ライフサイエンスコーパス: ascorbate

1 in all wines was achieved by the addition of ascorbate.

2 containing the antioxidants glutathione and ascorbate.

3 xygen and biological reducing agents such as ascorbate.

4 plasma membrane conductance and the reduced ascorbate.

5 (hESCs) or hESCs cultured in the presence of ascorbate.

6 g compounds such as urate, paracetamol and l-ascorbate.

7 the generation of H2O2 via the oxidation of ascorbate.

8 lecular weight 148), an oxidative product of ascorbate.

9 duce the rate of reduction of the prodrug by ascorbate.

10 abolites, including amino acids, sugars, and ascorbate.

11 on, either electrochemically or using sodium ascorbate.

12 s/ferric ion and reducing agents including L-ascorbate.

13 llet culture in serum-free medium containing ascorbate.

14 skeletal system formation in the absence of ascorbate.

15 desirable charge recombination with oxidized ascorbate.

16 ially increase the post-harvest retention of ascorbate.

17 ms, in a manner that was reversed by dietary ascorbate.

18 s related to apoptosis, was downregulated by ascorbate.

19 (Ascorbate); (3) 10 mm l-NAME; or (4) 10 mm ascorbate + 10 mm l-NAME (Ascorbate + l-NAME).

20 (forming with k = 0.6 min(-1), pH 7.4, 10 mm ascorbate, 10 mum IsdG-heme, 22 degrees C) was identifie

21 decreased (dimethylamine, 4-DTA, creatinine, ascorbate, 2-hydroxyisobutyrate, allantoin, 4-DEA, 4-hyd

22 ger solution (Control); (2) 10 mm ascorbate (Ascorbate); (3) 10 mm l-NAME; or (4) 10 mm ascorbate + 1

23 Ascorbate acted cell-autonomously to negatively regulate

24 Ascorbate alone does not promote goethite dissolution un

25 The addition of sodium ascorbate along with L-5-MTHF enabled a sustained stabil

26 It was shown that local infusion of ascorbate (an anti-oxidant) improves NO-dependent forear

27 Pathway analysis implicated ascorbate and aldarate metabolism (P=9.0x10(-6)), and pe

28 tion in antioxidants and perturbation of the ascorbate and aldarate metabolism.

29 The metabolic pathway for ascorbate and aldarate was disturbed in all exposed spin

30 with important nutraceuticals like lycopene, ascorbate and antioxidants.

31 the interaction between BRD4 and H4 by which ascorbate and BETi blocked the binding of BRD4 to acetyl

32 roxide (H2O2) produced by high-concentration ascorbate and cell culture medium iron efficiently kills

33 a result, DHAR regenerates a pool of reduced ascorbate and detoxifies reactive oxygen species (ROS).

34 Altered enzyme activities and levels of ascorbate and free thiols resulting in enhanced membrane

35 levels but had little effect on phenotype or ascorbate and glutathione pools in standard conditions.

36 letion of low-molecular-weight antioxidants (ascorbate and glutathione) from a synthetic model of the

37 e reductases (DHARs) in interactions between ascorbate and glutathione.

38 st information regarding the location of the ascorbate and GSH binding sites and their interacting re

39 ccounting for the concentrations of adsorbed ascorbate and HBED, a synergistic effect could still be

40 g the bone formation model in the absence of ascorbate and in the presence of phosvitin which support

41 Cotreatment with ascorbate and JQ1 induced apoptosis and inhibited prolif

42 t of meat cooking and endogenous addition of ascorbate and nitrite was evaluated on protein oxidation

43 g in response to chromium(VI) metabolism via ascorbate and nonascorbate reduction: implications for i

44 We find that both ascorbate and RA or retinol promote the derivation of in

45 he treatment of roots with the ROS scavenger ascorbate and the NADPH oxidase inhibitor diphenyliodoni

46 Although ascorbate and thrombin both required calcium for their r

47 ment with antioxidants (N-acetylcysteine and ascorbate) and placebo.

