ライフサイエンスコーパス: H2O2

1 H2O2 fluctuations can be monitored in real time using fa

2 H2O2 has been implicated in several neurodegenerative di

3 H2O2 is an early danger cue required for innate immune c

4 H2O2 levels were consistent across subsamples of the sam

5 H2O2 oxidizes capping agent CSH, modulating the growth o

6 H2O2 production is blocked by stigmatellin, indicating i

7 H2O2-induced modifications commence with oxidation of Ty

8 H2O2/Zn(2+) induced concentration-dependent increases in

9 ncentrations of H2O2 in the range of 0-0.144 H2O2 to protein ratios (HTPR) by the addition of the req

10 degrees C) by chemical oxidation with 5-15% H2O2 and investigated the changes in surface chemistry a

11 Impaired mitochondria and accumulated H2O2 production resulted in disturbance of redox-sensiti

12 nts for reactions containing O2 but no added H2O2 The kcat/Km for H2O2-driven degradation of chitin w

13 In addition, H2O2-treated cells had elevated rates of point mutations

14 ctra of purified recombinant TcAPx-CcP after H2O2 reaction denote the formation of a compound I-like

15 erous bacterial and fungal pathogens against H2O2-induced oxidative damage from host immune responses

16 ins provided the greatest protection against H2O2.

17 larly high relative to both oxygen, allowing H2O2 detection by its reduction, and reductants.

18 We hypothesize that although H2O2 serves as an early recruitment trigger for innate i

19 Given that defensin-1 and H2O2 are regular antibacterial components of all honeys,

20 tected erythrocytes from oxidative AAPH- and H2O2-induced hemolysis, but at high concentrations a pro

21 ecrease in both glucose oxidase activity and H2O2 production as well as defensin-1 amount was observe

22 nduced by dexamethasone (Dex), TNF-alpha and H2O2 treatment.

23 Formation of the stable adduct of CPA and H2O2 was also observed when the reaction mixture was eva

24 to stress, as stress signals doxorubicin and H2O2 each must free p53 from PEPD in order to achieve ro

25 enthalpic barriers for both epoxidation and H2O2 decomposition reactions.

26 s with oxo atom donors (PhIO, IBX-ester, and H2O2) to afford a rare example of a singly oxygenated su

27 and proanthocyanidins, in lignin-forming and H2O2-scavenging cultures and supported that monolignols

28 d digestion procedure using diluted HNO3 and H2O2 was developed for multi-element determination in gu

29 ition of 15mL of juice sample using HNO3 and H2O2 was performed in a digester block with reflux syste

30 f carbonyl compounds with hydroperoxides and H2O2 in acidic media, as such reactions involve alpha-ca

31 ion, Lon proteolytic activity induction, and H2O2 stress adaptation and produces the male-specific pa

32 istry involving redox-active labile iron and H2O2.

33 he aptamer; the resulting ECL of luminol and H2O2 at the anodic poles is monitored using a photomulti

34 Using menadione and H2O2 as positive controls, just 100 mug/mL of the test c

35 METHODS AND H2O2 induced endothelium-independent vasodilation in non

36 us stresses such as CdCl2, NaCl, NaHCO3, and H2O2 treatments.

37 m resulting in increased levels of O2(-) and H2O2 are capable of disrupting intracellular iron metabo

38 for Citrate-Fe(II) mediated O2 to O2(-) and H2O2 to OH were 3.0 +/- 0.7 and (4.2 +/- 1.7) x 10(3) M(

39 n antioxidant chain becomes overwhelmed, and H2O2 degradation stalls or ceases.

40 to simulate the relationship between VO2 and H2O2 emission as a function of lipid concentration.

41 tative iron transporter system (ybbKLM), and H2O2 scavenging enzymes.

