ライフサイエンスコーパス: Fenton

1 Fenton chemistry techniques were employed to identify th

2 Fenton reactions (Fe(2+)/Fe(3+) plus H2O2) were used for

3 Fenton reagent (Fe(II)/H2O2) oxidized PEO by the same ro

4 Fenton systems are interesting alternatives to advanced

5 Fenton's reagent oxidations were more specific for guani

6 d oxidation processes (AOP) was studied: (1) Fenton treatment using H2O2 with dissolved iron salts an

7 lobin heme iron could potentially serve as a Fenton reagent for the intracellular generation of hydro

8 eversible inactivation of ISPNAP occurs by a Fenton-type reaction which forms a strong oxidizing agen

9 at H(2)O(2) rapidly oxidizes this metal in a Fenton reaction.

10 tered and O-centered radicals generated in a Fenton-like fashion.

11 ol to the nucleus where it participates in a Fenton-like reaction that results in the production of h

12 oxidized their solvent-exposed clusters in a Fenton-like reaction.

13 es in dental caries by taking advantage of a Fenton reaction which requires metal ions such as iron o

14 ) generation for cancer therapy, based on a Fenton-like reaction between linoleic acid hydroperoxide

15 ron(V)-oxo-hydroxo species, in parallel to a Fenton-type process where hydroxyl radicals are formed.

16 submillimolar levels of H2O2 may be due to a Fenton-type reaction between H2O2 and intracellular iron

17 cuit in a 2-dimensional tissue strip using a Fenton-Karma model of cardiac tissue.

18 oxide and the combination, consistent with a Fenton chemical mechanism of pathophysiology, and this s

19 maged DNA generated from treating DNA with a Fenton-type reactive oxygen-generating system and is kno

20 comparison to conventional (purely abiotic) Fenton reactions, the microbially driven Fenton reaction

21 , it has been examined to what extent adding Fenton reaction promoting Fe impacted the toxicity of an

22 (AA) of 25 free L-amino acids (FAA) against Fenton system-mediated hydroxyl radical (HO(*)) producti

23 ding not only synchrotron radiation but also Fenton reactions involving chelated iron, have become an

24 3,4-DHPEA-EDA was oxidised by enzymatic and Fenton reactions.

25 atible with the recent proposal by Kubie and Fenton (2009) that navigation primarily depends on headi

26 d by two oxidants, catechol/Cu(2+)/NADPH and Fenton's reagent, were located and compared.

27 uted to sickle hemoglobin auto-oxidation and Fenton chemistry reactions catalyzed by denatured heme m

28 generation from polychlorinated phenols and Fenton system.

29 Exposure of isolated DNA to X/gamma-rays and Fenton reagents was shown to lead to the formation of in

30 ins that are carbonylated in a receptor- and Fenton reaction-dependent manner, including annexin A1,

31 between 2 and 4 V, using acid treatment and Fenton's reagent, and combined with differential electro

32 density and the potential elimination of any Fenton-type process involving exposed iron ions culminat

33 O2 or UV irradiation to regenerate Fe(II) as Fenton reagents.

34 onols quercetin and kaempferol on iron-based Fenton reaction were documented.

35 sed by ionizing radiation and that caused by Fenton reactions.

36 lting increase in .OH formation generated by Fenton chemistry is responsible for the observed enhance

37 ensitivity to hydroxyl radicals generated by Fenton chemistry.

38 uced injury to that thought to be induced by Fenton reactions.

39 mCG-->TT tandem double mutations induced by Fenton-type reagents.

40 , thus avoiding oxidative damage mediated by Fenton chemistry.

41 The latter is mediated by Fenton reaction and prevents H2O2 accumulation.

42 he degradation of the three TeCPs and PCP by Fenton reagents, and the type and yield of which were fo

43 ing deprivation of the epidermal Trp pool by Fenton chemistry.

44 the likely production of hydroxyl radical by Fenton chemistry with concomitant formation of AP sites

45 nuates the production of hydroxyl radical by Fenton chemistry.

