ライフサイエンスコーパス: GSH

1 GSH deficiency compromised the activation of mammalian t

2 GSH/Grx1 provide an alternative mechanism to thioredoxin

3 -1beta, IL-6, and IL-8, and increased IL-10, GSH, SOD, and CAT levels.

4 viors showed that dual stimuli (pH=5.3, 10mM GSH) induced the quickest release of siRNA from the NPs.

5 Therefore, we developed (1) a GSH-based photoaffinity probe (GSTABP-G) to target the "

6 igh mTORC1 signaling, based on cotargeting a GSH-controlled oxidative stress pathway.

7 structures reveal the structural basis for a GSH-mediated allosteric mode of activation of PrfA in th

8 he assay is based on the masking of GSH in a GSH and GSSG mixture via a 1,4-addition reaction with p-

9 hionylation during ischemia-reperfusion in a GSH-independent manner.

10 The GST active site is composed of a GSH binding "G site" and a substrate binding "H site".

11 the case of trypanothione disulfide (TS2), a GSH-spermidine bioconjugate, involved in the antioxidati

12 es were observed in the contents of TPC, AA, GSH and Cys and CUPRAC values in all samples that were d

13 l protein with phospholipase A2 (aiPLA2) and GSH peroxidase activities, protects lungs from oxidative

14 regarding the location of the ascorbate and GSH binding sites and their interacting residues.

15 (OsDHAR) in the native, ascorbate-bound, and GSH-bound forms and refined their resolutions to 1.9, 1.

16 over, a significant decrease in cysteine and GSH levels in the pancreas and brain, respectively, was

17 ich were previously ascribed to cysteine and GSH.

18 hypothesized that the degradation of Gln and GSH may lead to a deficiency for the host, possibly init

19 This indicates that Gln and GSH supplementation may help reducing tissue damage caus

20 effect of oral supplementation with Gln and GSH was assessed.

21 uch as antioxidant status (SOD, CAT, GPX and GSH) and lipid peroxidation was also studied.

22 n was reversed by glutaredoxin 1 (Grx1), and GSH plus Grx1 was able to support the peroxidase activit

23 f oxidized and reduced glutathione (GSSG and GSH) can be measured with essentially no additional effo

24 e total glutathione content (GSH + GSSG) and GSH in saliva is significantly greater than in plasma, e

25 for UV-induced covalent binding to GSTs and GSH-binding enzymes.

26 he reduced protein was treated with H2O2 and GSH.

27 e limits of detection (LOD) for Cys, Hcy and GSH were 0.156, 0.185, and 1.838 muM, respectively.

28 ing site probes to distinguish Cys, Hcy, and GSH is highlighted as a creative new direction in the fi

29 de insult in a pentose phosphate pathway and GSH-dependent manner.

30 h glutathione (GSH) based on the low pH- and GSH-sensitive arsenic-sulfur bond, and we termed the res

31 y crystal structure of GSTP1 bound to PL and GSH at 1.1 A resolution to rationalize previously report

32 dently manipulated superoxide production and GSH metabolism during reperfusion.

33 luding STAT3 and phospho-STAT3 (pSTAT3), and GSH attenuated these responses.

34 Trx and GSH inhibition may lead to a reprogramming of the immune

35 and could be selectively targeted by Trx and GSH inhibitors.

36 therapies based on silencing of the Trx and GSH pathways represent a promising approach for the cure

37 Dual inhibition of the Trx and GSH systems synergistically kills neoplastic cells in vi

38 ascorbate but not the endogenous antioxidant GSH.

39 nfected host cells and exogenous antioxidant GSH accelerated mutant invading growth without increasin

40 uated after cotreatment with the antioxidant GSH.

41 The antioxidative GSH pathway thus plays an unexpected role in metabolic i

42 Exogenously applied GSH could improve stress tolerance in wild-type plants b

43 eins and low molecular weight thiols such as GSH.

