ライフサイエンスコーパス: H(2)O(2)

1 H(2)O(2) enters cells through aquaporin membrane protein

2 H(2)O(2) is reduced to H(2)O by electrons supplied by NA

3 s as well as efficient bubble propulsion (1% H(2)O(2), 1,5% NaCh, speed 140 mum s(-1)).

4 Treatment under optimal condition (2% H(2)O(2) and 42 degrees C for 5 h) resulted in a 601% in

5 ibrinogen solution or blood containing 0.2mM H(2)O(2).

6 7 L m(-2)h(-1)bar(-1) with treatment by 0.3% H(2)O(2) for 12 min.

7 on of the HRP-labelled anti-human IgA with a H(2)O(2)/luminol/enhancers substrate.

8 e colloidal PtP(2) nanocrystals that achieve H(2)O(2) production at near zero-overpotential with near

9 pecies is used as a strategy to avoid adding H(2)O(2) in the solution during the detection of phenoli

10 In addition, H(2)O(2) production is only significant when the enzyme

11 t-corrole CoBr(8) as electrocatalyst affords H(2)O(2) as the main product in homogeneous solutions, w

12 duced haemolysis (p < 0.05), and ameliorated H(2)O(2)-induced toxicity by 8-23 and 15-83%.

13 ive intermediates ((3)RB(2-)*, O(2)(*-), and H(2)O(2)) that are not kinetically relevant for other co

14 cursors of CO(2), ammonia, acetaldehyde, and H(2)O(2) and that reaction byproducts can influence the

15 ect eggs, and they induce salicylic acid and H(2)O(2) accumulation, defense gene expression and cell

16 In conclusion, increases in ATP and H(2)O(2) constitute an essential signal that switches on

17 llowed by treatment with aqueous NH(4)Cl and H(2)O(2), gave unreacted cis-(+)-limonene oxide and dias

18 C. albicans biofilm synergy in a contact and H(2)O(2)-independent manner.

19 emical microscopy (SECM) in the feedback and H(2)O(2) collection modes to identify the role of the ge

20 s)-a potential fertilizer and fungicide- and H(2)O(2)-released from roots during plant stress respons

21 1,1,1,3,3,3-hexafluoroispropanol (HFIP) and H(2)O(2) is described.

22 cted signals from pH changes, histamine, and H(2)O(2).

23 of ~70% after 72 h, while UV-irradiated and H(2)O(2)-treated PolyRad showed a maximum drug release o

24 nd formate enhanced PGRP-induced killing and H(2)O(2) production in an FDH-dependent manner.

25 oxidase (HRP) in the presence of luminol and H(2)O(2).

26 inone (HQ) as electron transfer mediator and H(2)O(2) as the enzyme substrate was used to detect the

27 er UV(254) photolysis across varying PAA and H(2)O(2) concentrations and water pH (5.8-7.2).

28 zers [rose Bengal (RB), perinaphthanone, and H(2)O(2)] and (2) reactive species scavenging and quench

29 nions), the glutathione redox potential, and H(2)O(2) Simultaneous analyses of two signaling compound

30 onship between honey colloidal structure and H(2)O(2) production that change our traditional understa

31 kinetic mechanism of [Formula: see text] and H(2)O(2) production by SDH.

32 The results for ArOH + HO(2)(*) -> ArO(*) + H(2)O(2) neither afford a linear correlation nor agree w

33 d the utilization of a green oxidant such as H(2)O(2), and the products, arising from an oxidation-re

34 in response to an external stimulus, such as H(2)O(2), would provide control of the gelation rate ove

35 se of reactive and harmful chemical, such as H(2)O(2).

36 antioxidative stress potential in assuaging H(2)O(2) induced erythrocyte hemolysis and antioxidant a

37 l IL4 and cationic protein mEar1 in blocking H(2)O(2)- and hypoxia-induced mouse and human cardiomyoc

38 man colon tumor epithelial cells and blunted H(2)O(2)-induced STAT3 phosphorylation.

