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1 bate peroxidase) and its reducing substrate (ascorbate).
2 ially increase the post-harvest retention of ascorbate.
3 ms, in a manner that was reversed by dietary ascorbate.
4 s related to apoptosis, was downregulated by ascorbate.
5 in all wines was achieved by the addition of ascorbate.
6  containing the antioxidants glutathione and ascorbate.
7 omparable to that upon chemical reduction by ascorbate.
8 xygen and biological reducing agents such as ascorbate.
9  plasma membrane conductance and the reduced ascorbate.
10 (hESCs) or hESCs cultured in the presence of ascorbate.
11 g compounds such as urate, paracetamol and l-ascorbate.
12  the generation of H2O2 via the oxidation of ascorbate.
13 lecular weight 148), an oxidative product of ascorbate.
14 ripening fruit that exhibits high amounts of ascorbate.
15 oth NDMA and NPYR contents in the absence of ascorbate.
16 t to turnover by inclusion of the reductant, ascorbate.
17  (Ascorbate); (3) 10 mm l-NAME; or (4) 10 mm ascorbate + 10 mm l-NAME (Ascorbate + l-NAME).
18 (forming with k = 0.6 min(-1), pH 7.4, 10 mm ascorbate, 10 mum IsdG-heme, 22 degrees C) was identifie
19 decreased (dimethylamine, 4-DTA, creatinine, ascorbate, 2-hydroxyisobutyrate, allantoin, 4-DEA, 4-hyd
20 ger solution (Control); (2) 10 mm ascorbate (Ascorbate); (3) 10 mm l-NAME; or (4) 10 mm ascorbate + 1
21 ongest predictors of IA were change in serum ascorbate, 3-methyl-oxobutyrate, and the PTPN22 (rs24766
22 at involves a multivalent interaction with L-ascorbate 6-phosphate lactonase (UlaG), a protein marker
23                                            l-Ascorbate, a lactone, is oxidized and ring-opened by enz
24                                              Ascorbate acted cell-autonomously to negatively regulate
25                                              Ascorbate alone does not promote goethite dissolution un
26                       The addition of sodium ascorbate along with L-5-MTHF enabled a sustained stabil
27          It was shown that local infusion of ascorbate (an anti-oxidant) improves NO-dependent forear
28              In contrast, the combination of ascorbate and 15 g kg(-1) black pepper resulted in a dec
29 a bifunctional peroxidase that oxidizes both ascorbate and 4-coumarate at comparable rates.
30                  Pathway analysis implicated ascorbate and aldarate metabolism (P=9.0x10(-6)), and pe
31 t of branched-chain amino acid biosynthesis, ascorbate and aldarate metabolism, the tricarboxylic aci
32 tion in antioxidants and perturbation of the ascorbate and aldarate metabolism.
33                    The metabolic pathway for ascorbate and aldarate was disturbed in all exposed spin
34 with important nutraceuticals like lycopene, ascorbate and antioxidants.
35 the interaction between BRD4 and H4 by which ascorbate and BETi blocked the binding of BRD4 to acetyl
36 a result, DHAR regenerates a pool of reduced ascorbate and detoxifies reactive oxygen species (ROS).
37 levels but had little effect on phenotype or ascorbate and glutathione pools in standard conditions.
38 except OsMDHAR), as well as its metabolites (ascorbate and glutathione) and uptake of nutrients (Mg,
39 letion of low-molecular-weight antioxidants (ascorbate and glutathione) from a synthetic model of the
40 e reductases (DHARs) in interactions between ascorbate and glutathione.
41 st information regarding the location of the ascorbate and GSH binding sites and their interacting re
42 ccounting for the concentrations of adsorbed ascorbate and HBED, a synergistic effect could still be
43 d an additional pathway involving apoplastic ascorbate and iron can account for ROS production upon h
44                             Cotreatment with ascorbate and JQ1 induced apoptosis and inhibited prolif
45 t of meat cooking and endogenous addition of ascorbate and nitrite was evaluated on protein oxidation
46 g in response to chromium(VI) metabolism via ascorbate and nonascorbate reduction: implications for i
47                            We find that both ascorbate and RA or retinol promote the derivation of in
48 he treatment of roots with the ROS scavenger ascorbate and the NADPH oxidase inhibitor diphenyliodoni
49                                     Although ascorbate and thrombin both required calcium for their r
50 onation states of the electron/proton donor (ascorbate) and all of the residues involved in the elect
51 ment with antioxidants (N-acetylcysteine and ascorbate) and placebo.