42 Scavenging of apoplastic H2O2 by potassium iodide repressed lignin formation, in

43 lyses revealed that scavenging of apoplastic H2O2 resulted in remodulation of the transcriptome, with

44 In human arterioles, H2O2-induced dilation is impaired in CAD, which is assoc

45 ROS, such as H2O2, are important for carcinogenesis and activate MAPK

46 ting Akt-FoxO1 signaling and also attenuates H2O2-induced Bim activation via inhibiting JNK phosphory

47 The cell-based H2O2 generation is affected by the medium volume, the ce

48 oreover, we identify that BiVO4 has the best H2O2 generation amount of those oxides and can achieve a

49 MtrC as a new benchmark in biotechnological H2O2 reduction with scope for applications in fuel cells

50 The phophorothioated DNA reacted to both H2O2 and hydroxyl radicals in vivo, and protected genomi

51 llulosic chromophores and its degradation by H2O2 is well-established, the second intermediate, 1,4,5

52 ese proteins prevented PTP1B inactivation by H2O2 Intriguingly, we discovered that TrxR1/NADPH direct

53 horn inhibited lipid peroxidation induced by H2O2, however, the non-polar fraction reduced more power

54 duced more powerfully the process induced by H2O2/Fe as compared to the phenolic fraction.

55 suggest that TRPA1 activation is mediated by H2O2 and reactive oxygen species, early markers of tissu

56 ite, and iron-catalyzed oxidation of PerR by H2O2 leads to the dissociation of PerR from DNA.

57 s also inhibited carbonylation stimulated by H2O2/Fe.

58 ation, reduced oxidative stress triggered by H2O2 in CaCo-2 cells.

59 se of budding yeast to temporally controlled H2O2 stress patterns.

60 (7) M(-1)s(-1)) and catalytically decomposes H2O2 using Cc as the reducing substrate with higher effi

61 nd sdhaf2 showed lower rates of SA-dependent H2O2 production in vitro in line with their low SA-depen

62 n and streptococcal pyruvate oxidase-derived H2O2 production were required for cardiomyocyte killing.

63 Our method can detect H2O2 by its specific CEST signal at approximately 6.2 pp

64 ctrochemical sensor was used for determining H2O2 in apple juice, and the sensor electrode provided s

65 ctrochemical sensing ability for determining H2O2 with high sensitivity and selectivity.

66 Therefore, direct H2O2 transfer from chloroplasts to nuclei, avoiding the

67 te and hydrous ferric oxide for EC-O2 and EC-H2O2, respectively), regardless of pH and Fe(II) product

68 In addition, in the EC-H2O2 system, Mn(II) removal efficiency increased as pH d

69 in trapping, and MS analysis after equimolar H2O2 addition, supporting an alternative electron transf

70 not otherwise be possible using an existing H2O2 assay.

71 ivity to shield the cytoplasm from exogenous H2O2 However, it receives electrons from the quinone poo

72 a striking hormetic effect of extracellular H2O2 stress on replicative longevity.

73 or ablate XRCC1 chromatin binding following H2O2 treatment.

74 lation and XRCC1 chromatin binding following H2O2 treatment.

75 sitivity (2.4 +/- 0.24 mA cm(-2) mM(-1)) for H2O2 oxidation.

76 chieve a Faraday efficiency of about 98% for H2O2 production.Producing hydrogen peroxide via electroc

77 t SC is a considerable diffusion barrier for H2O2 penetration.

78 sensor using the GC/rGO-Nf@Ag6 electrode for H2O2 determination was calculated to be 5.35x10(-7)M wit

79 taining O2 but no added H2O2 The kcat/Km for H2O2-driven degradation of chitin was on the order of 10

80 ylation, providing a molecular mechanism for H2O2-induced chemotaxis deficiency.

81 The enriched pathways for H2O2 resistance included DNA repair, aromatic amino acid

82 S in an MPPC, and the energy requirement for H2O2 production was low ( approximately 0.87 kWh/kg H2O2

83 ensity functional theory predicted trend for H2O2 evolution is further confirmed by our experimental

84 new type of oscillation during recovery from H2O2 challenge.

85 Further, H2O2 decomposition (the undesirable reaction pathway) po

86 ished by reactive oxygen species (ROS), e.g. H2O2, which oxidize the catalytically indispensable acti

87 (Duox-1), a NADPH oxidases known to generate H2O2.