39 ng both the enzyme and the substrate, brings H(2)O(2) into a strained reactive conformation and guide

40 ults indicate that the oxidation of SO(2) by H(2)O(2) in the liquid water present in atmospheric aero

41 Dimer formation is accelerated by H(2)O(2) and hindered by reducing agents, resulting in f

42 d to the plasma membrane and is activated by H(2)O(2) via covalent modification of extracellular cyst

43 more sensitive to oxidative stress caused by H(2)O(2) Further, loss of Tat significantly attenuates B

44 prostaglandin E2 and was strongly induced by H(2)O(2) or TNFalpha only in presence of NRF2.

45 otection against oxidative damage induced by H(2)O(2).

46 und to be important for resisting killing by H(2)O(2) Finally, DeltamumR exhibited reduced fitness in

47 amage caused by oxidative stress promoted by H(2)O(2) in Saccharomyces cerevisiae cells.

48 ence of substrate accelerated reoxidation by H(2)O(2), whereas reoxidation by O(2) became slower, sup

49 of cysteines in the PKA catalytic subunit by H(2)O(2) and a significant proportion of the catalytic s

50 membrane side and subsequently terminated by H(2)O(2) oxidation on the anodic membrane side, is cruci

51 The proposed model for the catalytic H(2)O(2) reduction to H(2)O on DLC electrodes was attrib

52 In plant cells, H(2)O(2) triggers an influx of Ca(2+) ions, which is tho

53 In wild-type cells, H(2)O(2) caused cytochrome c release and apoptosis, both

54 el results suggest that, following cleaning, H(2)O(2) photolysis increased OH concentrations by 10-40

55 Cytoplasmic H(2)O(2) appears to derive, at least in part, from mitoc

56 metabolism of DA does not increase cytosolic H(2)O(2) but leads to mitochondrial electron transport c

57 (NOX4) to be the main producer of cytosolic H(2)O(2), which is essential for GSIS; an increase in AT

58 oxidation method, as it allows decentralized H(2)O(2) production.

59 hrombin and MnO(2) nanosheets that decompose H(2)O(2) to O(2) gas.

60 drial electron transport chain (ETC) derived H(2)O(2) versus cytosolic phospholipase A(2) (cPLA(2)) d

61 Our results suggest that NOX1-derived H(2)O(2) is a resource that governs bacterial growth and

62 with alkaline hydrogen peroxide at different H(2)O(2) concentrations and treatment temperatures on it

63 se, suggesting that surface uptake dominated H(2)O(2) loss.

64 e reduction reactions of the analytes (i.e., H(2)O(2) and 3-nitrotyrosine (3-NT)) at the Pd/Au thin f

65 e for detection of common ROS and RNS (i.e., H(2)O(2) and 3-NT).

66 in situ) and 'potentiated' conditions (i.e., H(2)O(2) production enhanced by addition of a reducing a

67 eptor-derived 661W cells treated with either H(2)O(2) or all-trans-retinal stressors implicated in th

68 t cells that express RBOHC and have elevated H(2)O(2) compared with adjacent atrichoblast cells that

69 Epithelial H(2)O(2) was significantly increased in villin-TLR4 mice

70 ng and mediated the production of epithelial H(2)O(2).

71 n, as an alternative to the highly explosive H(2)O(2), discarded orange peel powder (OP) is valorized

72 identify how the perception of extracellular H(2)O(2) is integrated with responses to various externa

73 tibody (mAb) that inhibited AQP3-facilitated H(2)O(2) and glycerol transport, and prevented liver inj

74 ior sensitivity (1.3-1.4 A.M(-1).cm(-2)) for H(2)O(2), as well as selectivity and long term stability

75 died aiming at the design of a biosensor for H(2)O(2) detection.

76 cess produced linear regression equation for H(2)O(2) as A = 0.00105C + 0.0630 (C:muM, R(2) = 0.9961)

77 4 mM with a detection limit of 0.036 muM for H(2)O(2).

78 However, whether sensors for H(2)O(2) also exist on the cell surface remains unknown.

79 ivity, fast response, and good stability for H(2)O(2) sensing.

80 ing that spontaneous water oxidation to form H(2)O(2) from water microdroplets is a general phenomeno

81 se COFs to efficiently reduce oxygen to form H(2)O(2).

