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1 a key enzyme that catalyzes the formation of lipid peroxides.
2 quires cellular iron and the accumulation of lipid peroxides.
3  and propagated by the accumulation of toxic lipid peroxides.
4 by the overwhelming accumulation of membrane lipid peroxides.
5 duced by accumulation of free iron and toxic lipid peroxides.
6 icating a role for iron in the production of lipid peroxides.
7   Prdx detoxify hydrogen peroxide and reduce lipid peroxides.
8 tathione-dependent peroxidases that detoxify lipid peroxides.
9  cell death induced by the build-up of toxic lipid peroxides.
10 y reduced hepatic inflammation, fibrosis and lipid peroxides.
11 NE) is one of the most abundant and reactive lipid peroxides.
12 dase 4 (GPx4), which preferentially degrades lipid peroxides.
13 ed selenium levels result in accumulation of lipid peroxides.
14 adation, a process dependent on PUFA-derived lipid peroxides.
15 leading to the 2-3-fold increase of cellular lipid peroxides.
16 oB-lipoproteins containing potentially toxic lipid peroxides.
17 ide, superoxide anion, hydroxyl radical, and lipid peroxides.
18 nt enzyme that reduces hydrogen peroxide and lipid peroxides.
19 s during brain ischemia is a major source of lipid peroxides.
20 tion of reactive oxygen species and membrane lipid peroxides.
21 diated partly through increased formation of lipid peroxides.
22 nted the twofold increase in oxidant-induced lipid peroxides.
23 ng antioxidant that halts the propagation of lipid peroxides.
24 bition was attenuated by the addition of the lipid peroxide 15-hydroperoxyeicosatertaenoic acid.
25 oxidative stress associated with circulating lipid peroxides (2-4), and in cases of severe maternal h
26 /- 9 versus 73 +/- 6 mmHg; P < 0.01), plasma lipid peroxides (2.6 +/- 0.3 versus 2.0 +/- 0.3 nM; P <
27  results from iron-dependent accumulation of lipid peroxide(5,6).
28              When GPX4 is overwhelmed, toxic lipid peroxides accumulate and disrupt membrane integrit
29  phospholipids (lipid peroxides); when these lipid peroxides accumulate in membranes, this culminates
30 ll death, is characterized by iron-dependent lipid peroxide accumulation in cell membranes from dysre
31 ndrial membrane potential hyperpolarization, lipid peroxide accumulation, and ferroptosis.
32  hApoD overexpression reduces age-associated lipid peroxide accumulation, suggesting a proximal mecha
33 -dependent regulated cell death triggered by lipid peroxide accumulation-has gained prominence in can
34  form of cell death driven by iron-dependent lipid peroxide accumulation.
35 the regulation of ferroptosis by controlling lipid peroxide accumulation.
36 ial membrane potential hyperpolarization and lipid peroxide accumulation.
37 ed production of reactive oxygen species and lipid peroxides, activation of nuclear factor-kappa B, a
38 piration followed by increased production of lipid peroxides and c-Jun N-terminal kinase activity.
39 r GSH in xCT-KO cells led to accumulation of lipid peroxides and cell swelling.
40 ficient T cells rapidly accumulated membrane lipid peroxides and concomitantly underwent cell death d
41 ve stress that included levels of myocardial lipid peroxides and Cu/Zn superoxide dismutase.
42 ed tissue levels of oxidized glutathione and lipid peroxides and elicited small intestinal tissue inj
43 pid peroxidase, cause lethal accumulation of lipid peroxides and induce ferroptotic cell death.
44 e 4 (GPX4), which catalyzes the reduction of lipid peroxides and is a target of ferroptosis inducers,
45 um of TLR4-deficient Cr mice contained fewer lipid peroxides and less complement deposition compared
46 feration and cell death, and accumulation of lipid peroxides and mitochondrial reactive oxygen specie
47 the formation of oxidative mediators such as lipid peroxides and nitric oxide (NO).
48 months of PC inhibited elevations in retinal lipid peroxides and NO levels by approximately 50%, but
49 erized by the accumulation of iron-dependent lipid peroxides and oxidative damage.