88 yzes the reduction of endogenously generated H2O2 Prx1 is synthesized on cytosolic ribosomes as a pre

89 myeloperoxidase was incubated with glycine, H2O2, malondialdehyde, and a lysine analog in PBS at a p

90 Higher H2O2 accumulation was concurrent with higher phenylalani

91 of the observed CBP21 inactivation at higher H2O2 levels, we conclude that controlled generation of H

92 hat this is the first report that identifies H2O2-induced covalent modifications as an essential comp

93 ble for substrate oxidation in the (L)Fe(II)/H2O2/AcOH catalytic system.

94 d repair after wounding, along with impaired H2O2 responses after exposure to the intestinal pathogen

95 genetic alteration that resulted in improved H2O2 tolerance by amplification of the CTT1 gene that en

96 8A expression decreased ERK1/2 activation in H2O2-treated cells.

97 ase and glutathione peroxidase activities in H2O2 treated CCD and Caco-2 cells compared to PEPS, EPS

98 gordonii, followed by a gradual decrease in H2O2 concentration (>30 min) to almost zero as lactate w

99 The mutants also exhibited a decrease in H2O2 reduction by the AhpF-AhpC ensemble.

100 wn-regulated plants revealed an elevation in H2O2 production within the guard cells, increased sensit

101 crease catalase activity that is involved in H2O2 breakdown; and 4) result in DNA strand breaks.

102 active oxygen species and malondialdehyde in H2O2 treated CCD 841 CoN (CCD) and Caco-2 cells were sig

103 S inhibitor L-NAME or specific eNOS siRNA in H2O2-treated cells.

104 sis monocytes, can be reversed by increasing H2O2 and sulfenylating SIRT6.

105 were more vulnerable to lenalidomide-induced H2O2 accumulation and associated cytotoxicity.

106 on reaction-diffusion principles that infers H2O2 degradation rates from intravital H2O2-biosensor im

107 ishmania mitochondrial SOD may also initiate H2O2-mediated redox signaling that regulates gene expres

108 oducts and SOA mass yields relative to input H2O2 concentrations, the second-generation dihydroxy hyd

109 chondria, a putative source of intracellular H2O2, have recently been demonstrated to be particularly

110 nfers H2O2 degradation rates from intravital H2O2-biosensor imaging data.

111 ction with NRX1, a process necessary for its H2O2-scavenging activity.

112 oduction was low ( approximately 0.87 kWh/kg H2O2) compared to previous studies using real wastewater

113 nocarcinoma cells generated micromolar level H2O2 during just 1 min of direct CAP treatment on these

114 we observed an initial increase in the local H2O2 concentration of approximately 12 +/- 5 muM above S

115 d to be particularly vulnerable to localized H2O2 perturbations, eliciting a dramatic cell death resp

116 n < 200 nmol/mg mito protein resulted in low H2O2 emission flux, increasing thereafter in Sham and T1

117 MM cells with lower H2O2-decomposition capacity were more vulnerable to lena

118 We speculate that micromolar H2O2 is created both biologically and abiotically at nat

119 ignaling by increased rates of mitochondrial H2O2 production, leading to part of the SA-dependent tra

120 edict that basal, steady-state mitochondrial H2O2 will be in the low nM range (2-4 nM) and will be in

121 chanistic understanding of the mitochondrial H2O2 reaction network in HeLa cells by creating a kineti

122 We could detect 65 +/- 10 muM H2O2 produced by Streptococcus gordonii (Sg) in a simula

123 We were also able to detect 30 muM H2O2 at 50 mum above the biofilm in the presence of the

124 protein content decreased on myeloperoxidase/H2O2 incubation.

125 mum diameter, highly sensitive, nonenzymatic H2O2 sensor with a detection limit of 250 nM and a broad

126 photosynthesis inhibitor) attenuates nuclear H2O2 accumulation and high light-responsive gene express

127 nd S3QELs, suppressors of mitochondrial O2()/H2O2 generation that do not inhibit oxidative phosphoryl

128 H2O2 We discuss their contributions to O2()/H2O2 production under native conditions in mitochondria

129 dvanced oxidation processes (AOPs) (i.e., O3/H2O2 and UV/H2O2) was investigated.

