ライフサイエンスコーパス: oxygen radical

1 der inert atmosphere, strongly implicate the oxygen radical.

2 respectively) CYP2E1, a potent generator of oxygen radicals.

3 ation and transplantation processes generate oxygen radicals.

4 enerates microbicidal (and pro-inflammatory) oxygen radicals.

5 hereby minimizing the formation of dangerous oxygen radicals.

6 lps protect cells against thermal injury and oxygen radicals.

7 cation of endogenous, metabolically produced oxygen radicals.

8 TLF does not kill trypanosomes by generating oxygen radicals.

9 le for trehalose in protecting cells against oxygen radicals.

10 , including a paradoxical protective role of oxygen radicals.

11 adykinin may be related to the production of oxygen radicals.

12 releases adenosine, bradykinin, opioids, and oxygen radicals.

13 ide synthase, could affect the generation of oxygen radicals.

14 otential and a 2-3-fold increase in reactive oxygen radicals.

15 s thought to occur through the generation of oxygen radicals.

16 d and the consequent production of injurious oxygen radicals.

17 damage through increased production of toxic oxygen radicals.

18 the ability of XDH to catalyze production of oxygen radicals.

19 des convert molecular oxygen to DNA-cleaving oxygen radicals.

20 oxidants reduced mitochondrial generation of oxygen radicals.

21 embled protein products from generating free oxygen radicals.

22 an overview of how S. pneumoniae copes with oxygen radicals.

23 aps to avoid creation of additional reactive oxygen radicals.

24 tases (SODs), enzymes capable of detoxifying oxygen radicals.

25 as well as its contribution to resistance to oxygen radicals.

26 ntiradical activity (DPPH) (95.4+/-0.3%) and oxygen radical absorbance capacity (ORAC) (0.82+/-0.07g

27 eptidyl peptidase IV (DPP-IV) inhibitory and oxygen radical absorbance capacity (ORAC) activities.

28 Antioxidant capacity was measured by Oxygen Radical Absorbance Capacity (ORAC) and Folin Cioc

29 ), ferric reducing antioxidant power (FRAP), oxygen radical absorbance capacity (ORAC) and Folin-Cioc

30 Antioxidant capacity measured as oxygen radical absorbance capacity (ORAC) and lipid pero

31 A linear relationship was observed between oxygen radical absorbance capacity (ORAC) and total mono

32 hytosteryl sinapates was observed using both oxygen radical absorbance capacity (ORAC) assay and cook

33 The oxygen radical absorbance capacity (ORAC) assay has been

34 The oxygen radical absorbance capacity (ORAC) assay indicate

35 xidant activity for Malbec GPE determined by oxygen radical absorbance capacity (ORAC) assay was 2,75

36 The oxygen radical absorbance capacity (ORAC) assay, frequen

37 By using the oxygen radical absorbance capacity (ORAC) assay, the oxy

38 This protocol describes the oxygen radical absorbance capacity (ORAC) assay, which m

39 luated for their antioxidant activity by the Oxygen Radical Absorbance Capacity (ORAC) assay.

40 n G was also demonstrated in vitro using the oxygen radical absorbance capacity (ORAC) assay.

41 ferric-reducing antioxidant power (FRAP) and oxygen radical absorbance capacity (ORAC) assays with a

42 g power (RP), antiradical activity (DPPH) or oxygen radical absorbance capacity (ORAC) assays.

43 ferric reducing antioxidant power (FRAP) and oxygen radical absorbance capacity (ORAC) compared to th

44 y HPLC and the total antioxidant capacity by Oxygen Radical Absorbance Capacity (ORAC) methods.

45 After simulated enzymatic digestion, the oxygen radical absorbance capacity (ORAC) of CPH obtaine

46 The oxygen radical absorbance capacity (ORAC) of the hydroly

47 The oxygen radical absorbance capacity (ORAC) of the obtaine

48 ts and diets supplemented with foods high in oxygen radical absorbance capacity (ORAC) reverse age-re

49 A significantly higher oxygen radical absorbance capacity (ORAC) value was obta

50 The Oxygen Radical Absorbance Capacity (ORAC) values for NaC

51 Oxygen radical absorbance capacity (ORAC) values of sele

52 ing plasma antioxidant capacity, measured as oxygen radical absorbance capacity (ORAC), and alpha-toc

53 ys, 2,2-diphenyl-1-picrylhydrazyl (DPPH) and Oxygen radical absorbance capacity (ORAC), and biologica

54 ric reducing/antioxidant power (FRAP) assay, oxygen radical absorbance capacity (ORAC), and total ant

55 mature calamondin peel exhibited the highest oxygen radical absorbance capacity (ORAC), reducing powe

56 ), ferric reducing antioxidant power (FRAP), oxygen radical absorbance capacity (ORAC), total phenoli

57 n that the Trp residue contributes to a high oxygen radical absorbance capacity (ORAC).

