ライフサイエンスコーパス: GSH

1 GSH deficiency induced in cultured hepatocytes caused an

2 GSH in dorsal anterior cingulate cortex (dACC) was acqui

3 GSH is a low-molecular-weight thiol-containing tripeptid

4 GSH levels correlated negatively with SBP, DBP and MBP v

5 GSH molecules within AtGAPC1 active sites are suggested

6 GSH plays an important role in P. aeruginosa physiology

7 GSH turnover also accelerated in the PPSB-deficient line

8 ), NADP/NADPH-Glo(TM), ROS-Glo(TM)/H(2)O(2), GSH/GSSG-Glo(TM) and Caspase-Glo(R) 3/7 assays.

9 Fe-2S] species, such as (FDX2:GLRX5:[2Fe-2S]:GSH) and (FDX2:BOLA3:GLRX5:[2Fe-2S]:GSH) are detected.

10 [2Fe-2S]:GSH) and (FDX2:BOLA3:GLRX5:[2Fe-2S]:GSH) are detected.

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

12 C3G was not altered during transport and a GSH conjugate was not formed.

13 ar; however, DJ-1 has been suggested to be a GSH-independent glyoxalase that detoxifies methylglyoxal

14 H-sensitive nanoparticles (CGPU) displayed a GSH-dose dependent release of cisplatin.

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

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

17 ve polyurethane nanoparticles (GPUs) using a GSH-cleavable disulfide bond containing polyurethane tha

18 H-MR spectroscopy data were acquired using a GSH-optimized MEGA-PRESS editing sequence and GSH/creati

19 We also noted that disulfides without a GSH are much slower oxidants, suggesting a strongly sele

20 We also studied the role of P. aeruginosa GSH biosynthesis in four mouse infection models, includi

21 conditions, grayscale value plotted against GSH concentration exhibited a linear relationship within

22 Altering GSH:GSSG ratios in mouse primary neurons in vitro also i

23 Although GSH may still play a biological role in trypanosomatid p

24 r role in intracellular cysteine balance and GSH biosynthesis.

25 ctivity in AtABCC2, and suggest that C3G and GSH bind closely, mutually enhancing each other's bindin

26 probed the putative binding sites of C3G and GSH through site-directed mutagenesis and functional stu

27 antioxidant enzymes, including catalase and GSH peroxidases, have supported a model in which beta-ce

28 ich were previously ascribed to cysteine and GSH.

29 evels of expression of antioxidant genes and GSH as assessed immediately following hyperoxia.

30 results indicate that co-targeting GLUT1 and GSH synthesis may offer a potential therapeutic approach

31 drug combination that co-targeted GLUT1 and GSH synthesis, we found that this combination induces sy

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

33 MY, TP and GLOB), antioxidants (SOD, GPx and GSH), and immune (IgM and lysozyme) parameters in LMB, e

34 ulfurs, mainly reduced glutathione (GSH) and GSH conjugates, were released by lys- cells during lysin

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

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

37 uction to l-cysteine depleted both NADPH and GSH pools, thereby allowing toxic accumulation of reacti

38 om the Grx reaction was reduced by NADPH and GSH reductase and this enzyme was essential because reac

39 ults provide evidence that increased ROS and GSH depletion underlie the cytotoxic effects of METH in

40 SH-optimized MEGA-PRESS editing sequence and GSH/creatine ratios were calculated for DLPFC (SZ: n = 3

41 l-cystine, and depletion of the antioxidant GSH.

42 rgy coenzymes (ATP, ADP, AMP), antioxidants (GSH, GSSG), and a vast pool of other metabolites using a

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

44 cytosed P. aeruginosa, half of the bacterial GSH was lost.

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

46 ealed one clean peak after treatment of both GSH and GSSH with the dielectric barrier discharge (DBD)

47 They hypothesized that coach-delivered CBT-GSH telemedicine sessions plus Noom Monitor would yield

48 Participants received eight CBT-GSH telemedicine sessions over 12 weeks administered by

49 Fifty-two-week outcomes for CBT-GSH plus Noom Monitor (N=114) were compared with outcome

50 emedicine trial of CBT-guided self-help (CBT-GSH) assisted with a smartphone app, Noom Monitor, for b

51 Participants who received CBT-GSH plus Noom Monitor reported significant reductions in

52 These results suggest that CBT-GSH plus Noom Monitor delivered via telemedicine by rout

53 ost of the bacteria oxidized half the cells' GSH, producing mainly glutathione disulfide (GSSG) and o

54 atresone, and agents that replenish cellular GSH ameliorate the effects of the toxin.