48 Measured rate constants for O2, GSH, ascorbate, and NAD(P)H are also large at approximately 1

49 ing PCR conditions, levels of copper ion and ascorbate, and reaction time.

50 nzymes that are dependent on oxygen, Fe(II), ascorbate, and the Kreb's cycle intermediate 2-oxoglutar

51 the demethylation of both DNA and histones, ascorbate appears to be a mediator of the interface betw

52 Conversely, CVC was elevated with Ascorbate ( approximately 72% CVCmax ; both P < 0.03) bu

53 es, that the anticancer/cytotoxic effects of ascorbate are completely abolished by iron at physiologi

54 The anti-cancer effects of ascorbate are hypothesized to involve the autoxidation o

55 containing histone demethylases also require ascorbate as a cofactor for histone demethylation.

56 In this study, we evaluated ascorbate as a mediator of thrombin-induced barrier perm

57 potential clinical utility of pharmacologic ascorbate as a radiosensitizer in the treatment of pancr

58 tic compounds and related to glutathione and ascorbate as key endogenous antioxidants in several in v

59 enics exhibited higher glutathione (GSH) and ascorbate (AsA) contents under salinity stress.

60 ochrome c peroxidase (CcP)], suggesting both ascorbate (Asc) and cytochrome c (Cc) peroxidase activit

61 etabolism of Cr(VI) by its principal reducer ascorbate (Asc) lacks a Cr(V) intermediate, which is abu

62 In vitro experiments have shown that ascorbate (ASC) oxidation products can form AGEs in prot

63 Renewed interest in using pharmacological ascorbate (AscH-) to treat cancer has prompted interest

64 actated Ringer solution (Control); (2) 10 mm ascorbate (Ascorbate); (3) 10 mm l-NAME; or (4) 10 mm as

65 Vitamin C (ascorbate, ascorbic acid) supplementation has reduced ox

66 nsitizer, and an equimolar mixture of sodium ascorbate/ascorbic acid electron donor in pure water.

67 ketones catalyzed by Cu(II)-TD@nSiO2/sodium ascorbate at room temperature.

68 after addition of biological reducing agent ascorbate at the physiological concentration (~1 mM).

69 Since humans are ascorbate auxotrophs, enhancing the nutritional quality

70 lular ATP levels, at the same time enhancing ascorbate availability in AngII-treated VSMC.

71 ation solution (3 g of disodium EDTA, 7 g of ascorbate, B vitamins, electrolytes, procaine, and hepar

72 for clinical trials of high-dose intravenous ascorbate-based treatment for cancer.

73 The location of the ascorbate-binding site overlaps with the GSH-binding sit

74 orylase (GGP), a major control enzyme in the ascorbate biosynthesis pathway.

75 Although the main reactions of the ascorbate biosynthesis, recycling and translocation path

76 DH) catalyses the last enzymatic step of the ascorbate biosynthetic pathway in plants.

77 a sativa L. japonica (OsDHAR) in the native, ascorbate-bound, and GSH-bound forms and refined their r

78 Thrombin exposure consumed intracellular ascorbate but not the endogenous antioxidant GSH.

79 reatment.Significance: This study shows that ascorbate can enhance the efficacy of BET inhibitors, pr

80 ts between biogenic ligands and a reductant (ascorbate) can occur in Fe mobilization from soil.

81 kimate coupling, but instead is coupled with ascorbate catabolism, and controls the synthesis of the

82 c pancreatic tumor xenografts, pharmacologic ascorbate combined with ionizing radiation decreased tum

83 Ascorbate concentration is tightly regulated in plants,

84 downstream GGP open reading frame under high ascorbate concentration.

85 Here, we demonstrate that ascorbate concentrations are determined via the posttran

86 tion of translation and results in increased ascorbate concentrations in leaves.