58 razyl (DPPH) radical scavenging activity and oxygen radical absorbance capacity (ORAC).

59 Ferric reducing antioxidant power (FRAP) and Oxygen radical absorbance capacity (ORAC)] and antioxida

60 ation regimens significantly increased serum oxygen radical absorbance capacity (P < 0.001) and LDL l

61 roxidation, anti-AAPH-induced hemolysis, and oxygen radical absorbance capacity activity.

62 quercetin derivatives, exhibited the highest oxygen radical absorbance capacity and effectively inhib

63 e by Trolox equivalent antioxidant capacity, oxygen radical absorbance capacity and nitric oxide scav

64 Antioxidant activity was measured by an oxygen radical absorbance capacity assay and against LDL

65 The Oxygen radical absorbance capacity assay indicated 5 of

66 using a database of foods analyzed with the oxygen radical absorbance capacity assay.

67 ape skin extracts were evaluated by using an oxygen radical absorbance capacity method (ORAC).

68 a database of common foods analysed with the oxygen radical absorbance capacity method.

69 The oxygen radical absorbance capacity of Alcalase, chymotry

70 Serum total antioxidant capacity measured by oxygen radical absorbance capacity was approximately 4%

71 PH (2,2-diphenyl-1-picrylhydrazyl) and ORAC (oxygen radical absorbance capacity) assays.

72 egetable intake or total antioxidant intake (oxygen radical absorbance capacity).

73 Serum oxygen radical absorbance capacity, plasma protein carbo

74 The oxygen-radical absorbance capacity (ORAC) assay has beco

75 itamin C, but not vitamin E, increased serum oxygen-radical absorbance capacity (P = 0.01).

76 londialdehyde + 4-hydroxyalkenals, and serum oxygen-radical absorbance capacity.

77 An oxygen radical absorbing capacity assay confirmed its fr

78 in and intervention, mean (95% CI) change in oxygen radical-absorbing capacity (U/mL) was -35 (-93, 1

79 (albumin, cholesterol, body mass index, and oxygen radical-absorbing capacity).

80 Serum oxygen radical-absorbing capacity, malondialdehyde (an i

81 sterol or albumin, body mass index, or serum oxygen radical-absorbing capacity.

82 All oat varieties had very similar oxygen radical absorption capacity compared with other w

83 s manifested by increased intracellular free oxygen radical accumulation and proportional changes in

84 rgy-dependent facets of cell death, blocking oxygen radical accumulation.

85 ction of CYP1A1 appears to lead to a leak of oxygen radicals and consequent oxidative DNA damage that

86 uene blocked the toxin A-induced increase in oxygen radicals and diminished cell rounding.

87 ssion appears to block production of harmful oxygen radicals and does not act directly or indirectly

88 nsequently display higher levels of reactive oxygen radicals and ERK1/2 phosphorylation following act

89 Oxygen radicals and heme are released during proteolysis

90 velopment by protecting tissues against free oxygen radicals and inhibiting cell proliferation, but o

91 iated with a decrease in reperfusion-induced oxygen radicals and inhibition of mitochondrial swelling

92 Increases in oxygen radicals and lipid peroxidation and depletion of

93 to resist intraphagosomal stresses, such as oxygen radicals and low pH, is critical for its persiste

94 Oxygen radicals and NO are likely to interact at the car

95 fected macrophages may enhance production of oxygen radicals and NO at sites of infection.

96 Oxygen radicals and other activated oxygen species gener

97 HA and toluene also correlate with those for oxygen radicals and other oxidants.

98 neration harmful byproducts such as reactive oxygen radicals and production of inflammatory cytokines

99 n the cellular steady-state concentration of oxygen radicals and that the greater effectiveness in p2

100 Citral increases intracellular oxygen radicals and this leads to activation of p53.

101 eptide polymyxin B and reactive nitrogen and oxygen radicals and to grow in acidic medium (pH 5.0).