82 ng materials (Au, Pt, and SiO(2)) and fuels (H(2)O(2) and alcohols).

83 Functionally, H(2)O(2) treatment inhibited both anterograde and retrog

84 Gaseous H(2)O(2) levels decreased rapidly and irreversibly, with

85 enervation atrophy, suggesting ETC generated H(2)O(2) is not a critical player.

86 ile the chitin-AcOH decomposed the generated H(2)O(2), as proved separately, by concurrent oxidation

87 s this limitation by cathodically generating H(2)O(2) in situ.

88 ses of condensate water microdroplets govern H(2)O(2) generation.

89 Higher gSAT H(2)O(2) production and lower aSAT mitochondrial respira

90 or-dependent increase: CuO NP-induced OMVs > H(2)O(2)-induced OMVs > control OMVs.

91 This discovery of heterogenized H(2)O(2) activators prepared by sol-gel and Stober proce

92 three stressors, which is enhanced at higher H(2)O(2) concentrations.

93 ric transduction using the hydroquinone (HQ)/H(2)O(2) system upon capturing the modified MBs on the s

94 Our study identifies H(2)O(2) from severe but not mild reactive astrocytes as

95 2+) ions, which is thought to be involved in H(2)O(2) sensing and signalling.

96 c enzymatic activity along with reduction in H(2)O(2) in the airways and had a significant protective

97 to wild-type germ-free mice caused increased H(2)O(2) production and tumorigenesis.

98 signaling cascade, which leads to increased H(2)O(2) and Ca(2+) levels and F-actin reorganization, b

99 ) also had completely abolished PGRP-induced H(2)O(2) production and high resistance to PGRP-induced

100 functional FDH-O had abolished PGRP-induced H(2)O(2) production and the highest resistance to PGRP-i

101 2)(*-), whereas only 2-OH and 3-OH inhibited H(2)O(2) and HO(*).

102 ach to catalyzing the reduction of O(2) into H(2)O(2), based on the use of redox-active carbenium spe

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

104 eak H(2)O(2) mixing ratios to decrease and k(H(2)O(2)) to increase, suggesting that surface uptake do

105 irreversibly, with removal rate constants (k(H(2)O(2))) 17-73 times larger than air change rate (ACR)

106 ble reuse, within 4 min using only 1.25 mg/L H(2)O(2).

107 h 7 mM salts for ionic strength and 2.5 mg/L H(2)O(2).

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

109 nd those with high total cholesterol and low H(2)O(2) levels.

110 xidase NOX1 is the primary source of luminal H(2)O(2) early after C. rodentium infection and is requi

111 gnificantly enhancing malondialdehyde (MDA), H(2)O(2), electrolyte leakage, oxidized glutathione (GSS

112 Under air-saturated conditions, mean H(2)O(2) contents were: 15.60 +/- 15.84; 1.39 +/- 2.06 a

113 Collectively, we show that SOD-1-mediated H(2)O(2) production regulates the redox environment and

114 liver injury by inhibition of AQP3-mediated H(2)O(2) transport and macrophage activation.

115 evidence for mAb inhibition of AQP3-mediated H(2)O(2) transport as therapy for macrophage-dependent l

116 jury, by a mechanism involving AQP3-mediated H(2)O(2) transport.

117 HPCA1 mediates H(2)O(2)-induced activation of Ca(2+) channels in guard

118 als, indicating that epidermal mitochondrial H(2)O(2) and its effectors could be targeted for therape

119 ous reports from other models, mitochondrial H(2)O(2) emission and oxidative damage were greater in T

120 Increased scavenging of mitochondrial H(2)O(2) does not protect against denervation atrophy, s

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

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

123 Treatment of cells with 1 mM H(2)O(2) for 10 min resulted in the degradation of Arl1

124 n plasma by the physiologically relevant MPO-H(2)O(2)-NO(2) (-) system.

