ライフサイエンスコーパス: oxygen radical

1 etal center, including rebound of a terminal oxygen radical.

2 der inert atmosphere, strongly implicate the oxygen radical.

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

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

5 ation and transplantation processes generate oxygen radicals.

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

7 hereby minimizing the formation of dangerous oxygen radicals.

8 lps protect cells against thermal injury and oxygen radicals.

9 cation of endogenous, metabolically produced oxygen radicals.

10 TLF does not kill trypanosomes by generating oxygen radicals.

11 le for trehalose in protecting cells against oxygen radicals.

12 , including a paradoxical protective role of oxygen radicals.

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

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

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

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

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

18 d and the consequent production of injurious oxygen radicals.

19 damage through increased production of toxic oxygen radicals.

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

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

22 oxidants reduced mitochondrial generation of oxygen radicals.

23 ation, which can be rescued by scavenging of oxygen radicals.

24 ubject to iron-mediated production of lethal oxygen radicals.

25 ge, iron leads to the formation of dangerous oxygen radicals.

26 cterial activities, including the release of oxygen radicals.

27 embled protein products from generating free oxygen radicals.

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

29 of ATP and a rapid increase in intracellular oxygen radicals.

30 aps to avoid creation of additional reactive oxygen radicals.

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

32 higher (p 0.05) antioxidant activity by the Oxygen Radical Absorbance Capacity (27 mM Trolox equival

33 gher (p <= 0.05) antioxidant activity by the Oxygen Radical Absorbance Capacity (27 mM Trolox equival

34 ioxidant capacities according to hydrophilic-oxygen radical absorbance capacity (H-ORAC(FL)) and ferr

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

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

37 sed on DPPH free radical savenging activity, oxygen radical absorbance capacity (ORAC) and beta-carot

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

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

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

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

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

43 The oxygen radical absorbance capacity (ORAC) assay confirme

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

45 The oxygen radical absorbance capacity (ORAC) assay indicate

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

47 y 2,2-diphenyl-1picrylhydrazyl (DPPH) assay, oxygen radical absorbance capacity (ORAC) assay, and fer

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

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

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

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

52 yl-1-picrylhydrazl radicals (DPPH) assay and oxygen radical absorbance capacity (ORAC) assay.

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

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

55 Ferric reducing antioxidant power (FRAP) and oxygen radical absorbance capacity (ORAC) assays.

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

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

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

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

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

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

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

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

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

65 Oxygen radical absorbance capacity (ORAC) values of sele

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

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

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

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

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

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

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

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

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

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

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

77 ity and phenolic content of saliva using the oxygen radical absorbance capacity and Folin-Ciocalteu a

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

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

80 The Oxygen radical absorbance capacity assay indicated 5 of

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

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

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

84 The oxygen radical absorbance capacity of Alcalase, chymotry

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

86 rom in vitro antioxidant assays (hydrophilic-oxygen radical absorbance capacity {H-ORAC(FL)} and ferr

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

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

89 Serum oxygen radical absorbance capacity, plasma protein carbo

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

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

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

93 An oxygen radical absorbing capacity assay confirmed its fr

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

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

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

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

98 lupulus (family Cannabaceae), utilizing the oxygen radical absorption capacity (ORAC) and ferric red

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

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

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

102 ucts is complex, initiated by regioselective oxygen radical addition to the carbon-carbon double bond

103 n peroxide reacts with iron to form reactive oxygen radicals after which oxidized iron is reduced by

104 A high level of free oxygen radicals and a low level of antioxidants were fou

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

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

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

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

109 Oxygen radicals and heme are released during proteolysis

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

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

112 Increases in oxygen radicals and lipid peroxidation and depletion of

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

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

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

116 Oxygen radicals and other activated oxygen species gener

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

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

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

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

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

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

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

124 tressors such as high salt, low pH, reactive oxygen radicals, and cell wall-targeting antibiotics, su

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

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

127 Oxygen radicals are generated when stigmatellin is added

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

129 Oxygen radicals are not generated when stigmatellin is a

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

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

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

133 itating the coupling kinetics of neighboring oxygen radicals at active sites.

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

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

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

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

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

139 the antioxidant capacity recovery, being the oxygen radical capacity of sole head and skin extracts s

140 quite common, but s-block compounds with an oxygen radical character remain rare.

141 the protein and cellular components through oxygen radical chemistry.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

159 IC-FPOMP generates reactive oxygen radicals from various precursors (TiO(2) nanopart

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

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

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

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

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

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

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

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

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

169 Oxygen radical generation was directly measured as dichl

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

188 , a well-known anti-aging element to capture oxygen-radicals in the human body, showing an "anti-agin

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

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

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

192 H(2)O(2), and (ii) elicited spontaneous and oxygen radical-induced rifampin-resistance (Rif(r)) muta

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

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

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

196 Terminal oxygen radicals involving p- and d-block atoms are quite

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

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

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

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

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

202 a cell death pathway exerted by an iron and oxygen-radical-mediated peroxidation of phospholipids co

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

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

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

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

207 t absorption studies reveal that the neutral oxygen radical (O(*)) is indeed an extraordinarily stron

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

209 n therapy, including the generation of toxic oxygen radicals or attenuation of endogenous protection

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

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

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

213 he inhibition of mouse platelet aggregation, oxygen radical output, and thrombus formation, and carot

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

215 It has been observed that oxygen radicals produced at a high cathodic voltage can

216 Reactive oxygen radicals produced by cytochrome P450 and the nico

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

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

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

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

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

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

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

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

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

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

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

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

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

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

231 Oxygen radical production was measured using the oxidant

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

233 % decrement in complex I activity, increased oxygen radical production, and increased susceptibility

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

235 -2-dependent activation of 6-OHDA oxidation, oxygen radical production, oxidative stress, and cytotox

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

237 e after transplantation because of decreased oxygen radical production.

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

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

240 almost completely blocked kainate-triggered oxygen radical production.

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

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

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

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

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

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

247 rough acid catalyzed transetherification and oxygen-radical reactions.

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

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

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

251 ion of these approaches is that the reactive oxygen radicals (ROS) generated at metal surfaces also d

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

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

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

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

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

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

258 The oxygen radical scavenger, N-acetylcysteine (NAC), attenu

259 anine cancer cells were pre-treated with the oxygen radical scavenger, N-acetylcysteine, the NKA inhi

260 led to the conclusion that it is a powerful oxygen radical scavenger, partially contributed by its m

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

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

263 Oxygen radical scavengers and calcium channel blockers h

264 These effects could be blocked by oxygen radical scavengers.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

280 ree filtrates occurred via reaction with the oxygen radical superoxide produced by soluble extracellu

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

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

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

284 mo, had significantly higher levels of free oxygen radicals than those prepared with rhTSH.

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

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

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

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

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

290 The natural product, plumbagin increases oxygen radicals through inhibition of oxidative phosphor

291 ular oxygen and the consumption of generated oxygen radicals, thus boosting the generation of halogen

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

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

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

295 d 2-related factor, quinone reductase-2, and oxygen radical trapping) and then in experiments of incr

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

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

298 Metabolism generates oxygen radicals, which contribute to oncogenic mutations

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

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