46 he influence of pore size on regeneration by Fenton oxidation for carbon materials with adsorbed meth

47 data point to depletion of epidermal Trp by Fenton chemistry and exclude melatonin as a relevant con

48 Iron-catalysed Fenton chemistry constitutes one mechanism of production

49 An accelerated catalytic Fenton (ACF) reaction was developed based upon a multica

50 ligosaccharides prepared by Cu(2+)-catalyzed Fenton-type and photochemical depolymerization.

51 (50) 53 muM), inhibiting the Cu(I)-catalyzed Fenton reaction at lower concentrations than GSH, ascorb

52 tion was OH., generated by a Cu(I)-catalyzed Fenton reaction.

53 Analogue 1c inhibited the Fe(II)-catalyzed Fenton reaction at about the same concentrations as asco

54 conclusion that increased levels of cellular Fenton chemistry played a role in the growth defects.

55 etter than other antioxidants in a chemical (Fenton reaction) system and neuronal cultures.

56 roxyl radical (OH(.)) generated in classical Fenton chemistry or spontaneous decomposition of peroxyn

57 In conclusion, Fenton-like conditions with low Fe(3+) concentrations an

58 s one of the major drawbacks of conventional Fenton processes.

59 H) species, followed by site-specific copper Fenton chemistry.

60 ctrons to free iron and drove a DNA-damaging Fenton system in vitro.

61 ial catalase and suppression of the damaging Fenton reaction.

62 ion of free cysteine that fuels the damaging Fenton reaction.

63 g force, which serves to inhibit deleterious Fenton chemistry.

64 tely cleaves DNA via a trace metal-dependent Fenton reaction.

65 ould be involved in avoiding metal-dependent Fenton reactions when photooxidation causes disassembly

66 n reductase, and these reduced flavins drive Fenton chemistry by transferring electrons to free iron.

67 ar whether flavins or other reductants drive Fenton chemistry in respiring cells.

68 rformance of BPA oxidation in an EDDS-driven Fenton reaction was found to be much higher at near neut

69 intermediates during the microbially driven Fenton degradation of 1,4-dioxane, an indication that co

70 ion that conventional and microbially driven Fenton degradation processes follow similar reaction pat

71 The microbially driven Fenton reaction completely degraded 1,4-dioxane (10 mM i

72 ic) Fenton reactions, the microbially driven Fenton reaction operated at circumneutral pH and did not

73 The microbially driven Fenton reaction provides the foundation for development

74 In the present study, a microbially driven Fenton reaction was designed to autocatalytically genera

75 croM Fe+3-EDTA to insure optimum O2-.-driven Fenton chemistry, NO enhanced modestly HX/xanthine oxida

76 ctive at inhibiting this classic O2-.-driven Fenton reaction.

77 oil environments based on a reductant-driven Fenton's reaction.

78 the biologically relevant superoxide-driven Fenton reaction.

79 ogen peroxide to the hydroxyl radical (i.e., Fenton chemistry), than are ligands of lower denticity.

80 ton exhibited higher efficiency than UV-EDDS-Fenton in the removal of acid extractable organic fracti

81 Both UV-NTA-Fenton and UV-EDDS-Fenton processes presented promoting effect on the acute

82 An electro-Fenton-based method was used to promote the regeneration

83 f the adsorbent material, this novel electro-Fenton approach could constitute an excellent alternativ

84 identified intermediates during the electro-Fenton oxidation process of the selected CECs.

85 ion and nature of toxicity along the electro-Fenton oxidative degradation of three representative CEC

86 In this work, we develop the electro-Fenton reaction as a means to generate hydroxyl radicals

87 The electro-Fenton treatment of sulfachloropyridazine (SCP), a model

88 a sequential combination of EC with electro-Fenton (EF) as post-treatment process was proposed.

89 n, a model protein, was labeled with electro-Fenton generated hydroxyl radicals and top-down proteomi

90 f hydroxyl radicals arises from an exogenous Fenton reaction and may stay either partially trapped on

91 'Fast Fenton' footprinting is a laboratory-based method for ti

92 A using a combination of time-resolved "Fast Fenton" hydroxyl radical footprinting and exhaustive kin

93 e cells from the medium is not available for Fenton chemistry, but is available for reconstitution of

94 from proteins and can act as a catalyst for Fenton chemistry to produce cytotoxic reactive oxygen sp

95 Fe(III) or Cu(II), setting up conditions for Fenton-type chemistry.

96 The pathway for Fenton-like systems driven by 1,2-DHBs with EDGs depends

97 re consistent with a biodegradative role for Fenton chemistry in which Fe(II) and H(2)O(2) react to f

98 ticipation of hydroxyl radicals derived from Fenton-like reaction mechanisms.