125 ses with the progression of oxidation by MPO/H(2)O(2)/Cl(-) due to the formation of graphene quantum

126 bit a good dynamic response range (1-200 muM H(2)O(2)), short response times (2 s) and a superior sen

127 tion occurs by (.)OH generation from neutral H(2)O(2) and that electrostatic repulsion of contaminant

128 ast to the conventional detection scheme, no H(2)O(2) was added to the analyte solution.

129 blethal bolus of glycine chloramine, but not H(2)O(2), significantly inhibited DNA methylation.

130 ) production, that the majority (~70-80%) of H(2)O(2) produced is reduced to H(2)O by electrons drawn

131 Several studies confirmed the ability of H(2)O(2) to antagonize susceptible oral bacterial specie

132 also successfully applied for assessment of H(2)O(2) and glucose in human serum and urine samples.

133 The initial cleavage of H(2)O(2) and subsequent hydrogen atom abstraction from c

134 nd under anodic conditions, a combination of H(2)O(2), Cl(*), HO(2)(*), Cl(2)(*-), and Cl(2) formatio

135 ard products; proteins; the concentration of H(2)O(2) at 3 and 24 h of incubation; and a tyrosine-con

136 Concentrations of H(2)O(2) in selected 'functional' (including energy, E,

137 and are inhibited by high concentrations of H(2)O(2) upon adsorption on an electrode.

138 acid-base reaction and the decomposition of H(2)O(2) by bovine liver catalase.

139 highly sensitive and selective detection of H(2)O(2) and 3-NT simultaneously.

140 he simultaneous degradation and detection of H(2)O(2).

141 sent excellent candidates for development of H(2)O(2) biosensors, since they exhibit a good dynamic r

142 guration can minimize the damaging effect of H(2)O(2) by two different pathways, oxidation at the pho

143 addition to delivering an acute exposure of H(2)O(2) to tumor cells, activates DUOX in pancreatic ca

144 re fueled by stereoelectronic frustration of H(2)O(2), the parent peroxide, where the lone pairs of o

145 ntify the site of PGRP-induced generation of H(2)O(2) in Escherichia coli.

146 rther, we identify an endogenous gradient of H(2)O(2) across the spermathecal tissue, which depends o

147 filters, selection of blue laser and lack of H(2)O(2) treatment.

148 f flavonol antioxidants control the level of H(2)O(2) and root hair formation.

149 n, but axons do not show increased levels of H(2)O(2).

150 ntration of 1 mol L(-1) HNO(3) and 2.5 mL of H(2)O(2).

151 eradish peroxidase (HRP) without the need of H(2)O(2) to be present in the solution.

152 ne (SLG) we observed a shift in the onset of H(2)O(2) generation which we traced back to photothermal

153 gin was believed to be the main predictor of H(2)O(2) concentration in honey.

154 air-saturated solution with the presence of H(2)O(2) enhancing the dynamic nature of the system.

155 In the presence of H(2)O(2) fuel, MOF motors (or MOFtors) exhibit jet-like

156 The presence of H(2)O(2) stimulated the generation of other long-lived R

157 onal polycyclic peroxides in the presence of H(2)O(2) under acid catalysis.

158 l for growth and survival in the presence of H(2)O(2), suggesting that MumR regulates additional gene

159 c current change measured in the presence of H(2)O(2)/hydroquinone (HQ) at screen-printed carbon elec

160 carbon electrodes (SPCEs) in the presence of H(2)O(2)/hydroquinone (HQ) upon magnetic capture of the

161 chanism is based on the reduction process of H(2)O(2) liberated from the enzymatic activity.

162 The production of H(2)O(2) in honey requires glucose oxidase (GOx) that ox

163 supplementation increases the production of H(2)O(2) in vitro.

164 uvate oxidase (SpxB)-dependent production of H(2)O(2) is widely distributed among oral commensal stre

165 These results show that the production of H(2)O(2) occurs in water microdroplets formed by not onl

166 s are related to the sustained production of H(2)O(2) over time, which in turn boosts the antibacteri

167 he metabolism caused excessive production of H(2)O(2) reactive oxygen species (ROS) to inflict cell d

168 cells, which provide sustained production of H(2)O(2).

169 ession of DUOX2 and epithelial production of H(2)O(2).