52         Measured rate constants for O2, GSH, ascorbate, and NAD(P)H are also large at approximately 1
53 ing PCR conditions, levels of copper ion and ascorbate, and reaction time.
54 nzymes that are dependent on oxygen, Fe(II), ascorbate, and the Kreb's cycle intermediate 2-oxoglutar
55  degradation and increase in soluble sugars, ascorbate, and TPC, together leading to higher germinati
56  the demethylation of both DNA and histones, ascorbate appears to be a mediator of the interface betw
57            Conversely, CVC was elevated with Ascorbate ( approximately 72% CVCmax ; both P < 0.03) bu
58                   The anti-cancer effects of ascorbate are hypothesized to involve the autoxidation o
59 ix (NAD, NADP, thioredoxin, glutathione, and ascorbate) are in kinetic steady state rather than therm
60 containing histone demethylases also require ascorbate as a cofactor for histone demethylation.
61                  In this study, we evaluated ascorbate as a mediator of thrombin-induced barrier perm
62  potential clinical utility of pharmacologic ascorbate as a radiosensitizer in the treatment of pancr
63 tic compounds and related to glutathione and ascorbate as key endogenous antioxidants in several in v
64  H16 (Cupriavidus necator ATCC 17699) uses l-ascorbate as sole carbon source via a novel catabolic pa
65 ent increased in sucuk both with and without ascorbate, as cooking level increased.
66 eyes and aqueous humor antioxidant levels of ascorbate (AsA) and total reactive antioxidant potential
67 ochrome c peroxidase (CcP)], suggesting both ascorbate (Asc) and cytochrome c (Cc) peroxidase activit
68 etabolism of Cr(VI) by its principal reducer ascorbate (Asc) lacks a Cr(V) intermediate, which is abu
69         Using an increased osmotic load with ascorbate (Asc), five new low-volume PEG-based bowel pre
70                                              Ascorbate (Asc; vitamin C) plays essential roles in deve
71 actated Ringer solution (Control); (2) 10 mm ascorbate (Ascorbate); (3) 10 mm l-NAME; or (4) 10 mm as
72 nsitizer, and an equimolar mixture of sodium ascorbate/ascorbic acid electron donor in pure water.
73                              TaAA9A oxidizes ascorbate at a rate similar to free copper but through a
74                             Since humans are ascorbate auxotrophs, enhancing the nutritional quality
75 lular ATP levels, at the same time enhancing ascorbate availability in AngII-treated VSMC.
76 Our findings suggest that higher exposure to ascorbate, beta-carotene, retinol, or urate does not low
77                          The location of the ascorbate-binding site overlaps with the GSH-binding sit
78 orylase (GGP), a major control enzyme in the ascorbate biosynthesis pathway.
79           Although the main reactions of the ascorbate biosynthesis, recycling and translocation path
80 DH) catalyses the last enzymatic step of the ascorbate biosynthetic pathway in plants.
81 a sativa L. japonica (OsDHAR) in the native, ascorbate-bound, and GSH-bound forms and refined their r
82                             Reduction of the ascorbate breakdown product 2-keto-l-gulonic acid to l-i
83                     PfCopC is not reduced by ascorbate but is a very strong Cu(II) chelator due to re
84     Thrombin exposure consumed intracellular ascorbate but not the endogenous antioxidant GSH.
85 reatment.Significance: This study shows that ascorbate can enhance the efficacy of BET inhibitors, pr
86 ts between biogenic ligands and a reductant (ascorbate) can occur in Fe mobilization from soil.
87 kimate coupling, but instead is coupled with ascorbate catabolism, and controls the synthesis of the
88 c pancreatic tumor xenografts, pharmacologic ascorbate combined with ionizing radiation decreased tum
89            S(Ca) and S(Mg) treatments raised ascorbate concentration and reduced nitrate levels in tr
90                                              Ascorbate concentration is tightly regulated in plants,
91                    Here, we demonstrate that ascorbate concentrations are determined via the posttran
92 tion of translation and results in increased ascorbate concentrations in leaves.
93 mined by ion chromatography, chlorophyll and ascorbate concentrations, and hydrophilic/lipophilic ant
94 rn, fruit firmness correlated inversely with ascorbate content and with alpha-l-arabinofuranosidase (
95 f knowledge that could impair improvement of ascorbate content in fruits and vegetables as degradatio
96                                              Ascorbate content in plants is controlled by its synthes
97 eas phenolic content remained invariable and ascorbate content peaked near S5 in both 'Ntopia' (108.6
98                                       Copper-ascorbate (Cu-As) was utilized as an oxidative stress ge
99 lved in sulfur assimilation, the glutathione-ascorbate cycle, and various antioxidant systems were up
100 sulfur causes dysfunction of the glutathione/ascorbate cycle, which reduces flavonoids.