130 ssed in oxyR2 mutants even in the absence of H2O2 Further genetic analyses suggest that OxyR2-activat

131 ould be significantly reduced by addition of H2O2.

132 ated products were formed than the amount of H2O2 consumed, suggesting that the controlled breakdown

133 the quantitative and mechanistic aspects of H2O2 signaling are still being elucidated.

134 suggesting that the controlled breakdown of H2O2 activates methane, which subsequently incorporates

135 we show that low oxidative concentrations of H2O2 also impede chemokinesis and chemotaxis of previous

136 ion rates and steady-state concentrations of H2O2 and its reaction partners within individual mitocho

137 ntaining low intracellular concentrations of H2O2 Furthermore, we showed that DeltaoxyR2 and Deltaahp

138 were treated with varying concentrations of H2O2 in the range of 0-0.144 H2O2 to protein ratios (HTP

139 Pathological concentrations of H2O2/Zn(2+) induced substantial cell death that was inhi

140 tion of IKZF1 and IKZF3 was a consequence of H2O2-mediated oxidative stress.

141 s of FeS2 dissolution and the degradation of H2O2 through the Fenton reaction.

142 This is the first demonstration of H2O2 production using PS in an MPPC, and the energy requ

143 be used to ensure the selective detection of H2O2, enabling confident characterization of the role th

144 ty, and its application for the detection of H2O2, glucose, and CN(-) ions.

145 e a potential candidate for the detection of H2O2.

146 based biosensor towards the determination of H2O2 and glucose in the real samples have been demonstra

147 and interference study for determination of H2O2 in wastewater samples demonstrated the selectivity

148 d well for the amperometric determination of H2O2 over a linear range of 0.03-1mM with a detection li

149 om 1.7 muM to 30 mM for the determination of H2O2 with a low limit of detection, 0.5 muM.

150 CSE overexpression alleviated the effects of H2O2 on H9c2 cardiomyocyte survival.

151 n this study, we investigated the effects of H2O2, a prototypical reactive oxygen species that is als

152 At longer times, substantial efflux of H2O2 from the mitochondria to the cytosol was evidenced

153 Neglecting efflux of H2O2 to the cytosol, the mitochondrial reaction network

154 rmance catalysis towards electroreduction of H2O2 with a high sensitivity of 1.5Acm(-2)M(-1).

155 The MitoB method allows an evaluation of H2O2 levels in living organisms over a timescale from ho

156 Provision of exogenous ROS in the form of H2O2 reversed the necrotic phenotype and restored CD95 e

157 ical results clearly proved the formation of H2O2 in the leaves of plants 3h after the E. cloacae ino

158 at 25 degrees C leading to the generation of H2O2.

159 sensor showed a promising chemical image of H2O2 produced by Sg biofilms.

160 esis and OXPHOS with significant increase of H2O2, sharply contrasting with a reduced ATP content.

161 kylhydroperoxide reductase, independently of H2O2 A conserved cysteine residue in OxyR2 is critical f

162 n factor and, consequently, an inhibition of H2O2 degradation and enhanced disease resistance.

163 n LPMO catalysis, such as the involvement of H2O2 Our results show that residues on the substrate-bin

164 We investigated the kinetics of H2O2 formation in aqueous suspensions of FeS2 microparti

165 grown bacteria were exposed to low levels of H2O2 or incubated in seawater.

166 leading to increased steady-state levels of H2O2; however, the mechanism(s) for cancer cell-selectiv

167 de sensor was used for in-situ monitoring of H2O2 produced in A. tequilana leaves after inoculation o

168 evel property resulting from nonlinearity of H2O2 scavenging by peroxiredoxins and our study reveals

169 eactions (NOx photo-oxidation, photolysis of H2O2, ozonolysis, or thermal decomposition of N2O5).

170 l death processes and shows the potential of H2O2 as a cellular damage biomarker, with a clear potenc

171 transcription requires both the presence of H2O2 and the absence of O2 Experiments show that Ccp lac

172 ) production rates, high pH, the presence of H2O2 instead of O2 as the initial Fe(II) oxidant, or a c

173 f the microelectrode sensor, the presence of H2O2 was detected in the root hairs by 3,3-diaminobenzid

174 etramethylbenzidine (TMB) in the presence of H2O2.