55 Herein, chiral GSH-anchored selenium nanoparticles (G@SeNPs) are fabric

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

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

58 Furthermore, the levels of dACC Glx and dACC GSH positively correlated with composite neuropsychologi

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

60 Cebpd(-/-) mice show decreased GSH/GSSG ratio, increased S-nitrosoglutathione and 3-nit

61 W is increased and associated with decreased GSH in patients with first-episode schizophrenia (SZ) co

62 highly positive correlation between detected GSH level and TMZ drug-resistance level in GBM cells.

63 gnificant negative correlation between DLPFC GSH and both whole-brain and DLPFC-specific gray matter

64 Doxorubicin-GSH adduct formation kinetics are thermodynamically esti

65 copically similar to that of a typical DSOR, GSH reductase, in which the active-site histidine had be

66 ghly negative glutathione redox potential (E(GSH) ) is maintained in the cytosol, plastids and mitoch

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

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

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

70 iates the uptake of cystine, a precursor for GSH biosynthesis.

71 H reductase (GR), the enzyme responsible for GSH recycling, promoted ULBP2/5 surface expression.

72 Current strategies for GSH detection often require sophisticated instruments th

73 r enter a futile thiol oxidase cycle forming GSH disulfide.

74 te known to be important for immune function-GSH-and the diffusion extracellular FW measure, which pr

75 GSH and thereby exhaust cells of functional GSH capacity.

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

77 Glutathione (GSH) is often upregulated in cancer, where it serves to

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

79 zenesulfonate (DNBS) group as a glutathione (GSH)-activated photosensitizer, a chemo-prodrug based on

80 tioxidants N-acetylcysteine and glutathione (GSH) abrogated ULBP2/5 upregulated by DMF.

81 s of inflammatory mediators and glutathione (GSH) after chelation therapy.

82 Metallothioneins (MTs) and glutathione (GSH) are abundant in the cytosol and nucleus.

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

84 Now, ultrasound (US) and glutathione (GSH) dual responsive vesicles of Janus Au-MnO nanopartic

85 al reaction between patulin and glutathione (GSH), in order to generate the conjugates that are forme

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

87 superoxide dismutase (SOD) and glutathione (GSH).

88 ndent on ME1-produced NADPH and glutathione (GSH).

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

90 redox stress is the antioxidant glutathione (GSH).

91 Biothiols, such as glutathione (GSH), homocysteine (Hcy), and cysteine (Cys), coexist in

92 levels of metabolites, such as glutathione (GSH).

93 s altered redox balance between glutathione (GSH) and oxidized glutathione (GSSG) and initiated mitoc

94 rate of ferrocenecarboxylic by glutathione (GSH) released from cardiomyocyte, which is the most abun

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

96 We developed glutathione (GSH)-responsive polyurethane nanoparticles (GPUs) using

97 ne residues of proteins to form glutathione (GSH) adducts, S-glutathionylation, that are selectively

98 ation and lactate, depletion in glutathione (GSH) level and inhibition at G0/G1 phase of cell cycle,

99 weight (LMW) thiols, including glutathione (GSH) and coenzyme A (CoA).

100 c7a11, S47 cells show increased glutathione (GSH) accumulation compared to cells with wild -type p53.

101 erivatives (YDs) with increased glutathione (GSH) enrichment.

102 replenishment of intracellular glutathione (GSH) levels.

103 he maintenance of intracellular glutathione (GSH).

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

105 Cys-3MH) and S-3-(hexan-1-ol)-l-glutathione (GSH-3MH) were quantified in the juices before and after

106 status due to bio-thiols, like glutathione (GSH), which constitute the most crucial defense system t

107 evels of malondialdehyde (MDA), glutathione (GSH), superoxide dismutase (SOD), catalase (CAT), matrix

108 evels of malondialdehyde (MDA), glutathione (GSH), total cholesterol, and myeloperoxidase activity (M

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

110 correlating with low levels of glutathione (GSH) and 25-hydroxyvitamin D3 (25(OH)VD(3)).

111 a PS by the mutual presence of glutathione (GSH) and hydrogen peroxide (H(2) O(2) ) with high specif

112 haracterize the contribution of glutathione (GSH) conjugation to kidney toxicity of PERC and the degr

113 recursor of the reduced form of glutathione (GSH), but also is an scavenger of soft electrophiles suc

114 depended on the co-transport of glutathione (GSH).