101                                       Sodium ascorbate decreased residual nitrite considerably.
102                                              Ascorbate deficiency as modeled in Gulo(-/-) mice dimini
103  in ascorbate synthesis, as evidenced by the ascorbate-deficient mutant vtc2-1 accumulating wild-type
104                           Of these pathways, ascorbate degradation is the least studied and represent
105 s study, we showed that erythrulose, a major ascorbate degradation product, reacts spontaneously with
106           Kynurenine pathway metabolites and ascorbate degradation products are present in human lens
107 ause l-ascorbate loss, but the mechanisms of ascorbate degradation remain incompletely understood, es
108                                              Ascorbate degradation was stimulated by darkness, and th
109 14)C]oxalate was the major product of [(14)C]ascorbate degradation, suggesting that commercial washin
110 thione (GSH)-dependent reduction of oxidized ascorbate (dehydroascorbate, DHA).
111                   This study highlights that ascorbate/dehydroascorbic acid are lost via the oxidativ
112                                Adding sodium ascorbate delayed degradation of divicine.
113 s signaling mechanism, suggesting a role for ascorbate-dependent peroxidase (APX), which degrades mit
114                              Pharmacological ascorbate depleted cellular NAD+ preferentially in cance
115 experience high respiratory rates leading to ascorbate depletion and a quickly fragile and perishable
116                                              Ascorbate depletion cooperated with Flt3 internal tandem
117 sion, oxidation of the glutathione pool, and ascorbate depletion in a cat2-2 genetic background upon
118                                     Systemic ascorbate depletion in mice increased HSC frequency and
119  Our findings show, for the first time, that ascorbate-derived xylosone can contribute to an increase
120 imately 60% CVCmax ; all P < 0.04); however, Ascorbate did not modulate CVC during exercise ( approxi
121 quired calcium for their respective effects, ascorbate did not prevent thrombin permeabilization by o
122  to (64)Cu(I) with the existence of sodium L-ascorbate, DL-Dithiothreitol or cysteine.
123 ach leaves were particularly prone to losing ascorbate during washing, especially with simultaneous m
124                                              Ascorbate enhanced the efficacy of BETi by decreasing ac
125 urrent study demonstrates that pharmacologic ascorbate enhances the cytotoxic effects of ionizing rad
126 s then possible to determine an AERC indice (Ascorbate Equivalent Reducing Capacity) and a CECC (Carn
127 ng acerola fruit ripening and shed lights on ascorbate, ethylene signalling, cellular respiration, su
128 abolite measurements, allowed us to focus on ascorbate, ethylene, respiration, sugar, and firmness, t
129            Disruption of this uORF stops the ascorbate feedback regulation of translation and results
130  by showing an activation of glutathione and ascorbate free radical scavenger systems.
131                                       Sodium ascorbate, glutathione, and kojic acid are promising inh
132 We investigated the antioxidant metabolites (ascorbate, glutathione, tocopherols, and polyphenols) an
133  anatomy, inhibited enzyme activities of the ascorbate-glutathione cycle (while transcripts of associ
134 ulation of Si channel and transporter genes, ascorbate-glutathione cycle and nutrient uptake, and low
135               A significant increase on most ascorbate-glutathione cycle components and on carbonylat
136                                In this work, ascorbate-glutathione cycle components, hydrogen peroxid
137 oxygenation rate (V(NO)), while depletion of ascorbate had no effect.
138                              Pharmacological ascorbate has been proposed as a potential anti-cancer a
139                    Pharmacological levels of ascorbate have long been suggested as a potential treatm
140  reaction mix contains iron(II) EDTA, sodium ascorbate, hydrogen peroxide and lysozyme.
141 y, and potential efficacy of pharmacological ascorbate in GBM and NSCLC therapy.
142               We identified a novel role for ascorbate in preserving cAMP during thrombin stimulation
143           The presence of copper ions and/or ascorbate in solution was necessary to efficiently decom
144 vidence and potential molecular mechanism of ascorbate in the demethylation of the genome, and it hig
145  hypothesis on mechanisms of accumulation of ascorbate in the later stages of fruit ripening.