175 Specifically, FLC-mediated production of H2O2 was shown to activate JAK2/STAT1 signaling, increas

176 selective electrochemical quantification of H2O2, because it is often enzymatically generated at bio

177 O is utilized herein for the quantitation of H2O2 in a wide concentration range, from 100nM to 100muM

178 by the addition of the required quantity of H2O2 and deionized water.

179 opy results indicated rapid initial rates of H2O2 disproportionation slowing concomitantly with the a

180 ameter sampling was used to explore rates of H2O2 efflux that could reconcile model predictions of Pr

181 trate oxidations coupled to the reduction of H2O2.

182 trate oxidations coupled to the reduction of H2O2.

183 The slow release of H2O2 by MgO2 decomposition (termed partial chemical oxid

184 In cells that underwent multiple rounds of H2O2 treatments, we identified a genetic alteration that

185 However, the significant secretion of H2O2 by cancer cells have been rarely observed.

186 olically controlled mitochondrial sources of H2O2 as well as glutathione- and thioredoxin-related pat

187 hat the improvement in the heat stability of H2O2 treated WPI solution was attributed to the signific

188 c model which explains the observed trend of H2O2, showing that FeS2 dissolution can act as a natural

189 immunoprecipitation experiments performed on H2O2-treated HCT116 cells, endogenous MLK3 associated wi

190 monoclonal FLC that was required for optimal H2O2 production and downstream signaling.

191 k electrons to oxygen to produce O2() and/or H2O2 We discuss their contributions to O2()/H2O2 product

192 ed sufficiently negative to drive the ORR or H2O2 reduction on the platinum surface, mainly using squ

193 Conversely, adding either superoxide or H2O2 from the outset strongly enhances catalysis.

194 to sustainability, relying on green oxidants H2O2 and O2 as the ultimate oxygen source.

195 -expression of stromal ascorbate peroxidase (H2O2 scavenger) or treatment with DCMU (photosynthesis i

196 -dependent) production of hydrogen peroxide (H2O2) and 4-hydroxynonenal (4-HNE), which sustains allod

197 tested for biosensing of hydrogen peroxide (H2O2) and as supercapacitor electrode materials.

198 tes superoxide (O2()) and hydrogen peroxide (H2O2) as bona fide products in reactions involving 1- or

199 on of cysteine (CSH) with hydrogen peroxide (H2O2) enzymatically generated by alcohol oxidase (AOx).

200 ceived that extracellular hydrogen peroxide (H2O2) generated by Duox diffuses through the tissue to d

201 noninvasively quantifying hydrogen peroxide (H2O2) in aqueous solutions based on chemical exchange sa

202 reported for detection of hydrogen peroxide (H2O2) in wastewater samples.

203 onradical species such as hydrogen peroxide (H2O2) or singlet molecular oxygen, rather than free-radi

204 One proposed signal is hydrogen peroxide (H2O2) produced by chloroplasts in a light-dependent mann

205 Hydrogen peroxide (H2O2) promotes a range of phenotypes depending on its in

206 n quantified by measuring hydrogen peroxide (H2O2) reduction by chronoamperometry at -0.35V (vs pseud

207 and NO3(-) in an alkaline hydrogen peroxide (H2O2) solution.

208 oped for the detection of hydrogen peroxide (H2O2) using a reduced graphene oxide-nafion@silver6 (rGO

209 es the reduction of O2 to hydrogen peroxide (H2O2), has been implicated in the cardiac and lung myofi

210 nerated ROS, particularly hydrogen peroxide (H2O2), impaired adenosine stimulated wound repair.

211 xidant in the presence of hydrogen peroxide (H2O2), we demonstrated that the resulting methanol incor

212 l Caco-2 cells exposed to hydrogen peroxide (H2O2)-induced oxidative stress.

213 targets enzymes of major hydrogen peroxide (H2O2)-scavenging pathways, including catalases.

214 rocesses applying gaseous hydrogen peroxide (H2O2).