50  defense systems that detoxify mitochondrial lipid peroxides and protect against ferroptosis, present
51                                       Tissue lipid peroxides and reactive carbonyls were increased in
52 ant strains each show a greater abundance of lipid peroxides and suffer more DNA damage and more prot
53 Prx silencing revealed an abrupt increase of lipid peroxides and the generation of several oxidized p
54                               In conclusion, lipid peroxides and their breakdown products are the cau
55 nocysteine-containing enzyme that dissipates lipid peroxides and thereby prevents the iron-mediated r
56        Plasma markers of lipid peroxidation (lipid peroxides and thiobarbituric acid-reactivity), pla
57  and prevented the increases in formation of lipid peroxides and tyrosine nitration as well as the in
58 Fsp1-knockout tumours had an accumulation of lipid peroxides, and inhibition of ferroptosis with gene
59 ts, including reactive oxygen species (ROS), lipid peroxides, and metals.
60  levels of molecular markers of hypertrophy, lipid peroxides, and oxidized mitochondrial DNA; and the
61 lmo1, as do the plasma levels of cystatin C, lipid peroxides, and TGFbeta1, and erythrocyte levels of
62  increases in the formation of nitric oxide, lipid peroxides, and the peroxynitrite biomarker nitroty
63 welling effect through cell populations in a lipid peroxide- and iron-dependent manner.
64                We hypothesized that selenium-lipid peroxide antagonism controls the above prognostic
65 e in reactive oxygen species detoxification, lipid peroxides are elevated in soz1, but not in wild ty
66  had partially beneficial effects on retinal lipid peroxides, but the levels of an endogenous antioxi
67   Serum nitrotyrosine was measured by ELISA, lipid peroxide by spectrophotometer, and microvascular f
68                        Moreover, decrease in lipid peroxides by glutathione peroxidase-4 or superoxid
69                            The hydrolysis of lipid peroxides by PON1 makes a major contribution to th
70 oprecipitation, SO by 2-hydroxyethidine, and lipid peroxides by thiobarbituric acid reactive substanc
71 Preeclamptic women had increased circulating lipid peroxides compared with normal pregnant women, as
72 ressing cells also showed significantly less lipid peroxide formation and decreased perturbation of t
73 e time-course curves of conjugated diene and lipid peroxide formation.
74  of peroxynitrite or other peroxides such as lipid peroxides formed at inflammatory sites might overw
75  systems, by accelerated selective uptake of lipid peroxides from HDL and by antioxidant molecules.
76  rates and sEV-mediated extrusion of harmful lipid peroxides from trophoblast cells into the circulat
77 s of paraoxonase 1, which are most active in lipid peroxide hydrolysis, as revealed by meta-analysis
78 s the capacity to retard the accumulation of lipid peroxides in LDL under oxidizing conditions in vit
79                  Rather, the accumulation of lipid peroxides in NKAP-deficient T cells was observed.
80      While detoxification reactions removing lipid peroxides in phospholipids such as that catalyzed
81 st the hypothesis that increased circulating lipid peroxides in preeclamptic women activate vascular
82 rape juices promoted significant decrease of lipid peroxides in serum and TBARS levels in plasma.
83                                          The lipid peroxides in the membrane were detected by fluores
84 h a reaction of methylselenol with PKC-bound lipid peroxides in the membrane.
85 ll death triggered by the lethal overload of lipid peroxides, in cancer therapy is impeded by our lim
86 min E) significantly abrogated H(2)O(2)- and lipid peroxide-induced 2',7'-dichlorofluorescein fluores
87 d ferroptosis, which is an iron-mediated and lipid peroxide-induced cell death pathway.
88  stellate cells strongly resist oxidant- and lipid peroxide-induced collagen synthesis in primary cul
89  sensitive to ferroptosis, an iron-dependent lipid peroxide-induced form of cell death.
90 Mito-Q and MitoVit-E inhibited H(2)O(2)- and lipid peroxide-induced inactivation of complex I and aco
91 ioxidant activity measurements (antiradical, lipid peroxide inhibition, H2O2 and NO scavenging) were
92  4 (GPX4) prevents ferroptosis by converting lipid peroxides into nontoxic lipid alcohols.
93 lease of eight different glycohydrolases and lipid peroxides into serum were determined and compared
94 mposition of polyunsaturated fatty acids via lipid peroxides is demonstrated.
95 st consider how the accumulation of membrane lipid peroxides leads to the execution of ferroptosis by
96             The twofold increase in vitreous lipid peroxide level in diabetic rabbits was completely
97                          Oxidized LDL with a lipid peroxide level of 80-100 nmol/mg of LDL protein an
98                            Nitrotyrosine and lipid peroxide levels (n = 102, 74 with OSA) were higher
99 ter 2 to 3 hours' postischemia and the serum lipid peroxide levels followed the same pattern.