146  a profound impact on the bioavailability of ascorbate in the nucleus.
147               Together, these data implicate ascorbate in the prevention of inflammatory endothelial
148         However, the downstream effectors of ascorbate in the regulation of endothelial permeability
149 cells, suggesting a limit of pharmacological ascorbate in treating cancer.
150  it highlights potential epigenetic roles of ascorbate in various diseases.
151 -N,N'-diacetic acid (HBED)) and a reductant (ascorbate) in goethite dissolution.
152 ngs under Hyg stress, and pre-treatment with ascorbate increased resistance to Hyg-induced toxicity i
153 reaction at RT when using CuSO(4) and sodium ascorbate independently of the click chemistry approach
154              Here we show that 100 microM of ascorbate induced apoptosis in A2058 melanoma cells.
155                              Pharmacological ascorbate induced cell death in pancreatic cancer cells
156   Lactoferrin did not have any effect on the ascorbate induced degradation of beta-glucan, whereas ov
157           Reductants such as glutathione and ascorbate inhibited both the oxidation of the substrate
158  and encodes a peptide that functions in the ascorbate inhibition of translation.
159 ng candidate for inhibiting the formation of ascorbate/iron(II) induced hydroxyl radicals in beta-glu
160 icroencapsulating L-5-MTHF along with sodium ascorbate is effective to produce a stable folate in for
161 espite historical controversy, pharmacologic ascorbate is emerging as promising cancer therapy via pr
162  by endothelial nitric-oxide synthase, which ascorbate is known to activate, and the subsequent gener
163         This posttranslational regulation of ascorbate is likely an ancient mechanism of control as t
164                The toxicity of pharmacologic ascorbate is mediated by the generation of H2O2 via the
165 sing interest in using high-dose intravenous ascorbate (IVC) in treating this disease partially becau
166 with l-NAME ( approximately 35% CVCmax ) and Ascorbate + l-NAME ( approximately 43% CVCmax ) compared
167 with l-NAME ( approximately 50% CVCmax ) and Ascorbate + l-NAME ( approximately 47% CVCmax ; all P >
168 NAME; or (4) 10 mm ascorbate + 10 mm l-NAME (Ascorbate + l-NAME).
169 nature of degradation products using [(14) C]ascorbate labelling in tomato, a model plant for fleshy
170  hypothesized to involve the autoxidation of ascorbate leading to increased steady-state levels of H2
171 re clinical trials with BETi should consider ascorbate levels in patients.
172 gII, leading to re-establishment of cellular ascorbate levels, increased VHL binding, and decreased H
173                     All leaves tested showed ascorbate loss during storage: lettuce showed the greate
174       We explored the extent and pathways of ascorbate loss in variously washed and stored salad leav
175 re-packaged salad leaves potentially cause l-ascorbate loss, but the mechanisms of ascorbate degradat
176  hypochlorite did not significantly increase ascorbate loss.
177 zes H4K5ac and H4K12ac, was downregulated by ascorbate mainly via the TET-mediated DNA hydroxymethyla
178                                       First, ascorbate maintained the cortical actin cytoskeleton in
179 O2 production by Cu-Abeta in the presence of ascorbate occurs mainly via a free O2 (-) intermediate.
180 t was hidden due to the inhibitory effect of ascorbate on HBED adsorption.
181             A synergistic effect of DFOB and ascorbate on the rate of goethite dissolution was observ
182  was constant and independent of the initial ascorbate or dehydroascorbic acid concentration over per
183 rricyanide serves as an oxidant and external ascorbate or dithionite provide a source of electrons to
184               However, they require unstable ascorbate or imidazole activation.
185                     Reactions conducted with ascorbate or N-acetylcysteine as a reductant under aerob
186 lusion of endogenous redox molecules such as ascorbate or nitrite.
187 ols with moderate reducing capacity, such as ascorbate or tyrosine.
188      In comparison, the dietary antioxidant, ascorbate or vitamin C, can substantially prevent such d
189 asing ROS levels by applying the antioxidant ascorbate, or the ROS-generation inhibitor diphenylene i
190 nts that have either high (PAO) or low (TAO) ascorbate oxidase (AO) activities relative to the wild t
191 e sequence of OsORAP1 was similar to that of ASCORBATE OXIDASE (AO) proteins.
192  dual-channel telemetric device, based on an ascorbate oxidase (AOx) biosensor, were developed for on
193                                     Finally, ascorbate oxidase was coated to eliminate interferences
194                      The enzymes uricase and ascorbate oxidase were used to remove uric and ascorbic
195 ascorbic acid based on the immobilization of ascorbate oxidase, a relatively unstable enzyme.