44 CBS in human breast cancer cells attenuated GSH/GSSG, total GSH, nuclear factor erythroid 2-related

45 ked increase in ROS production and augmented GSH reductase and antioxidant regulator NRF2 activity, b

46 ts GSTP1, which forms covalent bonds between GSH and various electrophilic compounds, through covalen

47 Our findings thus establish a link between GSH deficiency and Th1/Th2 disequilibrium in LP-BM5 infe

48 of glutamate cysteine ligase (Gclc) blocked GSH production specifically in murine T cells.

49 all those viral infections characterized by GSH deficiency and a Th1/Th2 imbalance to be more effect

50 bility for ACO1 was found to be increased by GSH, which explains our above observations.

51 The restoration of GSH levels by GSH-replenishing molecules can represent a new therapeut

52 ducible factor (HIF)-1alpha is stabilized by GSH adducts, and the genetic deletion of Glrx improves i

53 ing to PrfA in the cytosol of the host cell, GSH induces the correct fold of the HTH motifs, thus pri

54 ompounds were identified to elevate cellular GSH levels by a novel approach (i.e. post-translational

55 a resting-state H(+) 'shuttle' conductance (GSH) in VGCs and Ci VSP, and we now report that R1H is s

56 reversibly modified thiols, and MS confirms GSH adducts on Cys(520) (mouse Cys(533)).

57 stability of the total glutathione content (GSH + GSSG) and GSH in saliva is significantly greater t

58 s of H2S were obtained from the combined Cys/GSH and copper treatments in white wine.

59 glutathione (GSH) levels, although cytosolic GSH remained normal.

60 ounced apoptosis associated with a decreased GSH/GSSG ratio, augmented nuclear factor erythroid-relat

61 reased reactive oxygen species and decreased GSH.

62 Glibenclamide decreased GSH levels and glutathione peroxidase (GPx) of PMNs afte

63 sults showed that HT significantly decreased GSH content, the ratio of reduced to oxidized glutathion

64 arity switching electrospray MS/MS to detect GSH conjugates that form positive and/or negative ions.

65 erometric techniques were employed to detect GSH sensitively using a GCE modified with TCNQ/GO at -0.

66 The CNDs were also able to detect GSH very selectively over other biothiols like cysteine

67 ographic water acts as a general base during GSH thiolate formation, stabilized by interaction with A

68 uces significant deviations in subcellular E(GSH) between U937 and U1, which distinctly modulates sus

69 The ability of DMP to elevate GSH levels and attenuate LPS-induced pro-inflammatory cy

70 ionine beta-synthase (CBS) promotes elevated GSH/GSSG.

71 (Arabidopsis thaliana) plants with enhanced GSH content (AtECS) exhibited remarkable up-regulation o

72 and CML levels, via Nrf2 pathway, enhancing GSH/GSSG ratio, heme oxygenase-1 and glyoxalase 1 in liv

73 otypes were rescued by addition of exogenous GSH and overexpression of Sod2, which suppressed indices

74 Our results suggest that exogenous GSH enhances cucumber seedling tolerance of HT stress by

75 The exogenous GSH treatment clearly lessened the HT stress by increasi

76 results in an electrocatalytic activity for GSH oxidation and GSSG reduction, enabling the simultane

77 teine (L-Cys) production is insufficient for GSH synthesis.

78 etry reveals detection limits of 100 muM for GSH and 8.3 muM for GSSG, respectively.

79 Three oxidation waves for GSH were found at -0.05, 0.1 and 0.5V, respectively.

80 the presence of glutathione (GSH) generates GSH-protein adducts that are specifically reversed by th

81 Glutathione (GSH) and cysteine (Cys) were determined as the thiol con

82 Glutathione (GSH) has so far been considered to facilitate detoxifica

83 Glutathione (GSH) plays a fundamental role in plant defense-signaling

84 Glutathione (GSH)-induced degradation of self-immolative linkers rele

85 using dithiothreitol (DTT) and glutathione (GSH) as liberating agents.