99 ability of purified YggX to protect DNA from Fenton chemistry mediated damage in vitro and to decreas

100 ases the amount of .OH radical produced from Fenton chemistry whereas the ferroxidase site mutant 222

101 atalyzed production of hydroxyl radical from Fenton chemistry is greatly attenuated in the presence o

102 reactivity to produce hydroxyl radicals from Fenton-like reaction mixtures containing hydrogen peroxi

103 and molecular oxygen, and thereby generating Fenton chemistry reagents.

104 ion of free iron necessary for the genotoxic Fenton reaction.

105 the alachlor degradation in the Fe(III)/H2O2 Fenton oxidation system.

106 environmental benignity of PCA/Fe(III)/H2O2 Fenton system.

107 and 500 degrees C was modified using H3PO4, Fenton-like reaction, (NH4)2S2O8 with H2SO4 and HNO3 wit

108 h dissolved iron salts and (2) heterogeneous Fenton-like oxidation with Fe immobilized on the zeolite

109 2 nm particle size, to promote heterogeneous Fenton-like reactions for the removal of nalidixic acid

110 and oxygen concentration on the homogeneous Fenton degradation of bisphenol A (BPA) used as a model

111 N'-disuccinic acid (EDDS) in the homogeneous Fenton process.

112 The homogeneous Fenton-like oxidation of organic substrates in water wit

113 aerobic biodegradation, alkaline hydrolysis, Fenton-like degradation, debromination by Zn(0) and redu

114 ork, dG was oxidized by HO(*) via the Fe(II)-Fenton reaction or by X-ray radiolysis of water.

115 N-formylkynurenine and kynurenine, implying Fenton chemistry in the cascade (n=10).

116 In Fenton-like reactions driven by 1,2-DHBs with EWGs, the

117 obably due to the participation of copper in Fenton-like chemistry.

118 Such species might engage in Fenton chemistry to generate reactive oxygen species.

119 nd their ability to inhibit .OH formation in Fenton reactions was quantified by ESR measurements.

120 age induced by hydroxyl radical generated in Fenton reaction.

121 ge and by consuming constituents involved in Fenton chemistry.

122 s releases Fe(II) ions, which participate in Fenton chemistry that damages DNA.

123 and hence may be available to participate in Fenton-driven free radical generation in conjunction wit

124 for the oxidative C-H bond cleavage step in Fenton-like hydrocarbon hydroxylation.

125 drial Fe-S containing enzymes, and increased Fenton-mediated free radical production.

126 resides in the protein's ability to inhibit Fenton chemistry as found for Dps proteins has never bee

127 high molecular weight melanoidins to inhibit Fenton induced hydroxyl degradation of deoxyribose was o

128 Compound 7A inhibited Fenton reaction better than EDTA, IC50 of 37 vs 54 muM,

129 of transition metal ions that could initiate Fenton-like reactions.

130 The damage to DNA was shown to involve Fenton chemistry.

131 important relationship between O2 and iron (Fenton chemistry) a study was undertaken to characterize

132 ive stress by sequestering iron and limiting Fenton-catalyzed oxyradical formation.

133 tivity protects DNA and proteins by limiting Fenton chemistry, but it interferes with the ability of

134 by the presence of O2 during Fe(2+)-mediated Fenton reactions when H2O2 is in excess.

135 gs provide support for biologically mediated Fenton chemistry in the root zones of desert grasses, an

136 y sensitive to nicking via the Fe2+-mediated Fenton reaction.

137 icity and does not result from iron-mediated Fenton chemistry, since cells remain sensitive to Mn dur

138 Nicking of duplex DNA by the iron-mediated Fenton reaction occurs preferentially at a limited numbe

139 Damage by iron-mediated Fenton reactions under aerobic or anaerobic conditions t

140 non-enzymatically, likely via iron-mediated Fenton-chemistry, at levels supporting in vitro catalysi

141 at with the more intensive oxidation method (Fenton < (NH4)2S2O8 with H2SO4 < HNO3 with H2O2) the con

142 g that FeS2 dissolution can act as a natural Fenton reagent, influencing the oxidation of third-party

143 ed by myeloperoxidase and is linked to a non-Fenton oxidative event marked by POBN(.).