215 omponents, defensin-1 and hydrogen peroxide (H2O2).

216 en cells are treated with hydrogen peroxide (H2O2).

217 iaminobenzidine (DAB) and hydrogen peroxide (H2O2).

218 trigger by activation by hydrogen peroxide (H2O2).

219 nd selective detection of hydrogen peroxide (H2O2).

220 bated upon treatment with hydrogen peroxide (H2O2).

221 However, measuring ROS (hydrogen peroxide, H2O2) content in vivo is now possible using the MitoB pr

222 min) for a range of experimentally perturbed H2O2 generation rates.

223 GAPDH down-regulation potentiated H2O2-induced DNA damage and SMC apoptosis.

224 SPIN acts as a molecular plug that prevents H2O2 substrate access to the MPO active site.

225 Prolonged H2O2 treatment activated ERK1/2 and promoted invasion of

226 ) was found to be more effectively protected H2O2-induced IP3R1 dysfunction by reducing disulfide bon

227 To accurately quantify H2O2 in unknown samples, we also implemented a standard

228 , quick, and accurate method for quantifying H2O2 in aqueous solutions.

229 Here, we stably expressed the ratiometric H2O2 redox sensor roGFP2-Orp1 in the cytosol and the mit

230 er acids cleave the metal-O bonds, releasing H2O2.

231 ressed this problem by fabricating a robust, H2O2-selective electrode.

232 oreover, AMC provoked the production of ROS, H2O2, and NO, modulating the PI3K/Akt, MAPK, NFkappaB an

233 with C119S/C162S being incapable of sensing H2O2 Similarly, disulfide heterodimer formation was abol

234 n the metabolic activity of another species, H2O2-producing S. gordonii.

235 owth inhibition induced by oxidative stress (H2O2 or menadione), significantly ameliorated the H2O2-d

236 In the present study, H2O2 dose-dependently impaired the adenosine triphosphat

237 ular sensitivity to methylmethane sulfonate, H2O2, and 5-FU from DRC.

238 of hypertension with a mitochondria-targeted H2O2 scavenger, mitochondria-targeted hydrogen peroxide

239 We conclude that H2O2 is a biological modifier of the structure and ligan

240 We demonstrate that H2O2 acts through an Src kinase to activate a negative r

241 We find that H2O2 binds to Pd(II) followed by styrene binding to gene

242 We hypothesize that H2O2-elicited dilation involves different K(+) channels

243 Our findings illustrate that H2O2-producing S. gordonii is dominant while the bufferi

244 We show that H2O2 production under these conditions is related to Mg(

245 cy of the different catalysts and shows that H2O2 is formed with overpotentials as low as 90 mV.

246 e presence of aerobic bacteria suggests that H2O2 diffusion to the anode side caused inhibition of me

247 The H2O2 response of the fabricated electrodes was linear fr

248 or menadione), significantly ameliorated the H2O2-dependent increase in matrix keratinocyte apoptosis

249 This is because the H2O2 derives from a sub-population of chloroplasts close

250 UO126, or ERK1/2 siRNA knockdown blocked the H2O2-induced shift of MLK3, while MLK3 inhibition with C

251 utrophil myeloperoxidase (MPO) catalyzes the H2O2-dependent oxidation of chloride anion to generate h

252 1B from inactivation when present during the H2O2 exposure.

253 d RNA sequencing to uncover the scope of the H2O2 (peroxide)-stress regulon and to further explore th

254 mum above the biofilm in the presence of the H2O2-decomposing salivary lactoperoxidase and thiocyanat

255 roparticles by monitoring, in real time, the H2O2 and dissolved O2 concentration under oxic and anoxi

256 ygen species of two cancer cell lines to the H2O2-containing environments might result in the specifi

257 e catalytic activity of CoOxH-GO towards the H2O2-mediated oxidation of AR to form reddish resorufin

258 etection at -0.20V was carried out using the H2O2/hydroquinone (HQ) system.