86 (Cys), homocysteine (Hcy), and glutathione (GSH) play crucial roles in maintaining redox homeostasis

87 tems, the thioredoxin (Trx) and glutathione (GSH) systems, actually promote cancer growth and HIV inf

88 Cysteine (Cys) and glutathione (GSH) were associated with small increases in H2S concent

89 both for arsenic [As (III)] and glutathione (GSH) with high selectivity.

90 (Cys), homocysteine (Hcy), and glutathione (GSH), play a key role in an extensive range of physiolog

91 lular glutamine, glutamate, and glutathione (GSH).

92 thyroxine (T4, p = 0.042), and glutathione (GSH, p = 0.034) concentrations than control birds.

93 maintenance of the antioxidant glutathione (GSH) is essential for their survival and proliferation.

94 at synthesis of the antioxidant glutathione (GSH), driven by GCLM, is required for cancer initiation.

95 intracellular thiol antioxidant glutathione (GSH), thereby increasing levels of reactive oxygen speci

96 sis of the cellular antioxidant glutathione (GSH).

97 which trigger the antioxidative glutathione (GSH) response necessary to buffer rising ROS and prevent

98 cursor for antioxidants such as glutathione (GSH) and NADPH, and GLN deprivation is therefore predict

99 n of the commercially available glutathione (GSH).

100 mors, MnO2 /DVDMS is reduced by glutathione (GSH) and H2 O2 and reassembled into nanoDVD, which can b

101 esized that increasing cellular glutathione (GSH) levels would inhibit neuroinflammation.

102 formation within the cofactor, glutathione (GSH).

103 s Gln, H. suis can also convert glutathione (GSH) to glutamate, and both reactions are catalyzed by t

104 the presence of the cosubstrate glutathione (GSH).

105 ) stress mitigated by exogenous glutathione (GSH), cucumber (Cucumis sativus L.) seedlings were expos

106 llei in vitro showed lower free glutathione (GSH) levels compared with those of healthy individuals.

107 particularly those involved in glutathione (GSH) metabolism, were among the most prominently up-regu

108 genes involved in intracellular glutathione (GSH) biosynthesis and inactivation of 4-HNE-induced phos

109 miting enzyme for intracellular glutathione (GSH) synthesis.

110 Cys-SSH and its glutathione (GSH) counterpart (GSSH) have been recognized as redox re

111 resh and dry yeasts up to 81 mg glutathione (GSH) per 1g dry sample were found.

112 lease and reduced mitochondrial glutathione (GSH) levels, although cytosolic GSH remained normal.

113 an be triggered by depletion of glutathione (GSH) and accumulation of lipid reactive oxygen species (

114 sociated decreases in levels of glutathione (GSH) are known to play a central role in ALD.

115 gen sulfide (H2S) by 50% and of glutathione (GSH) by 40%.

116 idues to ROS in the presence of glutathione (GSH) generates GSH-protein adducts that are specifically

117 owever, a high concentration of glutathione (GSH) is present in cancer cells and can consume reactive

118 BAN and BAM shared depletion of glutathione (GSH) or cellular thiols as a molecular initiating event

119 to different concentrations of glutathione (GSH) showing a linear relationship between the slope of

120 tamate is used for synthesis of glutathione (GSH).

121 I(-) ligand in the presence of glutathione (GSH).

122 he ratio of reduced to oxidized glutathione (GSH/GSSG), chlorophyll content, photosynthesis and relat

123 ed ratio of reduced to oxidized glutathione (GSH/GSSG).

124 The redox pair glutathione (GSH) and glutathione disulphide (GSSG) forms the most im

125 expressed in hepatic pericytes, glutathione (GSH), and malondialdehyde (MDA) concentrations in liver;

126 cells cotreated with BITC plus glutathione (GSH).

127 ide bond formation and promotes glutathione (GSH) oxidation to GSSG.

128 glutathione imbalance, reduced glutathione (GSH) and cysteine were quantified in different organs.