196 These were partially explained by changes in ascorbate oxidation and recycling.
197 trate a novel biochemical mechanism by which ascorbate oxidation and the kynurenine pathway intertwin
198     We evaluated their catalytic activity in ascorbate oxidation based on redox cycling between Cu(I)
199 e-catalyzed oxygen activation, as well as on ascorbate oxidation.
200                              Pharmacological ascorbate (P-AscH(-), high-dose, intravenous vitamin C)
201                            Herein, palmitoyl ascorbate (PA) as a prooxidant for hydrogen peroxide (H2
202 vides an overview on the architecture of the ascorbate pathway.
203 al network by knocking in (KI) an engineered ascorbate peroxidase (APEX) gene to the endogenous locus
204                  Here, we applied engineered ascorbate peroxidase (APEX) to map the proteome at EMCs
205                       Here, we used enhanced ascorbate peroxidase (APEX)-tagged PB2 proteins and elec
206  live Drosophila tissues using an engineered ascorbate peroxidase (APEX).
207                                  We used the ascorbate peroxidase (APEX2) proximity labeling system,
208 ty, associated with lower catalase (CAT) and ascorbate peroxidase (APX) activities, leading to fruits
209     CuZn-superoxide dismutase (CuZn-SOD) and ascorbate peroxidase (APX) constitute first line of defe
210 ys of several enzymatic antioxidants such as ascorbate peroxidase (APX), catalase (CAT), superoxide d
211  This study aimed to investigate the role of ascorbate peroxidase (APX), guaiacol peroxidase (GPX), p
212 yl histidine (NMH) ligand into an engineered ascorbate peroxidase (APX2) overcomes the reliance on th
213 l downstream genes, including those encoding ascorbate peroxidase (AtApx2) and heat shock proteins [A
214                    We identified the plastid ascorbate peroxidase (cpAPX) genes across angiosperms an
215       Critically, over-expression of stromal ascorbate peroxidase (H2O2 scavenger) or treatment with
216  (2-Cys) peroxiredoxins (PRXs) and thylakoid ascorbate peroxidase (tAPX), have been proposed to be in
217             Arabidopsis mutants deficient in Ascorbate Peroxidase 1 showed attenuated hydrotropic roo
218 tagenesis, horseradish peroxidase (HRP), and ascorbate peroxidase 2 (APEX-2) proximity labelling, alo
219                    Using a modified enhanced ascorbate peroxidase 2 (APEX2) approach with rapamycin-d
220                We recently reported enhanced ascorbate peroxidase 2 (APEX2) as a broadly applicable g
221 ed higher superoxide dismutase, catalase and ascorbate peroxidase activities as compared to control.
222  by higher activity of superoxide dismutase, ascorbate peroxidase and phenylalanine ammonia-lyase.
223 the enzymes glutathione reductase, catalase, ascorbate peroxidase and superoxide dismutase together w
224 labeling technique, APEX-seq, which uses the ascorbate peroxidase APEX2 to probe the spatial organiza
225 tate of the iron(IV) oxo (or ferryl) form of ascorbate peroxidase compound II (APX-II) is a subject o
226 compound responses, with a high induction of ascorbate peroxidase expression.
227             Two mitochondrial-localized rice ascorbate peroxidase genes fused to DsRed and successful
228  in a position analogous to the substrate in ascorbate peroxidase is essential for both decarboxylati
229                        The Trypanosoma cruzi ascorbate peroxidase is, by sequence analysis, a hybrid
230                    Analysis of a thylakoidal ascorbate peroxidase mutant (tapx), the (1)O2-retrograde
231                                    Cytosolic ascorbate peroxidase over-expression has little effect o
232 howed that WKS1 phosphorylates the thylakoid ascorbate peroxidase protein and reduces its ability to
233                 A new study makes use of the ascorbate peroxidase proximity-labeling proteomics appro
234 antioxidant enzymes catalase, peroxidase and ascorbate peroxidase was also increased at harvest by SA
235 ation-modified cysteine residue on cytosolic ascorbate peroxidase was demonstrated using liquid chrom
236 alpha(1C) or beta(2B) subunits conjugated to ascorbate peroxidase(5) in mouse hearts, and use multipl
237 omplex formed between a redox metalloenzyme (ascorbate peroxidase) and its reducing substrate (ascorb
238 xin, glutathione peroxidase-like enzymes and ascorbate peroxidase, all of which have cell compartment
239 salt stress, including several genes such as ASCORBATE PEROXIDASE2, GLUTATHIONE S-TRANSFERASE TAU9, a
240 ed signal compared with previously described ascorbate peroxidases.