170 of H(2)O(2) and allows the quantification of H(2)O(2) in a wide linear range (from 5.0 x 10(-7) M to

171 ), which exponentially increases the rate of H(2)O(2) (JH(2)O(2)) production.

172 rated, potentiated conditions, mean rates of H(2)O(2) production were 21.7 +/- 33.3, 0.98 +/- 2.84, a

173 n the non-enzymatic catatalytic reduction of H(2)O(2) and allows the quantification of H(2)O(2) in a

174 results also indicated that the reduction of H(2)O(2)-induced-CYG oxidation rate (34.78%) at pH 3.0 w

175 pments that recognized the essential role of H(2)O(2) in metabolic redox control.

176 Our results demonstrated that the synergy of H(2)O(2) and gluconic acid is essential for the antibact

177 Electrochemical synthesis of H(2)O(2) through a selective two-electron (2e(-)) oxygen

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

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

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

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

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

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

184 nt conditions using either molecular O(2) or H(2)O(2).

185 nd MMT2 We show that exposure to the oxidant H(2)O(2) induced MMT1 expression but not MMT2 expression

186 -to-volume ratio within the room caused peak H(2)O(2) mixing ratios to decrease and k(H(2)O(2)) to in

187 such as ELISA tests based on the peroxidase-H(2)O(2)-ABTS system, should be carried out at pH 4.4 to

188 The UV/hydrogen peroxide (H(2)O(2)) advanced oxidation process (AOP) frequently em

189 mbranes were treated with hydrogen peroxide (H(2)O(2)) and sodium hypochlorite (NaOCl, liquid bleach)

190 Two species, hydrogen peroxide (H(2)O(2)) and the superoxide anion radical (O(2)(.-)), a

191 roxyl radical ((*)OH) and hydrogen peroxide (H(2)O(2)) are regarded as major oxidants associated with

192 x reactions, I identified hydrogen peroxide (H(2)O(2)) as a normal constituent of aerobic life in euk

193 Hydrogen peroxide (H(2)O(2)) is a major reactive oxygen species in unicellu

194 Hydrogen peroxide (H(2)O(2)) is a reactive oxygen species (ROS) that mediat

195 19294-19298 (2019)] that hydrogen peroxide (H(2)O(2)) is spontaneously produced in micrometer-sized

196 t is no more sensitive to hydrogen peroxide (H(2)O(2)) killing than wild-type A. baumannii However, m

197 echanistically, excessive hydrogen peroxide (H(2)O(2)) originated from monoamine oxidase B in severe

198 tococcus parasanguinis, a hydrogen peroxide (H(2)O(2)) producing oral commensal, has antimicrobial ac

199 respiratory capacity and hydrogen peroxide (H(2)O(2)) production than aSAT (p < 0.05).

200 resulting in promotion of hydrogen peroxide (H(2)O(2)) production.

201 catalytic activity toward hydrogen peroxide (H(2)O(2)) reduction.

202 robic respiration but for hydrogen peroxide (H(2)O(2)) respiration using cytochrome c peroxidase (Ccp

203 ioxidant power (FRAP) and hydrogen peroxide (H(2)O(2)) scavenging assays, showed that GG exhibited th

204 3+)) reducing power; (iv) hydrogen peroxide (H(2)O(2)) scavenging.

205 er of water, glycerol and hydrogen peroxide (H(2)O(2)) that is expressed in various epithelial cells

206 rocatalytic production of hydrogen peroxide (H(2)O(2)) using a rotating ring-disk electrode, further

207 Epithelial production of hydrogen peroxide (H(2)O(2)) was analyzed in murine colonic epithelial cell

208 us-mediated generation of hydrogen peroxide (H(2)O(2)) we developed a model of intranasal supplementa

209 cose to gluconic acid and hydrogen peroxide (H(2)O(2)) while the chitin-AcOH decomposed the generated

210 or for the degradation of hydrogen peroxide (H(2)O(2)) with a K(m) of about 13 mM and specific activi

211 ugars, gluconic acid, and hydrogen peroxide (H(2)O(2)), which result from the enzymatic conversion of

212 osed to a strong oxidant, hydrogen peroxide (H(2)O(2)).