129 raction with tripeptide reduced glutathione (GSH) bioreceptor directly immobilized on the dielectric

130 romotes regeneration of reduced glutathione (GSH) by supplying NADPH to glutathione reductase or thio

131 perometric detection of reduced glutathione (GSH) in pH 7.2 phosphate buffer solution (PBS) has been

132 high concentrations of reduced glutathione (GSH) inside the cells, thereby facilitating the decomple

133 Reduced glutathione (GSH) is an efficient antioxidant on limiting browning, l

134 d with higher cytosolic reduced glutathione (GSH) levels.

135 similarly oxidized the reduced glutathione (GSH) pool, phase II iron limitation exhibited transient

136 tivity, effect on total reduced glutathione (GSH) synthesis and protective effect against H2O2 and me

137 n is the conjugation of reduced glutathione (GSH) to endo- and xenobiotics.

138 of oxidized (GSSG) and reduced glutathione (GSH), biomarkers of oxidative stress, is demonstrated in

139 beta, IL-6, IL-8, IL10, reduced glutathione (GSH), superoxide dismutase (SOD), and catalase (CAT).

140 oducing an antioxidant, reduced glutathione (GSH), through HIF-1-mediated metabolic reprogramming.

141 sed in the detection of reduced glutathione (GSH).

142 the mean value for the [reduced glutathione (GSH)]/[oxidized glutathione (GSSG)] ratio was significan

143 d it was recently proposed that glutathione (GSH) could fulfill this function.

144 It catalyzes the glutathione (GSH)-dependent dealkylation of alkylcobalamins and the r

145 ascorbate, which catalyses the glutathione (GSH)-dependent reduction of oxidized ascorbate (dehydroa

146 and is especially sensitive to glutathione (GSH) compared to alternative assays.

147 The tripeptide glutathione (GSH) is a crucial intracellular reductant and radical sc

148 ion kinetics was studied, using glutathione (GSH) and cysteine (CYS) as model systems.

149 fficiency of the reaction using glutathione (GSH) as an oligopeptide stopper, we have employed cytoch

150 a Michael addition adduct with glutathione (GSH) and inhibits IKKbeta phosphorylation.

151 m albumin (HSA) pretreated with glutathione (GSH) based on the low pH- and GSH-sensitive arsenic-sulf

152 iety can directly interact with glutathione (GSH), thereby reducing its intracellular concentration.

153 rm stable mixed disulfides with glutathione (GSH).

154 under a redox environment (10mM glutathione, GSH), and demonstrated enhanced cytotoxicity against 4T1

155 murine aortic endothelial (MAE) cells, GSSG/GSH was over twice as high in EOMA cells.

156 mpared with in the cytosol, the nuclear GSSG/GSH ratio was 5-fold higher.

157 efficacy of internet-based guided self-help (GSH-I) compared with traditional, individual face-to-fac

158 Consistent with these findings, hepatic GSH was depleted at the onset of biliary injury, and in

159 y injury, and in situ mapping of the hepatic GSH redox potential using a redox-sensitive green fluore

160 et had a similar oxidation level, but higher GSH and lower SOD activities.

161 nd the beef protein group showed the highest GSH, Grx1 and Trx1 levels as reflected by RT-PCR, Wester

162 ydrolysis initiates the formation of the hPL-GSH conjugate, which blocks the active site of and inhib

163 rminus functionalization is likely to impair GSH homeostasis substantially through blocking the gamma

164 ne ligase (GCL), the rate-limiting enzyme in GSH biosynthesis).

165 creased by p62 attenuation and implicated in GSH production and utilization.

166 nnects Asp-49 to distal residues involved in GSH binding and is ligand dependent.

167 ne) and lipid (malondialdehyde) and increase GSH content both in bleomycin treated mouse lungs and TG

168 Finally, the ability of DMP to increase GSH via GCL activation was observed in mixed cerebrocort

169 Compound 25 increased GSH intracellular levels and showed no toxicity on mitoc

170 elease induced by lowering pH and increasing GSH levels, both occurring in cancer cells.