144 species, which are required for nonenzymatic Fenton-based decomposition of soil organic matter.

145 and II ionic species, and superoxide but not Fenton reaction generated hydroxyl radicals, are importa

146 alachlor degradation mechanism in this novel Fenton oxidation system.

147 , 48.7%, and 54.6%, correspondingly) and NTA-Fenton (69.6%, 35.3%, and 44.2%, correspondingly) proces

148 Both UV-NTA-Fenton and UV-EDDS-Fenton processes presented promoting

149 Under optimum conditions, UV-NTA-Fenton exhibited higher efficiency than UV-EDDS-Fenton i

150 aphthenic acids (NAs) removals in the UV-NTA-Fenton process (98.4%, 86.0%, and 81.0% for classical NA

151 therefore not the reason for acceleration of Fenton chemistry.

152 2)O(2) results in significant attenuation of Fenton chemistry.

153 nitration is mediated by species capable of Fenton-type chemistry.

154 e damage without deleterious side effects of Fenton chemistry.

155 d synergistically enhances the efficiency of Fenton reaction to degrade pectin into 5.5 kDa within on

156 any advantage, at the level of prevention of Fenton chemistry, radical trapping, or iron clearance, t

157 -DHBs) are able to amplify the reactivity of Fenton systems and have been extensively studied in biol

158 his, a systematic study of the reactivity of Fenton-like systems driven by 1,2-DHBs with different su

159 er hydroxyl radicals produced as a result of Fenton-Haber Weiss reactions of ascorbate and Cu(2+) rap

160 supports our hypothesis that the synergy of Fenton reaction and manganese peroxidase might play an i

161 truction of the HEDPA by ozonation or use of Fenton's reagent, Am, Pu, U, and Th are separated from e

162 whereas O(2)(*-) (ONOO(-) formation), (*)OH (Fenton reaction), and compound III are unlikely to contr

163 To develop efficient AOPs based on Fenton systems driven by 1,2-DHBs, the change in reactiv

164 This unexpected effect of pH on Fenton reaction efficiency could be due to the formation

165 OS) formed from gamma-radiolysis of water or Fenton reaction, and it can abstract one hydrogen atom f

166 ies produced by gamma-radiolysis of water or Fenton reaction.

167 t of Mn(II) during EC treatment and in other Fenton type systems.

168 (TAME) by chemical oxidation (permanganate, Fenton reagents), acid hydrolysis, and aerobic bacteria

169 l radical production from hydrogen peroxide (Fenton's reaction) and subsequent aqueous-phase oxidatio

170 Photo-Fenton experiments were performed in a pilot compound pa

171 Aerosol organics oxidized by photo-Fenton and H2O2 photolysis resemble ambient "aged" and "

172 s similar in both OH-aging mechanisms, photo-Fenton significantly increased the degree of oxidation (

173 f this paper was to develop a modified photo-Fenton treatment able to degrade micro pollutants in mun

174 responsible for the efficiency of such photo-Fenton process.

175 This work illustrates that photo-Fenton chemistry efficiently forms highly oxidized organ

176 roxide photolysis (H2O2 + hnu) and the photo-Fenton reaction (Fe (II) + H2O2 + hnu).

177 e from CN, while Dps sequesters it, quelling Fenton's reaction.

178 so leads to the production of free radicals (Fenton reaction) that can attack and damage lipids, prot

179 ogen peroxide, generating hydroxyl radicals (Fenton chemistry) and, ultimately, other related deleter

180 More recently Fenton and Perkins employed three of the most commonly u

181 ed this adduct formed under oxido-reductive (Fenton) conditions in Tris buffer.

182 in LambdaC/Br = 10.7 and 2.4, respectively; Fenton-like degradation resulted in carbon isotope fract

183 Ferritins are also antioxidants, scavenging Fenton chemistry reactants.

184 (III) in the protein rather than from simple Fenton chemistry.