102 otoxicity in brain involves the formation of oxygen radicals, and a decrease in intracellular levels

103 hondria are the main intracellular source of oxygen radicals, and based on the recently documented pr

104 e of the pancreatic tumor cells to thrombin, oxygen radicals, and trypsin, suggesting that common cel

105 This study determines whether oxygen radicals are generated in the mesenteric microvas

106 Oxygen radicals are generated when stigmatellin is added

107 Diminished ATP concentrations and increased oxygen radicals are likely to contribute to cytotoxicity

108 Oxygen radicals are not generated when stigmatellin is a

109 bility of heme-protein complexes to generate oxygen radicals, are consistent with HO-2, like five oth

110 mechanism of stunning involves generation of oxygen radicals as well as alteration in calcium homeost

111 significant reduction in the accumulation of oxygen radicals associated with this insult.

112 This intermediate had been described as an oxygen-radical bound to the trinuclear copper cluster wi

113 henotypes are due to a buildup of diffusible oxygen radicals brought on by the absence of cytochrome

114 protects organisms from potentially damaging oxygen radicals by catalyzing the disproportionation of

115 l formation of the teratogen acetaldehyde or oxygen radicals by fetal ethanol-oxidizing enzymes.

116 These oxygen radicals can explain the reactive nature of the s

117 the protein and cellular components through oxygen radical chemistry.

118 d the presence of IgG aggregates modified by oxygen radicals (chlorinated IgG [Cl-IgG]) and peroxynit

119 technique revealed the formation of a stable oxygen radical-containing transformation product resulti

120 Recent studies suggest that oxygen radicals contribute to the enhanced basal vascula

121 tive damage of DNA by endogenously generated oxygen radicals contributes to the mutagenic process.

122 nally, protein carbonyl content, a marker of oxygen radical damage, was decreased in Snell dwarfs.

123 ium, the trehalose content and resistance to oxygen radicals decreased rapidly.

124 y, we have examined the effects of aging and oxygen radical-dependent oxidation on the hydrophobicity

125 viously uncharacterized coordination between oxygen radical detoxification and thiol homeostasis is r

126 For the latter part, the oxygen radicals did not affect Bak oligomerization but i

127 ells from the mitogenic and toxic effects of oxygen radicals, did not reveal any mutations.

128 Spin density analyses reveal oxygen radical, diradical, and superoxide characters in

129 as oxidative phosphorylation, generation of oxygen radicals, dynamic morphological rearrangements, c

130 istatin-5-provoked yeast cell death in which oxygen radical formation is the ultimate and essential s

131 ew intracellular lipid signal that regulates oxygen-radical formation in neutrophils, a key response

132 The amount of oxygen radical formed is proportional to the amount of s

133 ion does not appear to involve a more potent oxygen radical formed upon metal-catalyzed oxidation.

134 man pathogen that regularly encounters toxic oxygen radicals from the atmosphere and from the host me

135 ts (BNNSs) is achieved by the solution-phase oxygen radical functionalization of boron atoms in the h

136 These data indicate that oxygen radicals generated by NADPH oxidase may contribut

137 hus suggesting that extracellular sources of oxygen radicals generated by plasma membrane reductases

138 y important in opposing the toxicity of free oxygen radicals generated by various pathogens, includin

139 Gas phase treatment of MoS2 with oxygen radicals generated in an upstream N2 -O2 plasma i

140 ormation of oxygen radicals in vivo; and (2) oxygen radicals, generated by the enzyme xanthine oxidas

141 ng pathway from death receptor engagement to oxygen radical generation and determined the mechanism b

142 al stresses, including exposure to methanol, oxygen radical generation by paraquat, high salt concent

143 als; at lower concentrations of L1 increased oxygen radical generation occurs.

144 Oxygen radical generation was directly measured as dichl

145 ic availability of iron for participation in oxygen radical generation.

146 rship after exposure to adriamycin, a potent oxygen radical generator.

147 dopamine and related compounds, rather than oxygen radicals have the ability to inhibit the proteaso

148 not influence the capacity of AA to generate oxygen radicals in a cell-free solution or the increase

149 omatous disease (X-CGD) to study the role of oxygen radicals in apoptosis.

150 tress such as exposure to toxic compounds or oxygen radicals in bacteria.

151 mpounds stimulate the production of reactive oxygen radicals in bacteria.

152 present study, we explored the role of free oxygen radicals in LacCer-mediated induction of cell pro

153 g recognition of the damaging role played by oxygen radicals in mediating necrotic neuronal injury.

154 nsmitter analogue, which generates cytolytic oxygen radicals in neuroblastoma cells that take it up.

155 to release both protective NO or deleterious oxygen radicals in normal and disease settings, respecti

156 her demonstrating the lack of involvement of oxygen radicals in proteasomal inhibition.