171 ablation stabilizes HIF-1alpha by increasing GSH adducts on Cys(520) promoting in vivo HIF-1alpha sta

172 a protein levels are increased by increasing GSH adducts with cell-permeable oxidized GSH (GSSG-ethyl

173 t during the very early phases of infection, GSH depletion and the downregulation of interleukin-12 (

174 MnO2 nanosheets are reduced by intracellular GSH.

175 ediated reprogramming elevated intracellular GSH levels, and consequently induced a radioresistant ph

176 for their ability to increase intracellular GSH levels in a murine microglial cell line (BV2), of wh

177 ncer cells due to depletion of intracellular GSH and ensuing elevated ROS; yet this treatment results

178 and also restored depletion of intracellular GSH levels, suggesting that free radical scavenging abil

179 nt with the PEEs increased the intracellular GSH content.

180 Intriguingly, GSH catalyzes their hydrolysis.

181 itivity, incorporated stable-isotope labeled GSH to avoid false positives, and used fast polarity swi

182 To study the biological effects of low GSH levels, we disrupted its synthesis both at birth by

183 he chicken and fish protein groups had lower GSH and higher SOD activities, the pork protein group sh

184 periodontitis group had significantly lower GSH and higher MDA concentration in the liver compared w

185 i) the mammalian antioxidant responses (MDA, GSH and SOD2 levels), (ii) tissue nutrient (glucose) and

186 Using the fabricated microwire, GSH can be detected with the sensitivity of 0.7 nA muM(-

187 ysis of the first breakdown step of modified GSH, and thus its timely reconstitution.

188 iza glabra, which was found to form multiple GSH conjugates upon metabolic activation.

189 glutathione stabilized copper nanoclusters (GSH-CuNCs).

190 arged glutathione capped gold nanoparticles (GSH-AuNPs) were electrostatically self-assembled onto th

191 Conversely, mice in which neuronal GSH levels were maintained by N-acetyl cysteine treatmen

192 nt and O2*(-) production rate compared to no GSH treatment in the HT condition.

193 hus be easily removed by the addition of non-GSH thiols.

194 Reinstating H2S but not GSH in CBS-silenced ECs restored Sp1 levels and its bind

195 includes a comparison with cyclic adducts of GSH and furan metabolites as reported in literature, and

196 ) s(-1)) for physiological concentrations of GSH to inhibit Prx disulfide formation and protect again

197 A marked redox imbalance, consisting of GSH and/or cysteine depletion, was found in the lymphoid

198 Intriguingly, the decrease of GSH, the production of O2 , and the formation of nanoDVD

199 H:GSSG ratio arising from the degradation of GSH and formation of GSSG.

200 thway that was characterized by depletion of GSH and ascorbic acid and accumulation of cytosolic and

201 These results point to possible depletion of GSH, an essential antioxidant, and its precursor gamma-G

202 uccessfully applied towards the detection of GSH in an eye drop solution.

203 electrode was used for the determination of GSH and GSSG in rat urine and plasma samples, intoxicate

204 e, this study aims to evaluate the effect of GSH addition (10, 20 and 30mgL(-1)) after the disgorging

205 The present study examines the effect of GSH deficiency on alcohol-induced liver steatosis in Gcl

206 emoassay analyses of the adduct formation of GSH with nine alpha,beta-unsaturated carbonyls employing

207 edox homeostasis confirmed the importance of GSH in modulating biliatresone-induced injury given that

208 th oxidative stress and direct inhibition of GSH biosynthesis by buthionine sulfoximine.

209 ly releasing Ce6 and decreasing the level of GSH for highly efficient PDT.

210 study, we investigated if enhanced levels of GSH and its derivatives can protect plants from Ag NPs a

211 hat are characterized by divergent levels of GSH, Cys, and Hcy.

212 KO mice, associated with increased levels of GSH-protein adducts, capillary density, vascular endothe

213 ry, even in the presence of normal levels of GSH.

214 e approximately 15% normal hepatic levels of GSH.