185 cted HLECs were exposed to oxidative stress (Fenton reaction) or HNE (30 microM) for 3 hours.

186 ing is blocked by iron chelators, suggesting Fenton's reaction.

187 tors prevent oxidative injury by suppressing Fenton chemistry and the formation of highly reactive hy

188 These results suggest that Fenton chemistry may be a useful methodology in identify

189 The Fenton reaction describes the reaction of Fe(II) with hy

190 The Fenton reaction is used to produce hydroxyl radicals for

191 The Fenton reaction, the oxidation of ferrous iron by hydrog

192 Fe(III) back to Fe(II) which accelerates the Fenton cycle and leads to faster contaminant degradation

193 oxidants such as ionizing radiation and the Fenton chemistry of Fe2+-EDTA/H2O2 poses a challenge to

194 lular iron levels; it thereby attenuates the Fenton reaction and the DNA damage that would otherwise

195 attenuate hydroxyl radical production by the Fenton reaction (Fe(2+) + H(2)O(2) --> Fe(3+) + OH(-) +

196 n binding capacity, oxidation of rRNA by the Fenton reaction formed 13 times more 8-hydroxyguanosine

197 the damage spectrum of the dC family by the Fenton reaction is compared with that by ionizing radiat

198 DNA is damaged in vivo by the Fenton reaction mediated by Fe2+ and cellular reductants

199 ve hydroxyl radical that is generated by the Fenton reaction with H2O2, might contribute to the sourc

200 ted ethanol in the presence of Fe(2+) by the Fenton reaction, establishing an acidic milieu.

201 d generation of free radical species, by the Fenton reaction, might contribute to the pathoetiology o

202 ely oxidized by the radical generated by the Fenton reaction.

203 cating that the DNA damage was caused by the Fenton reaction.

204 s against hydroxyl radicals generated by the Fenton reaction.

205 ng the generation of hydroxyl radical by the Fenton reaction.

206 , the hydroxyl radical (*OH) produced by the Fenton reaction.

207 e to attack by HO* radicals generated by the Fenton reaction.

208 uch more efficient than that obtained by the Fenton reagent at pH 3.

209 iptional regulation, enzyme degradation, the Fenton reaction and damage caused by *OH, oxidation of b

210 NADH could drive the Fenton reaction to cause damage to the dC family in vitr

211 hat vitamin C, a compound known to drive the Fenton reaction, sterilizes cultures of drug-susceptible

212 In contrast to restriction enzymes the Fenton reaction is known to cleave DNA without nucleotid

213 sal that NADH was the reducing agent for the Fenton reaction in vivo.

214 ascorbate, thus removing the metal from the Fenton cycle, and effective radical scavengers.

215 s of DMPO/.17OH and DMPO/.16OH formed in the Fenton reaction were 90% and 10%, respectively, reflecti

216 In the Fenton reaction, free intracellular iron transfers elect

217 e hydroxyl radical, which is produced in the Fenton reaction, is buffered by extracellular proteins,

218 of the attack of OH radicals produced in the Fenton way on DNA molecules is important from biological

219 NA in the presence of H2O2 and Cu(II) in the Fenton-type reaction.

220 E. coli eliminates substrates of the Fenton reaction by assimilating Fe(2+) and biosynthesizi

221 es generated in vivo and the key role of the Fenton reaction in this process may be important for und

222 The rate constant of the Fenton reaction measured at physiological pH was much hi

223 l formation by eliminating substrates of the Fenton reaction, by assimilating ferrous iron (Fe(2+)) a

224 sistance was not caused by inhibition of the Fenton reaction, for copper-supplemented cells exhibited

225 me iron enzymes and in the first step of the Fenton reaction.

226 iron-sulfur clusters, and stimulation of the Fenton reaction.

227 mechanism to avoid the toxic effects of the Fenton reaction.

228 t with an Fe(II)-mediated stimulation of the Fenton/Haber-Weiss reaction and hydroxyl radical-mediate

229 footprinting has been developed based on the Fenton reaction, Fe(II) + H2O2 --> Fe(III) + *OH + OH-.

230 ng ferrous (Fe2+) form which can promote the Fenton reaction.

231 roxyl-radical formation, confirming that the Fenton reaction was responsible.