259 of the CoOxH-GO nanohybrid in detail via the H2O2-mediated oxidation of Amplex Red (AR) to form fluor

260 ll KIM-PTP family members to determine their H2O2 oxidation profiles and identify their reversible in

261 Our results indicate that at high tissue H2O2 levels the peroxiredoxin-thioredoxin antioxidant ch

262 ytes studied using the sensor combining TMB, H2O2, and GBR in phosphate buffer of pH 4.48, the S(2-)

263 Exposure of H9c2 cardiomyocytes to H2O2 or pharmacologic inhibition of H2S production incre

264 of ribosomes did not appear to change due to H2O2 treatment, nor did posttranslational modifications,

265 This further leads to H2O2 production and PKCalpha activation, inhibiting A2AA

266 phic bacteria, that converts methanethiol to H2O2, formaldehyde, and H2S, an activity not previously

267 ly selective two-electron reduction of O2 to H2O2 (93-99%) using decamethylferrocene (Fc*) as the red

268 ahpC rendered V. cholerae more resistant to H2O2 RNA sequencing analyses indicated that OxyR1-activa

269 restored bacterial viability in response to H2O2 treatment.

270 expected to control perturbations well up to H2O2 generation rates ~50 muM/s (0.25 nmol/mg-protein/s)

271 Melatonin treatment at 100mumol/L triggered H2O2 accumulation, which result from higher superoxide d

272 Increased ER glutathione import triggers H2O2-dependent Bip oxidation through Ero1 reductive acti

273 rate analog revealed a highly unconventional H2O2-activating distal environment with the reactive pro

274 6c is essential for bacterial survival under H2O2 stress.

275 d on an ITO electrode displays unprecedented H2O2 reduction activity.

276 However, upon H2O2 exposure, the membrane potential was significantly

277 t has recently been shown that LPMOs can use H2O2, instead of O2, as a cosubstrate.

278 talyze hydrocarbon oxidation reactions using H2O2 in the presence of added carboxylic acids.

279 in vitro exposure to oxidative stress using H2O2 induces miR-500a-5p overexpression and downregulati

280 ted (253.7 nm, 310-410 nm), and oxidized (UV-H2O2, ozone) poultry litter extracts.

281 ation processes (AOPs) (i.e., O3/H2O2 and UV/H2O2) was investigated.

282 ter are interested in converting from the UV/H2O2 to the UV/free chlorine advanced oxidation process

283 for the oxygen reduction reaction (water vs H2O2) was evaluated in the presence and absence of Pt-Al

284 grow on a nonfermentable carbon source when H2O2 was supplied.

285 ritical need to identify mechanisms by which H2O2 modulates cellular processes in general and how it

286 benign oxidation of conjugated alkenes with H2O2.

287 t turnover number (TON) 3-fold compared with H2O2, highlighting the importance of oxidant choice as a

288 oxidation was significantly correlated with H2O2 generation (Pearson's r = 0.91), no correlation was

289 o sequential oxidative decarboxylations with H2O2 as the oxidant, coproheme III as substrate and cofa

290 s(pyridyl-2-methyl)amine) ligand family with H2O2/AcOH or AcOOH at -40 degrees C reveal the formation

291 re, we show that the enzyme reacts fast with H2O2 (k = 2.9 x 10(7) M(-1)s(-1)) and catalytically deco

292 (Fenton < (NH4)2S2O8 with H2SO4 < HNO3 with H2O2) the concentration of oxygen-containing surface gro

293 ilical vein endothelial cells incubated with H2O2 for 2 hours, accompanied with restoration of BH4.

294 s are modeled by treating keratinocytes with H2O2.

295 2O4 up to -2.5 mA/cm(2) at 0.6 V vs RHE with H2O2 as an electron scavenger, and they show a charge se

296 ll viability compared to control stress with H2O2 (5mM/2h), recovering viability to values between 34

297 in the oxidation of the same substrates with H2O2 catalyzed by manganese complexes, supporting the hy

298 The WPI solution treated with H2O2 (>0.072 HTPR) remained in the liquid state after he

299 rectal carcinoma (HCT116) cells treated with H2O2, extracellular signal-regulated kinases 1 and 2 (ER

300 Although the wound H2O2 gradient reaches deep into the tissue, it likely ov