87 f knowledge that could impair improvement of ascorbate content in fruits and vegetables as degradatio

88 Ascorbate content in plants is controlled by its synthes

89 eas phenolic content remained invariable and ascorbate content peaked near S5 in both 'Ntopia' (108.6

90 The availability of ascorbate could have significant consequences for health

91 sulfur causes dysfunction of the glutathione/ascorbate cycle, which reduces flavonoids.

92 Ascorbate deficiency as modeled in Gulo(-/-) mice dimini

93 talyzed by dioxygenases is incomplete due to ascorbate deficiency.

94 in ascorbate synthesis, as evidenced by the ascorbate-deficient mutant vtc2-1 accumulating wild-type

95 Finally, in embryos of the ascorbate-deficient mutants vtc2-4, vtc5-1, and vtc5-2,

96 Of these pathways, ascorbate degradation is the least studied and represent

97 s study, we showed that erythrulose, a major ascorbate degradation product, reacts spontaneously with

98 Kynurenine pathway metabolites and ascorbate degradation products are present in human lens

99 ause l-ascorbate loss, but the mechanisms of ascorbate degradation remain incompletely understood, es

100 Ascorbate degradation was stimulated by darkness, and th

101 14)C]oxalate was the major product of [(14)C]ascorbate degradation, suggesting that commercial washin

102 thione (GSH)-dependent reduction of oxidized ascorbate (dehydroascorbate, DHA).

103 This study highlights that ascorbate/dehydroascorbic acid are lost via the oxidativ

104 Adding sodium ascorbate delayed degradation of divicine.

105 Pharmacological ascorbate depleted cellular NAD+ preferentially in cance

106 Ascorbate depletion cooperated with Flt3 internal tandem

107 sion, oxidation of the glutathione pool, and ascorbate depletion in a cat2-2 genetic background upon

108 Systemic ascorbate depletion in mice increased HSC frequency and

109 Our findings show, for the first time, that ascorbate-derived xylosone can contribute to an increase

110 imately 60% CVCmax ; all P < 0.04); however, Ascorbate did not modulate CVC during exercise ( approxi

111 quired calcium for their respective effects, ascorbate did not prevent thrombin permeabilization by o

112 to (64)Cu(I) with the existence of sodium L-ascorbate, DL-Dithiothreitol or cysteine.

113 ced by common interfering substances such as ascorbate, dopamine and dihydroxyphenylacetic acid.

114 Additions of ascorbate dose- and time-dependently enhance the generat

115 ach leaves were particularly prone to losing ascorbate during washing, especially with simultaneous m

116 Moreover, the ascorbate efflux activity was also measured in Arabidops

117 Ascorbate enhanced the efficacy of BETi by decreasing ac

118 Our findings suggest that ascorbate enhances 5-hmC generation, most likely by acti

119 These results suggest that ascorbate enhances 5-hmC generation, most likely by acti

120 urrent study demonstrates that pharmacologic ascorbate enhances the cytotoxic effects of ionizing rad

121 Further, blocking ascorbate entry into cells by phloretin and knocking dow

122 s then possible to determine an AERC indice (Ascorbate Equivalent Reducing Capacity) and a CECC (Carn

123 tween 14 and 82% of the total As was citrate-ascorbate extractable.

124 Disruption of this uORF stops the ascorbate feedback regulation of translation and results

125 th each type of cysteine modification (e.g., ascorbate for SNO).

126 by showing an activation of glutathione and ascorbate free radical scavenger systems.

127 During chase in ascorbate- free medium, anMan-containing HS disappeared

128 w in mouse embryonic fibroblasts cultured in ascorbate-free medium.

129 Sodium ascorbate, glutathione, and kojic acid are promising inh

130 We investigated the antioxidant metabolites (ascorbate, glutathione, tocopherols, and polyphenols) an

131 A significant increase on most ascorbate-glutathione cycle components and on carbonylat

132 In this work, ascorbate-glutathione cycle components, hydrogen peroxid

133 one S-transferases, indicated a key role for ascorbate/glutathione cycles.