157 etic hyperactivity after MI in mice and that oxygen radicals in the brain may be important new target

158 M-1 and by inducing the accumulation of free oxygen radicals in the chondrocyte cytoplasm.

159 ase (SOD) were studied to assess the role of oxygen radicals in the mechanism of action of 2'-NH2-MPT

160 Evidence has accumulated for a role of toxic oxygen radicals in the pathogenesis of ischemia-reperfus

161 ts are useful tools for studying the role of oxygen radicals in the pathogenesis of neuronal death af

162 1) METH treatment increases the formation of oxygen radicals in vivo; and (2) oxygen radicals, genera

163 rome P450 together generate acetaldehyde and oxygen radicals including the hydroxyl radical (HO.).

164 ation by hematoxylin-eosin staining, and for oxygen radical-induced lipid peroxidation by malondialde

165 ndogenous genotoxic product of enzymatic and oxygen radical-induced lipid peroxidation whose adducts

166 e deficient in the generation of nitrogen or oxygen radicals (inducible NO synthase 2 or gp91(phox) g

167 propose an atomistic mechanism in which the oxygen radical initiates the etching process.

168 binding site on Ca(2+)-ATPase is involved in oxygen radical injury, SR vesicles containing bound Ca(2

169 ils that have been activated by ANCA release oxygen radicals, lytic enzymes, and inflammatory cytokin

170 BHA), indicating that the generation of free oxygen radicals may be responsible for inducing cell dea

171 pathogenicity, protecting Salmonella against oxygen radical-mediated host defences.

172 Increased expression of MnSOD can diminish oxygen radical-mediated injuries and the cytotoxic effec

173 Transepithelial PRK causes oxygen radical-mediated lipid peroxidation on the superf

174 an important, yet unknown feature of airway oxygen radical metabolism.

175 ansduction pathways as well as to changes in oxygen radical metabolism.

176 Pathophysiological levels of oxygen radical metabolites have been studied as indicato

177 was not associated with production of toxic oxygen radicals, nitric oxide, or the restriction of int

178 n interactions between nitric oxide and free oxygen radicals on the other, might help determine a per

179 digm of having canonical enzymes to detoxify oxygen radicals or homologues of typical oxidative stres

180 uction of nitric oxide, prostaglandin E2, or oxygen radicals or the release of interleukin-1beta, tum

181 nted by inhibitors of protein kinase C, free oxygen radicals, or AA metabolic pathways.

182 Taken together, these data suggest that oxygen radicals, possibly generated by mitochondria, pla

183 Reactive oxygen radicals produced by cytochrome P450 and the nico

184 Mitochondrial DNA is exposed to oxygen radicals produced during oxidative phosphorylatio

185 Our previous studies have indicated that oxygen radicals, produced during reoxygenation following

186 ly oxidized LDL generated by incubation with oxygen radical-producing xanthine/xanthine oxidase (X/XO

187 Oxidized ATP also inhibited oxygen radical production and activation of NF-kappaB an

188 These data indicate that oxygen radical production and lung injury in response to

189 dose-related impairment of stimulus-induced oxygen radical production and of phagocytic killing.

190 pendent on IFN-gamma activation and reactive oxygen radical production by activated macrophages after

191 s iNOS and gp91-phox, thereby decreasing net oxygen radical production by means of negative feedback.

192 icated that NO(radical) affected the rate of oxygen radical production by modulating the rate of O(2)

193 ls expressed on GABAergic neurons results in oxygen radical production comparable to that triggered b

194 es galectin-3, abrogating its stimulation of oxygen radical production in human neutrophils and incre

195 t of NMDA, kainate, and high K+ exposures on oxygen radical production paralleled the effect of these

196 etween high glucose utilization and elevated oxygen radical production was also observed in vitro by

197 to the mitochondria and that the majority of oxygen radical production was dependent on Bid.

198 Oxygen radical production was measured using the oxidant

199 ilization may increase longevity by reducing oxygen radical production, a potential cause of aging.

200 % decrement in complex I activity, increased oxygen radical production, and increased susceptibility

201 NAD(P)H oxidase, though a major source of oxygen radical production, is not the oxygen sensor in m

202 -2-dependent activation of 6-OHDA oxidation, oxygen radical production, oxidative stress, and cytotox

203 hotodynamic therapy are thought to result in oxygen radical production.

204 e after transplantation because of decreased oxygen radical production.

205 drial Ca2+ overload and consequent injurious oxygen radical production.

206 tudies have not found evidence of comparable oxygen radical production.

207 almost completely blocked kainate-triggered oxygen radical production.

208 ot have any effect on TNF-alpha secretion or oxygen radicals production in U937 cells.