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

116 m, i.e., a low reduced/oxidized glutathione (GSH-GSSG) ratio.

117 racellular glutathione/oxidized glutathione (GSH/GSSG) and nicotinamide adenine dinucleotide reduced/

118 one levels and reduced/oxidized glutathione (GSH/GSSG) ratios.

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

120 Organosulfurs, mainly reduced glutathione (GSH) and GSH conjugates, were released by lys- cells dur

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

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

123 Decreases in reduced glutathione (GSH) mimic the effects of biliatresone, and agents that

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

125 total glutathione (GT), reduced glutathione (GSH), catalase (CAT), peroxidase (POD), superoxide dismu

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

127 methylglyoxal requires reduced glutathione (GSH), which accumulates to high levels in NSCLC relative

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

129 Herein, we report glutathione (GSH) reaction rates for N-phenyl acrylamides with varied

130 active oxygen species scavenger glutathione (GSH) was upregulated in chRCC due to decreased expressio

131 ey marker for oxidative stress, glutathione (GSH), may associate with central neurochemicals or neuro

132 barrier discharges (DBD) on the glutathione (GSH) and glutathione disulphide (GSSG) molecules as the

133 igation was related to both the glutathione (GSH) redox molecule and the enzyme peroxidase (PO), whic

134 h wild-type plants; besides the glutathione (GSH) steady-state levels in roots of PPSB-deficient line

135 -DDP is not a substrate for the glutathione (GSH) transferase activity of GST P1-1.

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

137 escribe the synthesis of a thin glutathione (GSH)-cleavable covalently crosslinked polymer coating, c

138 of the abundant cellular thiol glutathione (GSH).

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

140 successfully prepared by using glutathione (GSH) and copper (II) chloride as precursors via a facile

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

142 igher in AD, p < 0.001; reduced glutathione [GSH]: higher in AD, p < 0.001); (3) polyamine synthesis/

143 In particular, melatonin heightened GSH content as well as the ratio of GSH/GSSG when compar

144 MM affected only hepatic GSH, with lower values in fish fed the OM diets.

145 tion (IFD) and Geometry of the Selfish Herd (GSH) to address an apparent conflict in their prediction

146 nregulated in the livers of mice fed an HFD (GSH- deficient) compared with control diet-fed group.

147 The micelles could dissociate under the high GSH level in cancer cells, triggering a release of pacli

148 ciated with higher GGT expression and higher GSH levels in tumor tissue compared to normal brain.

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

150 T(SH)(2) (4.8 x 10(6) m(-1) s(-1)); however, GSH-mediated reduction was extremely slow (39 m(-1) s(-1

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

152 Changes in GSH and oxidative state are associated with neurodegener

153 we found that biliatresone and decreases in GSH upregulated RhoU/Wrch1, a Wnt signaling family membe

154 created a P. aeruginosa mutant defective in GSH biosynthesis to examine how loss of GSH biosynthesis

155 YDs enriched in GSH appeared on average 3.3 times more efficient at quen

156 ing radical species than YDs not enriched in GSH.

157 lutamyl-transferase (GGT) is a key enzyme in GSH homeostasis, and compared to normal brain its expres

158 no significant difference between groups in GSH in either voxel.

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

160 decreased expression of proteins involved in GSH degradation.

161 urface of cellular membranes and involved in GSH metabolism and maintenance of redox homeostasis.

162 iptionally regulated by Nrf2 and involved in GSH, NADPH, and NADH generation were significantly lower

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

164 toxicity by decreasing ROS through increased GSH.

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

166 of quinone redox cycling, and adduct-induced GSH depletion.

167 HFD-induces GSH deficiency and epigenetically alters VD-biosynthesis

168 pathological progress of acute liver injury, GSH levels are decreased, and this is significantly reco

169 ferences provides evidence for an integrated GSH and IFD strategy that may represent an evolutionary

170 onditions, after activation by intracellular GSH and H(2) O(2) .

171 n removal of the DNBS group by intracellular GSH.

172 oxidative stress by enhancing intracellular GSH levels.

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

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

175 Moreover, rapid depletion of intracellular GSH in xCT-KO cells led to accumulation of lipid peroxid

176 Intriguingly, GSH catalyzes their hydrolysis.

177 ubunits cross-linking, while maintaining its GSH-conjugation activity.

178 ids GSSG accumulation in an organism lacking GSH reductase.