134 n the native state; exposure to ascorbate or ascorbate/glutathione leads to nitroxide reduction and a

135 Pharmacological ascorbate has been proposed as a potential anti-cancer a

136 ese findings show that anticancer effects of ascorbate have been significantly overestimated in previ

137 Pharmacological levels of ascorbate have long been suggested as a potential treatm

138 a marked increase in pyrimidines as well as ascorbate, heme, and other indices of oxidative stress.

139 reaction mix contains iron(II) EDTA, sodium ascorbate, hydrogen peroxide and lysozyme.

140 Increased cortex ascorbate in embryos carrying extra copies of the SVCT2

141 y, and potential efficacy of pharmacological ascorbate in GBM and NSCLC therapy.

142 sues known to possess high concentrations of ascorbate in mice.

143 Thus, we have uncovered a novel role for ascorbate in modulating the epigenetic control of genome

144 We identified a novel role for ascorbate in preserving cAMP during thrombin stimulation

145 The presence of copper ions and/or ascorbate in solution was necessary to efficiently decom

146 vidence and potential molecular mechanism of ascorbate in the demethylation of the genome, and it hig

147 hypothesis on mechanisms of accumulation of ascorbate in the later stages of fruit ripening.

148 a profound impact on the bioavailability of ascorbate in the nucleus.

149 f fluorescent CuNPs through the reduction by ascorbate in the presence of dsDNA templates.

150 Together, these data implicate ascorbate in the prevention of inflammatory endothelial

151 However, the downstream effectors of ascorbate in the regulation of endothelial permeability

152 cells, suggesting a limit of pharmacological ascorbate in treating cancer.

153 it highlights potential epigenetic roles of ascorbate in various diseases.

154 mple Sharpless-Fokin catalyst CuSO4 + sodium ascorbate in water under ambient conditions leading to e

155 -N,N'-diacetic acid (HBED)) and a reductant (ascorbate) in goethite dissolution.

156 ngs under Hyg stress, and pre-treatment with ascorbate increased resistance to Hyg-induced toxicity i

157 Here we show that 100 microM of ascorbate induced apoptosis in A2058 melanoma cells.

158 Pharmacological ascorbate induced cell death in pancreatic cancer cells

159 Lactoferrin did not have any effect on the ascorbate induced degradation of beta-glucan, whereas ov

160 generated in endosomes by an endogenously or ascorbate-induced S-nitrosothiolcatalyzed reaction.

161 that expression of APP/APLP2 is required for ascorbate-induced transport of HS from endosomes to the

162 Reductants such as glutathione and ascorbate inhibited both the oxidation of the substrate

163 and encodes a peptide that functions in the ascorbate inhibition of translation.

164 ng candidate for inhibiting the formation of ascorbate/iron(II) induced hydroxyl radicals in beta-glu

165 icroencapsulating L-5-MTHF along with sodium ascorbate is effective to produce a stable folate in for

166 espite historical controversy, pharmacologic ascorbate is emerging as promising cancer therapy via pr

167 by endothelial nitric-oxide synthase, which ascorbate is known to activate, and the subsequent gener

168 This posttranslational regulation of ascorbate is likely an ancient mechanism of control as t

169 The toxicity of pharmacologic ascorbate is mediated by the generation of H2O2 via the

170 Vitamin C (ascorbate) is likely to be essential for skeletal muscle

171 sing interest in using high-dose intravenous ascorbate (IVC) in treating this disease partially becau

172 with l-NAME ( approximately 35% CVCmax ) and Ascorbate + l-NAME ( approximately 43% CVCmax ) compared

173 with l-NAME ( approximately 50% CVCmax ) and Ascorbate + l-NAME ( approximately 47% CVCmax ; all P >

174 NAME; or (4) 10 mm ascorbate + 10 mm l-NAME (Ascorbate + l-NAME).

175 nature of degradation products using [(14) C]ascorbate labelling in tomato, a model plant for fleshy

176 hypothesized to involve the autoxidation of ascorbate leading to increased steady-state levels of H2

177 proteins are strongly associated with plasma ascorbate levels and likely impact tissue cellular vitam

178 re clinical trials with BETi should consider ascorbate levels in patients.