213 ction of oxygen (O(2)) to hydrogen peroxide (H(2)O(2)).

214 ght to generate cytosolic hydrogen peroxide (H(2)O(2)).

215 sustainable production of hydrogen peroxide (H(2)O(2)).

216 s the rapid production of hydrogen peroxide (H(2)O(2)).(1)(,)(2) This then acts as an activation sign

217 ([Formula: see text]) and hydrogen peroxide (H(2)O(2)); however, the precise mechanisms are unknown.

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

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

220 the polyamine spermine into spermidine plus H(2)O(2), is associated with increased human gastric can

221 ignificantly prevented by AAD-2004, a potent H(2)O(2) scavenger.

222 bstrate dopamine (DA) in especially prepared H(2)O(2) reaction solution.

223 uction of O(2) to H(2)O at pH 0, but produce H(2)O(2) at higher pH.

224 taining redox-active compounds might produce H(2)O(2) during shelf storage and potentially be consume

225 scle mitochondrial hydroperoxide production (H(2)O(2) and lipid hydroperoxides (LOOHs)).

226 physiological levels in the nanomolar range, H(2)O(2) is the major agent signalling through specific

227 ring and real-time detection of the released H(2)O(2).

228 o the starting dication while also releasing H(2)O(2).

229 In addition, repeatable H(2)O(2) sensing with the low concentration of 10 pM as

230 We identified a specific role for one ROS, H(2)O(2), in driving root hair initiation and demonstrat

231 We show that the small ROS, H(2)O(2), is increased in basal keratinocytes following

232 inguishable in the presence of exogenous ROS/H(2)O(2) Together, these data provide a molecular explan

233 fects both these functions not by scavenging H(2)O(2), but by repressing the nutrient signaling Ras-c

234 ricular myocytes expressing wild-type SERCA, H(2)O(2) caused a 25% increase in mitochondrial calcium

235 t unidentified chemoattractant.(3-5) Similar H(2)O(2)-activated signaling pathways are also critical

236 w death profile in stressed cells (starved + H(2)O(2)), while cell proliferation was stagnant.

237 adaptability to increased oxidative stress (H(2)O(2)).

238 Structurally, H(2)O(2) treatment reduced the number of cisternal membr

239 y enriched in cells survived after sublethal H(2)O(2) challenge.

240 ase (HRP) is uncompetitive for the substrate H(2)O(2) while it is competitive for the substrate ABTS.

241 l dimension between the electrode and target H(2)O(2) and 3-NT molecules.

242 der greater for the production of H(2)O than H(2)O(2).

243 Here we report that H(2)O(2) is spontaneously produced in water microdroplet

244 tion in condensate microdroplets showed that H(2)O(2) was generated from microdroplets with sizes typ

245 rates of Mg alloys were controlled, and the H(2)O(2) release kinetics was accelerated when the degra

246 calcium content was decreased by 31% and the H(2)O(2)-stimulated rise in mitochondrial calcium concen

247 enhances the sulfate formation rate for the H(2)O(2) oxidation pathway compared to the dilute soluti

248 Importantly, the H(2)O(2) formation kinetics can be precisely controlled

249 Time-course observations of the H(2)O(2) production in condensate microdroplets showed t

250 and further electrochemical detection of the H(2)O(2) released, enabling high-throughput analysis.

251 trains is inefficient, using only 10% of the H(2)O(2).

252 nges, however, decreased the toxicity of the H(2)O(2)/gluconic acid.

253 ting Thr241 phosphorylation can overcome the H(2)O(2) sensitivity of Tsa1-deficient cells.

254 We also found that the H(2)O(2) production yield strongly depends on environmen

255 These H(2)O(2)(-)-induced pathological features of AD in GiDs

256 By combining Mg alloys with Ti, H(2)O(2), which is an oxidizing agent that kills bacteri

257 lification was thereby translated into a TMB/H(2)O(2)-resulted electrochemical signal, acquired by sc

258 PGRP-induced incomplete reduction of O(2) to H(2)O(2) is downstream from dehydrogenases and ubiquinon

259 leads to O(2) rather than by 2e(-)/2H(+) to H(2)O(2).