100          The effect of AG on rabbit vitreous lipid peroxide levels was also determined.
101                                 In contrast, lipid peroxide levels were reduced by treatment with fer
102 ractility with enhancing urinary and cardiac lipid peroxide levels, compared to wild type and TRPC3-d
103 nt both fluorescence decay and generation of lipid peroxides (LOOH) when peroxidation was initiated b
104 nditions concentration of fatty acids (FAs), lipid peroxides (LP) and a-lactalbumin (a-La) were on a
105 nditions concentration of fatty acids (FAs), lipid peroxides (LP) and alpha-lactalbumin (alpha-La) we
106 tment decreases nitric oxide (NO) by 27% and lipid peroxide (LPO) by 18% as compared to injury, which
107  Oxidative stress was estimated by measuring lipid peroxides (measured as thiobarbituric acid reactiv
108 rosis and ones involved in detoxification of lipid peroxide-mediated oxidative stress to be different
109 n contrast, no detectable changes (P>.05) in lipid peroxide occurred within 2h except for samples wit
110 eath triggered by the lethal accumulation of lipid peroxides on cellular membranes, has emerged as on
111 h that is triggered by the toxic build-up of lipid peroxides on cellular membranes.
112                                The levels of lipid peroxide, oxidatively modified DNA, electron trans
113 h characterized by the accumulation of toxic lipid peroxides, particularly in the plasma membrane, le
114                            Concentrations of lipid peroxides precardiopulmonary bypass were similar t
115 bituric acid reactive substances (TBARs) for lipid peroxide products and by colorimetric assay for hy
116 ipid peroxidation, and the concentrations of lipid peroxide products in the wild-type mice were lower
117 omarkers examined, in which the formation of lipid peroxides, protein carbonyls and DNA oxidised prod
118 ither tertiary butyl hydroperoxide, TBOOH (a lipid peroxide prototype) (T cells), or H2O2 (H cells).
119 lenge with another type of peroxide, TBHP, a lipid peroxide prototype.
120 e than 2-fold elevation of the intracellular lipid peroxides, resulting in apoptosis.
121 tabolites, including adenosine, lactate, and lipid peroxides, such that energetically costly processe
122 urated fatty acids and lower accumulation of lipid peroxides than did wild-type seeds.
123 cantly less vitamin E and significantly more lipid peroxides than do livers of wild-type mice.
124  T1D and produces proinflammatory lipids and lipid peroxides that exacerbate beta-cell dysfunction an
125 karyotic cells where it reduces hydrogen and lipid peroxides to alcohols.
126 ndent of GPX4 regulation, but the ability of lipid peroxides to stimulate ferroptosis by modulating p
127            During ferroptosis, mitochondrial lipid peroxides trigger PRDX3 hyperoxidation, a posttran
128 e synthesis in cancer and are generated from lipid peroxides underlying the non-caspase-dependent for
129                    Reduction of pre-existing lipid peroxides using ebselen delayed HbLDL kinetics and
130 thione peroxidase 4 (GPX4), which detoxifies lipid peroxides using glutathione.
131         The levels of mitochondrial iron and lipid peroxides were also markedly increased in cardiomy
132                                LV myocardial lipid peroxides were greater (CIH, 1,258+/-703; HC 715+/
133                                              Lipid peroxides were increased in both septic patients (
134                                          The lipid peroxides were localized exclusively in the photor
135 gh levels of SO were higher (+44%); those of lipid peroxides were similar, and their reduction by alp
136 injury (e.g. chemokine transcript levels and lipid peroxides) were disproportionately increased in th
137 lation of oxidatively damaged phospholipids (lipid peroxides); when these lipid peroxides accumulate
138 roptosis, and protects cells by neutralizing lipid peroxides, which are by-products of cellular metab
139 zyme catalyzes the reduction of hydrogen and lipid peroxides, which limits the availability of these
140 ckout animals may be due to the formation of lipid peroxides, which serve as substrates for GPX-1.
141  infection also markedly increased levels of lipid peroxides within infected cells.
142 ion of GPX4 did not reduce the production of lipid peroxides within infected cells.
143 ophils induce iron-dependent accumulation of lipid peroxides within tumor cells by transferring myelo
144 ium, a cofactor of peroxidases that detoxify lipid peroxides, would inhibit atherosclerosis more effe

 
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