179 no significant effect on antioxidant levels (GSH, SOD, and CAT) (P >0.05).

180 Cisplatin-loaded GSH-sensitive nanoparticles (CGPU) displayed a GSH-dose

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

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

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

184 tions in glutathione metabolism, where lower GSH/GSSG ratios decrease labile Cu(I) availability witho

185 On the other hand, the mean GSH level increased significantly from 3.3 +/- 3.3 to 13

186 osis assays and LC-MS analyses, we monitored GSH oxidation in Pseudomonas aeruginosa to gauge their e

187 ular-weight (LMW) S-nitrosothiols (S-nitroso-GSH (GSNO) and S-nitroso-CoA (SNO-CoA)).

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

189 scavenging activity shed light on other non-GSH compounds present.

190 1 each form hydrogen bonds with two atoms of GSH spanning the gamma-glutamyl bond.

191 the VD-deficiency and potential benefits of GSH treatment in reducing 25(OH)VD(3)-deficiency.

192 on of fumarate, likely by depleting cells of GSH antioxidant capacity.

193 der cytosolically relevant concentrations of GSH and MT.

194 and is highly reactive with the cysteine of GSH, with a calculated rate constant of 2 x 10(5) m(-1)

195 with the carboxyl oxygen of the cysteine of GSH.

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

197 indicated elevated levels and a decrease of GSH/GSSG ratio in PER group compared with the CTRL group

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

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

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

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

202 oach to be used for on-site determination of GSH levels in a rapid (i.e., within 30 min), simple (i.e

203 dine dithiocarbamate (PDTC) on the efflux of GSH and Cys from HepG2 cells.

204 interstrain variability in both formation of GSH conjugation metabolites of PERC and its kidney effec

205 In line with this, inhibition of GSH reductase (GR), the enzyme responsible for GSH recyc

206 enzymes adapted to using T(SH)(2) instead of GSH, including the glutaredoxins (Grxs).

207 ment was associated with increased levels of GSH and decreased levels of proinflammatory cytokines an

208 urethane that responds to elevated levels of GSH within lung cancer cells.

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

210 e in GSH biosynthesis to examine how loss of GSH biosynthesis affects P. aeruginosa virulence.

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

212 Also interesting, no nitrosylation of GSH/GSSG was oberved in the presence of iron complexes,

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

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

215 hile those with pK(a)'s < 7 slow the rate of GSH addition at pH 7.4, relative to a hydrogen substitue

216 ightened GSH content as well as the ratio of GSH/GSSG when compared to non-sprayed water stressed pla

217 /ml of methanolic extract showed recovery of GSH and trolox equivalent antioxidants in rat blood/hemo

218 Replenishment of GSH by its prodrugs treatment beneficially altered epige

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

220 However, the role of GSH biosynthesis during mammalian infection is not well

221 and complementary data regarding the role of GSH in P. aeruginosa during mammalian infection.

222 etermined, which is 3.49 units below that of GSH.

223 max) values for Grx are strongly depended on GSH concentrations.

224 the time-dependent chemical modifications on GSH and GSSG in the presence of iron(II) and iron(III) c

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

226 Further research included studies on GSH, toxicological aspects (the concept of "redox cyclin

227 ollowed by OP(DTT) ( R(CV)(2) = 0.32) and OP(GSH) ( R(CV)(2) = 0.22).

228 or OP(DTT) ( R(CV)(2) = 0.55) followed by OP(GSH) ( R(CV)(2) = 0.50) and OP(AA) ( R(CV)(2) = 0.23).

229 ne/ascorbate-related oxidative potential (OP(GSH) and OP(AA)) and dithiothreitol depletion (OP(DTT)).

230 (i.e., Fe, Cu, and black carbon) whereas OP(GSH) was not a strong marker for traffic during either s

231 ntioxidants (N-acetylcysteine, vitamin E, or GSH ethyl ester) did not prevent this ROS increase.

232 ifting equilibria like in the NAD(+)/NADH or GSH/GSSG couples), on non-natural molecules such as dyes

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

234 ROS formation, downregulated anti-oxidative GSH and SOD activity;si-TTP upregulated pro-apoptotic cl

235 l-d,l-penicillamine), nitric oxide, oxidized GSH, and hydrogen peroxide to post-translationally modif

236 Blood pressure, lipid panel, oxidized (GSH) & reduced glutathione (GSSG) were also evaluated fo

237 -based resistances include cytochromes P450, GSH S-transferases, glucosyl and other transferases, ary

238 een systemic oxidative stress (in particular GSH), central glutamate, and cognition in SZ will benefi

239 d declining fitness benefits within a patch (GSH).