179 gII, leading to re-establishment of cellular ascorbate levels, increased VHL binding, and decreased H

180 All leaves tested showed ascorbate loss during storage: lettuce showed the greate

181 We explored the extent and pathways of ascorbate loss in variously washed and stored salad leav

182 re-packaged salad leaves potentially cause l-ascorbate loss, but the mechanisms of ascorbate degradat

183 hypochlorite did not significantly increase ascorbate loss.

184 zes H4K5ac and H4K12ac, was downregulated by ascorbate mainly via the TET-mediated DNA hydroxymethyla

185 First, ascorbate maintained the cortical actin cytoskeleton in

186 ith a total of 19 traits, including sucrose, ascorbate, malate, and citrate levels.

187 g radiolabeled (55)Fe demonstrated that this ascorbate-mediated reduction is an obligatory step for t

188 revealed superior regenerability by each of ascorbate, N-acetylcysteine, and urate when compared to

189 e and changes in amino acids, phospholipids, ascorbate, nucleotides and nicotinate/nicotinamide.

190 O2 production by Cu-Abeta in the presence of ascorbate occurs mainly via a free O2 (-) intermediate.

191 (siRNA) significantly inhibit the effect of ascorbate on 5-hmC.

192 t was hidden due to the inhibitory effect of ascorbate on HBED adsorption.

193 A synergistic effect of DFOB and ascorbate on the rate of goethite dissolution was observ

194 nitroxides in the native state; exposure to ascorbate or ascorbate/glutathione leads to nitroxide re

195 was constant and independent of the initial ascorbate or dehydroascorbic acid concentration over per

196 However, they require unstable ascorbate or imidazole activation.

197 Reactions conducted with ascorbate or N-acetylcysteine as a reductant under aerob

198 ols with moderate reducing capacity, such as ascorbate or tyrosine.

199 In comparison, the dietary antioxidant, ascorbate or vitamin C, can substantially prevent such d

200 asing ROS levels by applying the antioxidant ascorbate, or the ROS-generation inhibitor diphenylene i

201 nts that have either high (PAO) or low (TAO) ascorbate oxidase (AO) activities relative to the wild t

202 e sequence of OsORAP1 was similar to that of ASCORBATE OXIDASE (AO) proteins.

203 dual-channel telemetric device, based on an ascorbate oxidase (AOx) biosensor, were developed for on

204 Thus, an ascorbate oxidase was introduced to remove the ascorbic

205 ascorbic acid based on the immobilization of ascorbate oxidase, a relatively unstable enzyme.

206 A new carbon ascorbate oxidase-based sensor-biosensor system (SB) was

207 These were partially explained by changes in ascorbate oxidation and recycling.

208 trate a novel biochemical mechanism by which ascorbate oxidation and the kynurenine pathway intertwin

209 Herein, palmitoyl ascorbate (PA) as a prooxidant for hydrogen peroxide (H2

210 vides an overview on the architecture of the ascorbate pathway.

211 Here, we applied engineered ascorbate peroxidase (APEX) to map the proteome at EMCs

212 Here, we used enhanced ascorbate peroxidase (APEX)-tagged PB2 proteins and elec

213 live Drosophila tissues using an engineered ascorbate peroxidase (APEX).