215 Pharmacological and genetic manipulation of GSH redox homeostasis confirmed the importance of GSH in

216 The assay is based on the masking of GSH in a GSH and GSSG mixture via a 1,4-addition reactio

217 r, the data demonstrate a novel mechanism of GSH elevation by post-translational activation of GCL.

218 utathionyl-cobalamin by a second molecule of GSH yields GSSG.

219 e (n = 153) failed to show noninferiority of GSH-I (adjusted effect, 1.47; 95% CI, -0.01 to 2.91; P =

220 on to VitC with concomitant normalization of GSH concentration and Nox4 expression in diabetic mice.

221 nd CblC, as well as into the organization of GSH and a base-off cobalamin in the active site of this

222 ow p62 helps maintain intracellular pools of GSH needed to limit mitochondrial dysfunction in tumor c

223 building block in the facile preparation of GSH bioconjugates in a satisfying overall yield was exem

224 ecially CaCl2 improved the oxidation rate of GSH.

225 generation and perturbations in the ratio of GSH to oxidized GSH, whereas MIOX-siRNA or N-acetyl cyst

226 ylation always forms the initial reaction of GSH with Michael-acceptor carbonyls.

227 normalized redox balance via regeneration of GSH from existing cellular pools.

228 at promote GSH synthesis and regeneration of GSH from GSSG.

229 ike 2 (Nrf2), a transcriptional regulator of GSH synthesis, inhibited EHC injury.

230 The restoration of GSH levels by GSH-replenishing molecules can represent a

231 Our results portray the role of GSH and GSSG as markers of oxidative stress in live orga

232 the possible adsorption over the surface of GSH-CuNCs.

233 terminus of the gamma-glutamyl (Glu) unit of GSH.

234 link between the effect of glibenclamide on GSH and PMN functions in response to B. pseudomallei tha

235 the time-dependent chemical modifications on GSH and GSSG that are caused by dielectric barrier disch

236 The effects of Hv1 mutations on GSH and GAQ are used to constrain the positions of key s

237 yses also showed the superiority of CBT over GSH-I by the 6-month (adjusted effect, 0.36; 95% CI, 0.2

238 ing GSH adducts with cell-permeable oxidized GSH (GSSG-ethyl ester) or 2-acetylamino-3-[4-(2-acetylam

239 substances and ratios of reduced to oxidized GSH) or organ masses between exposed and control birds.

240 erturbations in the ratio of GSH to oxidized GSH, whereas MIOX-siRNA or N-acetyl cysteine treatment a

241 The nano-assembly PM-GSH-CuNCs was applied for the selective detection of nit

242 Advantageously, the nano-assembly PM-GSH-CuNCs was chemically adsorbed over the cellulosic st

243 of picric acid (PA), the fluorescence of PM-GSH-CuNCs was selectively quenched at 410nm and 625nm

244 Immunotherapy based on the use of pro-GSH molecules would permit LP-BM5 infection and probably

245 nd processes downstream of Nrf2 that promote GSH synthesis and regeneration of GSH from GSSG.

246 We used quantitative GSH and GSSG biosensors to monitor glutathione import in

247 ometric titrations at biologically realistic GSH/Cu(I) ratios, enabled by our recently developed Cu(I

248 eport that R1H is sufficient to reconstitute GSH in Hv1 without abrogating GAQ.

249 Carbon monoxide (CO) reduced GSH/GSSG in three breast cancer cell lines by inhibiting

250 t thiol oxidase activity, converting reduced GSH to oxidized GSSG with concomitant scrubbing of ambie

251 to determine the concentrations of reduced (GSH) and oxidized glutathione (GSSG), and it enables the

252 re developed to accurately quantify reduced (GSH), oxidized (GSSG) and total (tGSH) glutathione in bi

253 or of the modified electrode toward reduced (GSH) and oxidized (GSSG) forms of glutathione was assess

254 ngiocytes to the toxin, whereas replenishing GSH level by N-acetylcysteine administration or activati

255 52), an N-acetyl-cysteine supplier, restored GSH/cysteine levels in the organs, reduced the expressio

256 uel types were observed for S-glutathione (S-GSH) and S-gamma-glutamylcysteine (S-gamma-GluCys), both

257 yrene, the largest reductions in levels of S-GSH and S-gamma-GluCys relative to controls were observe

258 sing the modified intention-to-treat sample, GSH-I was inferior to CBT in reducing OBE days at the en

259 185A/H) and S4 (N4R) experimentally separate GSH and GAQ gating, which report thermodynamically disti

260 logical doses of VC induce oxidative stress, GSH depletion, and increased glucose flux through the ox

261 ay be a better initial treatment option than GSH-I.