209 ent increases TNF-alpha secretion, increases oxygen radicals production, and lowers cAMP levels in U9

210 of CT-1 seem to be mediated by reduction in oxygen-radical production, increased superoxide dismutas

211 to injure pulmonary endothelium by releasing oxygen radicals, proteases, and proinflammatory cytokine

212 d to precipitate this Mn, photosystem II and oxygen radical protection mechanisms must have evolved b

213 ribution based upon (a) steric demand in the oxygen-radical reaction and (b) the influence of substit

214 rough acid catalyzed transetherification and oxygen-radical reactions.

215 Lytic enzymes and oxygen radicals released by PMN are important in clearin

216 ctivates the drug to produce highly reactive oxygen radicals, resulting in local cell and tissue dama

217 of apoptosis through generation of reactive oxygen radicals (ROR).

218 Because Cu(2+) facilitates formation of oxygen radicals (ROS) which inhibit pyruvate dehydrogena

219 t N-(2-mercaptopropionyl)-glycine and by the oxygen radical scavenger 2-acetamidoacrylic acid.

220 Cotreatment of cells with the oxygen radical scavenger dimethyl sulfoxide significantl

221 The addition of oxygen radical scavenger enzymes (catalase, superoxide d

222 LPS or IL-1beta, an effect inhibited by the oxygen radical scavenger PDTC.

223 canoylphorbol-13-acetate , is blocked by the oxygen radical scavenger pyrrolidine dithiocarbomate.

224 ron chelator, or 1,3-dimethyl-2-thiourea, an oxygen radical scavenger, prior to addition of H(2)O(2)

225 In HC animals, tissue endogenous oxygen radical scavengers and antioxidant vitamins were

226 Oxygen radical scavengers and calcium channel blockers h

227 These effects could be blocked by oxygen radical scavengers.

228 L was generated in the presence of different oxygen radical scavengers.

229 ected by nitric oxide synthase inhibitors or oxygen radical scavengers.

230 adical absorbance capacity (ORAC) assay, the oxygen radical scavenging ability of the SWCNT antioxida

231 sugar content, total phenolic content (TPC), oxygen radical scavenging absorbance capacity (ORAC), hy

232 The oxygen radical scavenging capacity (ORAC) was the highes

233 es exhibited higher DPPH radical-scavenging, oxygen radical-scavenging capacity (ORAC) and ferric red

234 and endothelial damage are prevented by the oxygen-radical-scavenging enzyme superoxide dismutase.

235 us and cell killing was explored by using an oxygen radical sensitive probe (dihydroethidium).

236 otic lesions may activate a broad cascade of oxygen radical-sensitive signaling pathways affecting ap

237 the surface density of catalytically active oxygen radical sites on a MoVTeNb oxide (M1 phase) catal

238 It causes increased cellular production of oxygen radical species and selectively decreases mitocho

239 nalized water-soluble fullerene that reduces oxygen radical species associated with neurodegeneration

240 Recently, oxygen radical species have been implicated in the proce

241 se, and matrix metalloproteinases (MMPs) and oxygen radical species, which damage alveolar-capillary

242 Because short-lived reactive oxygen radicals such as superoxide have been implicated

243 It is postulated that oxygen radicals, superoxide in particular, are involved

244 Abnormalities of nitric oxide (NO) and oxygen radical synthesis and of oxygen consumption have

245 TNF alpha-treated hepatocytes generated more oxygen radicals than did controls.

246 halose was much more sensitive to killing by oxygen radicals than wild-type cells.

247 o the generation of reactive metabolites and oxygen radicals that can readily adduct DNA, lipids, and

248 ght, MLu facilitates production of cytotoxic oxygen radicals that mediate apoptosis.

249 such as cytokine withdrawal or generation of oxygen radicals, that culminates in mitochondrial dysfun

250 s of Sod1 beyond protection of the cell from oxygen radicals, the involvement of this protein in copp

251 related to the receptor-mediated release of oxygen radicals to inactivate nitric oxide.

252 veness to jasmonic acid and paraquat-induced oxygen radicals to mutant plants.

253 ations and other factors which might enhance oxygen radical toxicity.

254 -alpha or anti-Fas antibody-induced burst of oxygen radicals was mainly derived from the mitochondria

255 was not decreased by anoxia, suggesting that oxygen radicals were not involved.

256 Metabolism generates oxygen radicals, which contribute to oncogenic mutations

257 iggered mechanism includes the generation of oxygen radicals, which in turn stimulate tumor necrosis

258 in may be due to increased susceptibility to oxygen radicals within macrophages; and (iii) other anti