214 ty, associated with lower catalase (CAT) and ascorbate peroxidase (APX) activities, leading to fruits

215 CuZn-superoxide dismutase (CuZn-SOD) and ascorbate peroxidase (APX) constitute first line of defe

216 ant enzymes viz. superoxide dismutase (SOD), ascorbate peroxidase (APX), guaiacol peroxidase (GPX) an

217 This study aimed to investigate the role of ascorbate peroxidase (APX), guaiacol peroxidase (GPX), p

218 yl histidine (NMH) ligand into an engineered ascorbate peroxidase (APX2) overcomes the reliance on th

219 l downstream genes, including those encoding ascorbate peroxidase (AtApx2) and heat shock proteins [A

220 Interestingly, cytosolic ascorbate peroxidase (cAPX), a key enzyme controlling H2

221 Critically, over-expression of stromal ascorbate peroxidase (H2O2 scavenger) or treatment with

222 (2-Cys) peroxiredoxins (PRXs) and thylakoid ascorbate peroxidase (tAPX), have been proposed to be in

223 Arabidopsis mutants deficient in Ascorbate Peroxidase 1 showed attenuated hydrotropic roo

224 We recently reported enhanced ascorbate peroxidase 2 (APEX2) as a broadly applicable g

225 We show that HSEs from the promoter of the ASCORBATE PEROXIDASE 2 (APX2) gene were necessary and su

226 hat catalase activity increased in roots and ascorbate peroxidase activity decreased in leaves.

227 the enzymes glutathione reductase, catalase, ascorbate peroxidase and superoxide dismutase together w

228 ol to 78.8 in 750 mg kg(-1) treatment; while ascorbate peroxidase decreased from 21.9 to 14.1 in 500

229 compound responses, with a high induction of ascorbate peroxidase expression.

230 Two mitochondrial-localized rice ascorbate peroxidase genes fused to DsRed and successful

231 in a position analogous to the substrate in ascorbate peroxidase is essential for both decarboxylati

232 The Trypanosoma cruzi ascorbate peroxidase is, by sequence analysis, a hybrid

233 Analysis of a thylakoidal ascorbate peroxidase mutant (tapx), the (1)O2-retrograde

234 Cytosolic ascorbate peroxidase over-expression has little effect o

235 A new study makes use of the ascorbate peroxidase proximity-labeling proteomics appro

236 ation-modified cysteine residue on cytosolic ascorbate peroxidase was demonstrated using liquid chrom

237 salt stress, including several genes such as ASCORBATE PEROXIDASE2, GLUTATHIONE S-TRANSFERASE TAU9, a

238 drogen peroxide-scavenging enzyme, cytosolic ASCORBATE PEROXIDASE6 (APX6), yet its specific function

239 degradation rate was evaluated at 63% of the ascorbate pool per day, a percentage that was constant a

240 n-reversible and leads to a depletion of the ascorbate pool.

241 negligible levels without marked effects on ascorbate pools, (2) the cytosolic isoforms are particul

242 tion of TET2 and TET3 transcription, whereas ascorbate potentiates TET activity and 5hmC production t

243 Second, ascorbate prevented actin polymerization and formation o

244 hmC) is an epigenetic hallmark of cancer and ascorbate promotes 5 hmC generation by serving as a cofa

245 The rate of ascorbate radical (Asc(-)) formation (and stability) was

246 dation as determined by the concentration of ascorbate radical [Asc*-] and the rate of oxygen consump

247 Treatment with catalase reduced the ascorbate radical contents by as much as 67%.

248 Treatment with DTPA further reduced ascorbate radical signals to below quantifiable levels i

249 The infant formulas contained ascorbate radicals ranging from about 138 nM to 40 nM.

250 Ascorbate radiosensitization was associated with an incr

251 gradation could be partially affected by the ascorbate recycling pathway, as lines under-expressing m

252 association was found between PM2.5 mass or ascorbate-related oxidative burden and FeNO levels.