262 Together, these results confirm that GSH is critical for cytosolic Fe-S protein biogenesis an

263 ating biliatresone-induced injury given that GSH depletion sensitized both EHCs and the otherwise res

264 complete SQR catalytic cycle indicates that GSH serves as the physiologically relevant sulfur accept

265 ant ethylene insensitive2-1, indicating that GSH-mediated resistance to these stresses occurs via an

266 We further observed that GSH induced ACS2 and ACS6 transcription in a WRKY33-depe

267 We report that GSH is essential for T cell effector functions through i

268 The results show that GSH concentration decreased to the level of the control

269 The GSH concentration and GCL activity are declining with ag

270 The GSH reduces browning and acetaldehyde formation for up t

271 The GSH treatment remarkably improved soluble protein conten

272 The GSH-Cu(I) interaction is thus a key consideration for bo

273 ectric function at the RPH condition and the GSH concentration.

274 ed a further 3 orders of magnitude below the GSH/Cu(I) affinity limit, consistent with the most recen

275 ing-compatible structure without binding the GSH activator molecule.

276 Besides enriching the GSH adductome and potential biomarker applications, elec

277 evels, while they were down-regulated in the GSH-depleted phytoalexin deficient2-1 (pad2-1) mutant.

278 ficantly higher in the CBT group than in the GSH-I group at 6-month follow-up (adjusted effect, -0.4;

279 vestigation, the nature and stability of the GSH-Cu(I) complexes formed under biologically relevant c

280 In particular, formation of the GSH-N single adduct contradicts the traditional view tha

281 inimizes the in vitro underestimation of the GSH:GSSG ratio arising from the degradation of GSH and f

282 GSSG), and it enables the calculation of the GSH:GSSG ratios in human plasma and saliva samples.

283 dicate that I-152 can be used to restore the GSH level and a balanced Th1/Th2 response in infected mi

284 acellular viability after treatment with the GSH synthesis inhibitor buthionine sulfoximine, and amin

285 the ascorbate-binding site overlaps with the GSH-binding site, suggesting a ping-pong kinetic mechani

286 I/MAVS-dependent cytokine production through GSH depletion, mitochondrial dysfunction, the activation

287 Total GSH levels were slightly increased after pretreatment wi

288 east cancer cells attenuated GSH/GSSG, total GSH, nuclear factor erythroid 2-related factor 2 (Nrf2),

289 unexpected electrocatalytic activity towards GSH oxidation, compared to GCE modified with only GO, TC

290 migration capacity of infected PMNs, whereas GSH could restore these functions.

291 also single, double and triple adducts with GSH involving beta-carbon attack at the much harder N-te

292 can form thiolato and sulfenato adducts with GSH, and react with H2 O2 generating hydroxyl radicals.

293 e crystal structures of PrfA in complex with GSH and in complex with GSH and its cognate DNA, the hly

294 PrfA in complex with GSH and in complex with GSH and its cognate DNA, the hly operator PrfA box motif

295 it also stabilized the ternary complex with GSH.

296 onishingly, supplementation of the feed with GSH, another GGT substrate, resulted in inflammation and

297 ylated when its disulfide was incubated with GSH and when the reduced protein was treated with H2O2 a

298 chemotypes are electrophiles that react with GSH, and LC/MS determined the cysteine adducts formed up

299 C3 olefin of PL was postulated to react with GSH.

300 seedlings were exposed to HT with or without GSH treatment for 4 days and following with 4 days of re