentrations <1 mic

100 londialdehyde, acetaldehyde, acrolein, and 4-hydroxynonenal are all products of fatty acid oxidation

101 Ethanol increased 4-hydroxynonenal as a maker of oxidative stress in both Ad

102 to albumin at a rate that exceeded that of 4-hydroxynonenal by several orders of magnitude: >50% of L

103 cts of acrolein, crotonaldehyde, and trans-4-hydroxynonenal can form cross-links with the tetrapeptid

104 vel, oxidative adducts (malonyldialdehyde, 4-hydroxynonenal, carbonyls), hypertrophic gene expression

105 -deoxy-Delta(12,14)-prostaglandin J(2) and 4-hydroxynonenal, contain a highly reactive alpha,beta-uns

106 ted by the decrease of malondialdehyde and 4-hydroxynonenal content in BAL of RSV-infected mice.

107 GDP-sensitive proton conductance induced by hydroxynonenal correlated with tissue expression of UCPs

108 idative stress markers 3'-nitrotyrosine or 4-hydroxynonenal expression (P<0.05).

109 cells to oxidative (amyloid beta-peptide, 4-hydroxynonenal, ferrous sulfate) and excitotoxic (glutam

110 n levels of the lipid peroxidation product 4-hydroxynonenal following the excitotoxic insult was lowe

111 the cell-permeable esters of glutathionyl-4-hydroxynonenal (GS-HNE) or glutathionyl-1,4-dihydroxynon

112 -functionalized endogenous reactive signal 4-hydroxynonenal (HNE(alkyne)) and the HaloTag-targetable

113 t reduction in the levels of protein-bound 4-hydroxynonenal (HNE) [a lipid peroxidation product], 3-n

114 nd the membrane lipid peroxidation product 4-hydroxynonenal (HNE) after exposure to the apoptotic ins

115 y reactive products of lipid peroxidation, 4-hydroxynonenal (HNE) and acrolein, both elevated in Alzh

116 8-hydroxydeoxyguanosine (OHdG) and 4-hydroxynonenal (HNE) and enzyme activity of glutathione

117 dative damage evaluated by the presence of 4-hydroxynonenal (HNE) and iron accumulation and expressio

118 Acrolein and 4-hydroxynonenal (HNE) are reactive aldehydes generated du

119 that levels of ceramide, sphingomyelin, and hydroxynonenal (HNE) are significantly increased in brai

120 The addition of the reactive aldehyde 4-hydroxynonenal (HNE) caused carbonylation, and HNE-gluta

121 GDM cells, the lipid peroxidation product 4-hydroxynonenal (HNE) failed to induce nuclear Nrf2 accum

122 4-Hydroxynonenal (HNE) has been widely implicated in the m

123 ignificantly lower levels of alpha-SMA and 4-hydroxynonenal (HNE) in CsA-treated knockout mice.

124 trans-4-Hydroxynonenal (HNE) is a major peroxidation product of

125 trans-4-Hydroxynonenal (HNE) is a major peroxidation product of

126 trans-4-Hydroxynonenal (HNE) is a peroxidation product of omega-

127 4-Hydroxynonenal (HNE) is a pro-apoptotic electrophile gen

128 oteins by the cytotoxic, reactive aldehyde 4-hydroxynonenal (HNE) is known to alter protein function

129 difficult-to-degrade and age-associated 2,4-hydroxynonenal (HNE) modification.

130 ted by photoinducible targeted delivery of 4-hydroxynonenal (HNE) to the proteins Keap1 and PTEN.

131 A marker of lipid peroxidation 4-hydroxynonenal (HNE) was elevated in the cerebrospinal f

132 4-hydroxynonenal (HNE), a highly reactive lipid peroxidati

133 te that p75(NTR) signaling is activated by 4-hydroxynonenal (HNE), a lipid peroxidation product gener

134 4-Hydroxynonenal (HNE), a metastable lipid peroxidation pr

135 port increased modification of proteins by 4-hydroxynonenal (HNE), a product of membrane lipid peroxi

136 was highly correlated with the presence of 4-hydroxynonenal (HNE), a toxic aldehyde and downstream pr

137 ination for the lipid peroxidation product 4-hydroxynonenal (HNE), a toxic compound that contributes

138 cultures to A beta induced conjugation of 4-hydroxynonenal (HNE), an aldehydic product of lipid pero

139 We now provide evidence that 4-hydroxynonenal (HNE), an aldehydic product of membrane l

140 eased levels of 8-hydroxyguanosine (8OHG), 4-hydroxynonenal (HNE), and heme oxygenase-1 (HO-1) in the

141 oxic products of oxidative damage, such as 4-hydroxynonenal (HNE), can react with proteins to impair

142 ty acid composition, residual tocopherol and hydroxynonenal (HNE), canola oil containing the formulat

143 An earlier study showed that 4-hydroxynonenal (HNE), formed as a result of increased li

144 he role of the lipid peroxidation product, 4-hydroxynonenal (HNE), in ethanol-related damage of cytoc

145 ein oxidation, and TBARs and protein-bound 4-hydroxynonenal (HNE), markers of lipid oxidation.