240 In this work, the formation of patulin-GSH conjugates activated by the application of pulsed li

241 ted individuals declined near the periphery (GSH).

242 Total plasma GSH levels were also positively correlated with the leve

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

244 ion (redox) changes in the glutathione pool (GSH), glutaredoxins (GRX) and thioredoxins (TRX) are imp

245 ced glutathione/oxidative glutathione ratio [GSH/GSSG]), and matrix metalloproteinase-8 (MMP-8) level

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

247 tillin-1 as a protein that binds recombinant GSH S-transferase-tagged PP2A-B55alpha.

248 eductase (NTR)/thioredoxin (TRX) and reduced GSH/GRX systems of the cytosol, chloroplasts, mitochondr

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

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

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

252 We observed that Grx1 reduces GSH-containing disulfides (including oxidized trypanothi

253 n of enzymes downstream of Nrf2 and restored GSH and GTP.

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

255 ion, requiring the interaction with a second GSH molecule, was enabled by switching additional residu

256 omes were the changes in the levels of serum GSH and inflammatory mediators such as tumor necrosis fa

257 Subsequently, GSH-triggered MnO degradation simultaneously released sm

258 At neutral pH, GSSH reacted faster than GSH because of increased availability of the anion and,

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

260 nd indeed requires a reductant stronger than GSH to increase its efficiency.

261 We found that GSH is critical for normal growth in vitro and provides

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

263 The GSH content and the PO activity were increased when the

264 The GSH disulfide resulting from the Grx reaction was reduce

265 The GSH level controls the growth of gold nanoparticles (AuN

266 asparagine that is proposed to activate the GSH cofactor.

267 targets are generally not stable against the GSH/MT system, which creates a challenge for their futur

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

269 Spearman correlation rho = 0.46) between the GSH concentration released from YDs and their radical sc

270 hich are then auto-analyzed to calculate the GSH concentrations by smartphone with an auto-analysis s

271 We demonstrate that CblC catalyzes the GSH-dependent denitration of NO(2)Cbl forming 5-coordina

272 ion, increase cellular ROS, and decrease the GSH/GSSG ratio.

273 e carrier family 7 member 11), decreased the GSH/GSSG ratio, and increased ROS levels.

274 5-hydroxymethylcytosine were observed in the GSH-deficient hepatocytes and the liver of HFD-fed mice.

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

276 ggesting a strongly selective binding of the GSH molecule.

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

278 nd here that the catalytic efficiency of the GSH-Grx system is 4-6 times higher than that of the Trx1

279 udy of patulin degradation and effect of the GSH/Fe(2+) molar ratio showed that a molar ratio of 5 al

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

281 We discovered that the GSH biosynthesis mutant was slightly less virulent in th

282 We find that the GSH reaction rates can generally be understood in terms

283 1 have a crucial catalytic role and that the GSH-Grx system favors the R1-p53R2 enzyme for DNA replic

284 ted with the bacterial cells, oxidized their GSH, and was sufficient to be solely responsible for bac

285 This is in sharp contrast to GSH/GSSG treatment with DBD plasma in the absence of met

286 The glutamine pathway leading to GSH production was suppressed, and ATP and GTP levels we

287 sfer of radiolabel from [(35)S]methionine to GSH.

288 ction and to determine their relationship to GSH.

289 Total GSH levels in plasma positively correlated with composit

290 We observed lower peripheral total GSH in SZ compared to controls in extracellular (plasma)

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

292 variability in TK of S-(1,2,2-trichlorovinyl)GSH (TCVG), S-(1,2,2-trichlorovinyl)-L-cysteine (TCVC),

293 acid and ALT levels also increased, whereas GSH and HDL levels showed lower values.

294 This study investigated whether GSH deficiency induces epigenetic alterations that impai

295 ico framework provides a platform from which GSH depletion can be explored as a function of a compoun

296 shows that nucleophiles co-accumulated with GSH during the enrichment of YDs are responsible for the

297 ent with kidney injury being associated with GSH conjugation.

298 Fumarate can complex with GSH and thereby exhaust cells of functional GSH capacity

299 it also stabilized the ternary complex with GSH.

300 s enzyme was essential because reaction with GSH alone yielded only little activity.