232 tion of hydroxyl radical ((*)OH) through the Fenton reaction in mitochondria.

233 the generation of free radicals through the Fenton reaction, ferritin acts as an anti-oxidant.

234 tion and the degradation of H2O2 through the Fenton reaction.

235 ting hydroxyl-radical production through the Fenton reaction.

236 lled cells by damaging their DNA through the Fenton reaction.

237 se iron-loaded enzymes are vulnerable to the Fenton reaction, the substitution of manganese may preve

238 set of oxidative reactions in analogy to the Fenton reaction, thus widening the scope of electrochemi

239 ctive hydroxyl radical (.OH) [formed via the Fenton reaction (Fe2++H2O2+H+-->Fe3++H2O+.OH)], interfer

240 important source of hydroxyl radical via the Fenton reaction in cloudwater.

241 The hydroxyl radical ions produced via the Fenton reaction inactivate GTF, a factor in the producti

242 Supporting the role of killing via the Fenton reaction, binding of iron by Dps significantly mi

243 Free iron, via the Fenton reaction, is known to exacerbate UV-induced and o

244 ecies, such as the hydroxyl radical, via the Fenton reaction.

245 f free radical generation by formate via the Fenton reaction.

246 active and damaging hydroxyl radical via the Fenton reaction.

247 ociated with DNA in vivo, presumably via the Fenton reaction.

248 , whose killing is amplified by iron via the Fenton reaction.

249 ultimately leading to cell apoptosis via the Fenton reaction.

250 of highly reactive hydroxyl radicals via the Fenton reaction.

251 for the generation of free radicals via the Fenton/Haber-Weiss reactions.

252 hlor degradation rate by 10000 times in this Fenton oxidation system at pH = 3.6.

253 PCA could be effectively mineralized in this Fenton system, suggesting the environmental benignity of

254 manganese superoxide dismutase, and through Fenton chemistry, iron may counteract the benefits of no

255 avoiding hydroxyl radical production through Fenton chemistry.

256 by generating reactive oxygen species due to Fenton reaction or by substituting for other transition

257 at CN enhances plasmid DNA relaxation due to Fenton's reaction in vitro.

258 exposure of tyrosine-containing peptides to Fenton conditions.

259 eactions: homolytic cleavage via traditional Fenton chemistry, heterolytic cleavage, and nucleophilic

260 carboxymethyllysine via Fenton reaction (UHP-Fenton pathway).

261 echanism of the ensuing damage, uncontrolled Fenton chemistry, are discussed.

262 of reactive oxygen species from unregulated Fenton type reactions.

263 n addition, the antioxidant activities of US-Fenton-treated pectin was significantly elevated.

264 combining ultrasound with Fenton system (US-Fenton), we show that ultrasound synergistically enhance

265 action of water-soluble alkyl nitriles using Fenton's reagent (Fe(II) and H2O2) is described.

266 er agent than EDDS for the application of UV-Fenton process in the treatment of OSPW.

267 The application of UV-Fenton processes with two chelating agents, nitrilotriac

268 n of pentosidine and carboxymethyllysine via Fenton reaction (UHP-Fenton pathway).

269 pparently formed from hydrogen peroxide, via Fenton's reaction.

270 hus avoiding hydroxyl radical production via Fenton chemistry.

271 en species (especially hydroxyl radical, via Fenton chemistry).

272 s most likely not a major target for ROS via Fenton reaction.

273 d by hydroxyl radical generated from UHP via Fenton reaction.

274 When Fenton's reagent was used, the (.)OH adduct of MDL 101,0

275 s pristine nanotubes do not degrade, whereas Fenton catalysis results in the homolytic cleavage of H(

276 The extracts were analyzed with Fenton systems containing Fe(II)-sulfate and Fe(II)-Quin

277 can be induced in isolated DNA treated with Fenton reagents and in cultured human cells exposed to g

278 r X-rays and in calf thymus DNA treated with Fenton reagents.

279 lastic Sediment Separator and treatment with Fenton's reagent enabled analysis via Attenuated Total R

280 etic double-stranded DNA upon treatment with Fenton-type reagents [i.e. H2O2, ascorbate together with

281 By combining ultrasound with Fenton system (US-Fenton), we show that ultrasound syner