253 Between-city differences in ascorbate-related oxidative potential did not modify the

254 Controlling for interference by ascorbate revealed that AqH augmented NO production in M

255 An anti-oxidant ascorbate reversed albumin-induced inhibition of prolyl-

256 multi-targeting mechanism of pharmacological ascorbate's anti-cancer action, with minimal toxicity, a

257 reactive oxygen species drive pharmacologic ascorbate's selective toxicity to cancer cells in vitro,

258 ve stress associated with an accumulation of ascorbate-sensitive ROS impairs NO-dependent cutaneous v

259 Ascorbate serves as a cofactor for Ten-eleven translocat

260 In contrast, ascorbate supplementation lowered the effective dose of

261 Furthermore, ascorbate supplementation might help reduce the severe s

262 ars to be independent of the role of GLDH in ascorbate synthesis, as evidenced by the ascorbate-defic

263 pH 5) and the photochemical [Ru(phen)3](2+)/ascorbate system.

264 Instead, embryos efflux high amounts of ascorbate that chemically reduce iron(III) from citrate-

265 ngly potentiated in oocytes preinjected with ascorbate (the canonical electron donor for cytochrome b

266 Emerging evidence suggests that ascorbate, the dominant form of vitamin C under physiolo

267 Ascorbate therefore accumulates within HSCs to promote T

268 Upon addition of hydrogen peroxide and ascorbate, these L7Ae-tethered nucleases were expected t

269 cer cells are sensitive to H2O2 generated by ascorbate, they would also be expected to become sensiti

270 ncer (NSCLC) and glioblastoma (GBM) cells to ascorbate through pro-oxidant chemistry involving redox-

271 impending therapeutic role of physiological ascorbate to potentiate apoptosis in melanoma.

272 have been associated with severely decreased ascorbate transport and lower systemic concentrations.

273 isk of CD has implications for understanding ascorbate transport in CD patients and provides a novel

274 acil symporter is a member of the nucleobase/ascorbate transporter (NAT) family of proteins, and is r

275 suggest that the SLC4, SLC26, and nucleobase-ascorbate transporter families all share an elevator tra

276 , a xanthine transporter from the nucleobase-ascorbate transporter family, show that the downward piv

277 SLC23A1 is a major ascorbate transporter in the intestinal tract, and some

278 enetic variant (rs10063949-G) in the SLC23A1 ascorbate transporter locus was identified and is associ

279 The role of ascorbate transporters in IBD remains to be determined.

280 Our previous work demonstrated that ascorbate treatment at physiological level (100 muM) inc

281 ic nuclear CLU was largely maintained, after ascorbate treatment.

282 ncentrations and compared this relation with ascorbate uptake by leukocytes.

283 nt transport, alternative carbon pathways (l-ascorbate utilization and metabolism), growth arrest res

284 etinoic acid (RA) or retinol (vitamin A) and ascorbate (vitamin C) act as modulators of TET levels an

285 Intracellular ascorbate (vitamin C) has previously been shown to tight

286 Ascorbate (vitamin C) is an essential antioxidant and en

287 Ascorbate (vitamin C) is best known for its role in scur

288 Cells were pretreated with or without ascorbate (vitamin C), which promotes DNA demethylation

289 new osteoid/bone formation in the absence of ascorbate (vitamin C).

290 Ascorbate was assayed by 2,6-dichlorophenolindophenol ti

291 However, we observed that EC50 of ascorbate was at a similar level for cultured healthy me

292 However, preservation of cAMP by ascorbate was found to depend on both the production of

293 Glutathione and ascorbate were less effective.

294 e presence of physiological concentration of ascorbate, were quickly reduced to their active form, ox

295 is a key enzyme involved in the recycling of ascorbate, which catalyses the glutathione (GSH)-depende

296 and mouse HSCs had unusually high levels of ascorbate, which decreased with differentiation.

297 hat AqH augmented NO production in MPhis via ascorbate, which limited degradation of H(4)B.

298 to a decrease in the rate of reduction with ascorbate, which makes the electrochemical reduction pot

299 ), and it has no cleavage in the presence of ascorbate, which reduces Cu(2+) to Cu(+).

300 In situ reduction with sodium ascorbate yields Cu(I)-containing MONPs that serve as hi