146 The by-product of lipid peroxidation, 4-hydroxynonenal (HNE), was shown to cause apoptosis in PC

147 The trans-4-hydroxynonenal (HNE)-derived exocyclic 1, N(2)-dG adduct

148 metabolites, a principal end product being 4-hydroxynonenal (HNE).

149 peroxidation was visualized by staining for hydroxynonenal (HNE).

150 aturated aldehydes, including acrolein and 4-hydroxynonenal (HNE).

151 ensitive to the lipid peroxidation product 4-hydroxynonenal (HNE).

152 rates a highly reactive and toxic product, 4-hydroxynonenal (HNE).

153 oxidation products acrolein (AC) and trans-4-hydroxynonenal (HNE).

154 steines are modified by the well-known LDE 4-hydroxynonenal (HNE)], establishing the functional conse

155 f AR increased atherosclerosis and increased hydroxynonenal in arteries.

156 dismutase in microglia, nitrotyrosine and 4-hydroxynonenal in neurons, as well as induction of endot

157 rocirculation, and accumulation of tubular 4-hydroxynonenal in the kidney in vivo.

158 One of these products, trans-4-hydroxynonenal, inactivates P450, particularly alcohol-i

159 Levels of nitrotyrosine and 4-hydroxynonenal increased in Ins2(Akita/+) retinas, but w

160 aldehyde, allyl isothiocyanate (AITC), and 4-hydroxynonenal, increased [Ca(2+)](i) in myenteric neuro

161 has been shown to protect against UV- and 4-hydroxynonenal-induced cellular damage, mainly by metabo

162 4-Hydroxynonenal-induced reactive oxygen species productio

163 Hydroxynonenal-induced uncoupling was inhibited by poten

164 Our findings indicate that hydroxynonenal is not merely toxic, but may be a biologi

165 antibodies binding to copper-oxidized LDL, 4-hydroxynonenal-LDL, acrolein-LDL, and LDL modified with

166 Plasma 4-hydroxynonenal levels were increased in obese asthmatic

167 The accumulation of 4-hydroxynonenal (lipid peroxidation) and 3-nitrotyrosine

168 yethyl)lysine, malondialdehyde-lysine, and 4-hydroxynonenal-lysine.

169 % increase; P < 0.05), lipid peroxidation (4-hydroxynonenal, measured by ELISA: 0.30 +/- 0.02 compare

170 on (Western blot), and lipid peroxidation (4-hydroxynonenal Michael adducts) were evaluated in brain

171 cell death.The lipid peroxidation product 4-hydroxynonenal might play a central role in MLP-induced

172 ated with the putative fibrogenic mediator 4-hydroxynonenal or iron/ascorbate, little or no increase

173 ipid peroxidation (malondialdehyde (MDA) and hydroxynonenal) or carbohydrate oxidation (glycolaldehyd

174 0.001) and oxidative stress with increased 4-hydroxynonenal (P < 0.001).

175 by streptozotocin significantly increased 4-hydroxynonenal production and decreased coronary artery

176 35% resulted in increases in formation of 4-hydroxynonenal protein adducts accompanied by evidence o

177 cies and mitochondrial 3-nitrotyrosine and 4-hydroxynonenal protein adducts and decreased mitochondri

178 reases in 8-hydroxy-2'-deoxy-guanosine and 4-hydroxynonenal protein adducts in the regressing epithel

179 cumulation of 8-hydroxy-2'-deoxyguanosine, 4-hydroxynonenal protein adducts, and nitrotyrosine, prima

180 feeding increased accumulation of hepatic 4-hydroxynonenal protein adducts, expression of hepatic tu

181 dox homeostasis, as assessed by changes in 4-hydroxynonenal protein adducts, protein carbonyl content

182 reased protein carbonyls, malondialdehyde, 4-hydroxynonenal-protein adducts, elevated levels of induc

183 17G) generated malondialdehyde-protein and 4-hydroxynonenal-protein epitopes, which were detectable o

184 we found that oxidation products (such as 4-hydroxynonenal) released from the heart trigger peroxiso

185 ative stress in the retina was assessed by 4-hydroxynonenal staining or ELISA for protein carbonyl co

186 elate with the degree of oxidative stress (4-hydroxynonenal staining) or with the abundance of balloo

187 within 20 s, whereas approximately 50% of 4-hydroxynonenal still remained unadducted after 1 h.

188 The carboxyatractylate-sensitive hydroxynonenal stimulation correlated with ANT content i

189 e exposure did result in the production of 4-hydroxynonenal, the timing of the increased levels of pr

190 roducts produced in the vascular wall (ie, 4-hydroxynonenal) upregulate adiponectin gene expression i

191 h as menadione, antimycin A, H(2)O(2), and 4-hydroxynonenal was lower in the CYP2E1 expressing cells

192 Malondialdehyde and 4-hydroxynonenal were measured in bronchoalveoar lavage (B

193 y lipid peroxidation end products, such as 4-hydroxynonenal, whose levels are elevated in the cerebro