241 degradation rate was evaluated at 63% of the ascorbate pool per day, a percentage that was constant a
242 n-reversible and leads to a depletion of the ascorbate pool.
243  negligible levels without marked effects on ascorbate pools, (2) the cytosolic isoforms are particul
244 tion of TET2 and TET3 transcription, whereas ascorbate potentiates TET activity and 5hmC production t
245                                      Second, ascorbate prevented actin polymerization and formation o
246 hmC) is an epigenetic hallmark of cancer and ascorbate promotes 5 hmC generation by serving as a cofa
247                                  The rate of ascorbate radical (Asc(-)) formation (and stability) was
248          Treatment with catalase reduced the ascorbate radical contents by as much as 67%.
249          Treatment with DTPA further reduced ascorbate radical signals to below quantifiable levels i
250                The infant formulas contained ascorbate radicals ranging from about 138 nM to 40 nM.
251                                              Ascorbate radiosensitization was associated with an incr
252 on and higher alpha-amylase activity, higher ascorbate (RAsA) and TPC were observed in the tolerant c
253 gradation could be partially affected by the ascorbate recycling pathway, as lines under-expressing m
254  association was found between PM2.5 mass or ascorbate-related oxidative burden and FeNO levels.
255 o, Canada (2016-2017), including glutathione/ascorbate-related oxidative potential (OP(GSH) and OP(AA
256                  Between-city differences in ascorbate-related oxidative potential did not modify the
257 ically determined differences in circulating ascorbate, retinol, and urate are not associated with di
258                              An anti-oxidant ascorbate reversed albumin-induced inhibition of prolyl-
259 multi-targeting mechanism of pharmacological ascorbate's anti-cancer action, with minimal toxicity, a
260  reactive oxygen species drive pharmacologic ascorbate's selective toxicity to cancer cells in vitro,
261 ve stress associated with an accumulation of ascorbate-sensitive ROS impairs NO-dependent cutaneous v
262                                              Ascorbate serves as a cofactor for Ten-eleven translocat
263                                 In contrast, ascorbate supplementation lowered the effective dose of
264                                 Furthermore, ascorbate supplementation might help reduce the severe s
265 ars to be independent of the role of GLDH in ascorbate synthesis, as evidenced by the ascorbate-defic
266 ngly potentiated in oocytes preinjected with ascorbate (the canonical electron donor for cytochrome b
267              Emerging evidence suggests that ascorbate, the dominant form of vitamin C under physiolo
268                                              Ascorbate therefore accumulates within HSCs to promote 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  antioxidant exposure (ranging from 1.00 for ascorbate to 1.05 for retinol).
272  impending therapeutic role of physiological ascorbate to potentiate apoptosis in melanoma.
273 de (MDA) as a measure of lipid peroxidation, ascorbate, total phenolic concentration (TPC), and activ
274 ipid peroxidation correlated negatively with ascorbate, TPC, and with ROS scavengers.
275 acil symporter is a member of the nucleobase/ascorbate transporter (NAT) family of proteins, and is r
276 karyotic member of the ubiquitous nucleobase ascorbate transporter (NAT) family.
277 suggest that the SLC4, SLC26, and nucleobase-ascorbate transporter families all share an elevator tra
278 , a xanthine transporter from the nucleobase-ascorbate transporter family, show that the downward piv
279                                Pharmacologic ascorbate treatment (P-AscH(-), high-dose, intravenous v
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 pepper levels (5, 10 or 15 g kg(-1)), sodium ascorbate usage and cooking level (raw, medium, medium w
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                                            l-Ascorbate (vitamin C) is ubiquitous in both our diet and
288 NPs) that determine variation in circulating ascorbate (vitamin C), beta-carotene, retinol (vitamin A
289        Cells were pretreated with or without ascorbate (vitamin C), which promotes DNA demethylation
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  to a decrease in the rate of reduction with ascorbate, which makes the electrochemical reduction pot
298 ), and it has no cleavage in the presence of ascorbate, which reduces Cu(2+) to Cu(+).
299 in the presence of copper sulfate and sodium ascorbate, while the modification of the catalytic syste
300                In situ reduction with sodium ascorbate yields Cu(I)-containing MONPs that serve as hi

 
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