260 egulates additional genes that contribute to H(2)O(2) resistance.

261 s replaced by serine (C674S) were exposed to H(2)O(2) (100 umol/Lmu).

262 by stressful stimuli induced by exposure to H(2)O(2) or S-nitrosoglutathione and DNA damage inducers

263 n mobility separation shows that exposure to H(2)O(2) results in the accumulation of a compact state

264 xidation pathway in peroxisomes and leads to H(2)O(2) production.

265 ate that P promotes hydrogenation of OOH* to H(2)O(2) by weakening the Pt-OOH* bond and suppressing t

266 iously that a partial reduction of oxygen to H(2)O(2) can facilitate damage to proteins hence, limits

267 lly more accessible 2e(-)/2H(+) reduction to H(2)O(2).

268 is required for both promoting resistance to H(2)O(2) and extending lifespan upon caloric restriction

269 affects the mitochondrial sensor response to H(2)O(2).

270 luding a peroxiredoxin-dependent response to H(2)O(2).

271 t is not redox active, but very sensitive to H(2)O(2), which accelerates the release of Cu ions from

272 sses the hypersensitivity of both strains to H(2)O(2) These results establish CydDC as a reducer of c

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

274 p a non-toxic, selective, and stable O(2)-to-H(2)O(2) electrocatalyst for realizing continuous on-sit

275 13.2 min with 7 mM salts and 4.5 mg/L total H(2)O(2) dosed in three separate injections in 5 min int

276 )-OCNT) shows nearly 100% selectivity toward H(2)O(2) and a positive shift of ORR onset potential by

277 nd showed excellent peroxidase-mimic towards H(2)O(2) using chronoamperometry (CA).

278 erve the loss of cellular antioxidants under H(2)O(2) induced oxidative stress and disturbances cause

279 n at near zero-overpotential with near unity H(2)O(2) selectivity at 0.27 V vs. RHE.

280 inhibited increases in albuminuria, urinary H(2)O(2), and mesangial matrix accumulation in db/db mic

281 , mesangial matrix accumulation, and urinary H(2)O(2) Administration of MTP-131 significantly inhibit

282 Recent reports indicate that LPMOs can use H(2)O(2) as an oxidant and thus carry out a novel type o

283 Using H(2)O(2) as oxidant, up to ~300 turnovers for the oxidat

284 ent mineralization of target compounds using H(2)O(2) or S(2)O(8)(2-) under UVA irradiation.

285 amplified amperometric peaks developed using H(2)O(2) activator and hydroquinone mediator.

286 he catalyst off the resulting polymers using H(2)O(2) oxidation.

287 The method used low-pressure UV/H(2)O(2) as the (*)OH generation system, methylene blue

288 enerates a lower (*)OH concentration than UV/H(2)O(2) at equivalent oxidant concentrations, with CH(3

289 AOP featured lower reagent costs than the UV/H(2)O(2) AOP but higher electricity costs that could be

290 s study investigated the influence of the UV/H(2)O(2) AOP on the elemental composition and DBP format

291 The UV/H(2)O(2) process is a promising advanced oxidation proce

292 c conditions, the primary oxidant formed was H(2)O(2), and under anodic conditions, a combination of

293 an <1 mum can contain up to 35% of the water+H(2)O(2) extractable arsenic as methylated species, but

294 ing wounding in larval zebrafish,(6-9) where H(2)O(2) activates the SFK Lyn to drive neutrophil chemo

295 d and gynoid fat decreased (p < 0.05), while H(2)O(2) production reduced in both depots, and mtDNA de

296 the ingredient significantly associated with H(2)O(2) production in combination with other ingredient

297 tion of LPMO-Cu(I) is 2,000-fold faster with H(2)O(2) than with O(2), the latter being several orders

298 s also observed when cells were treated with H(2)O(2) In vivo, high CCL-2 production was detected on

299 irradiation with UV light or treatment with H(2)O(2).

300 s dissociation of the HOO(-) ligand to yield H(2)O(2).