ライフサイエンスコーパス: N-acetyl-L-cysteine

1 evates cellular levels of glutathione (i.e., N-acetyl-L-cysteine).

2 treatment with a cell-permeable antioxidant, N-acetyl-l-cysteine.

3 ytokines, and this induction is inhibited by N-acetyl-l-cysteine.

4 , is abrogated by the glutathione precursor, N-acetyl-l-cysteine.

5 as not blocked by the free-radical scavenger N-acetyl-L-cysteine.

6 expression was blocked with the antioxidant N-acetyl-L-cysteine.

7 suppressed by treatment with the antioxidant N-acetyl-l-cysteine.

8 require expression of p53 and was blocked by N-acetyl-l-cysteine.

9 , being virtually inhibited by coinfusion of N-acetyl-l-cysteine.

10 and H(2)O(2) was blocked by the antioxidant N-acetyl-l-cysteine.

11 ss was blocked by antioxidant agents such as N-acetyl-L-cysteine.

12 d by treatment with the chemical antioxidant N-acetyl-L-cysteine.

13 c benefits from thiol-rich antioxidants like N-acetyl-L-cysteine.

14 the reactive oxygen species (ROS) scavenger N-acetyl-L-cysteine.

15 onal activity by using the antioxidant agent N-acetyl-L-cysteine.

16 of PC cells with the free radical scavenger N-acetyl-L-cysteine.

17 and diphenyleneiodonium, or the antioxidant, N-acetyl-L-cysteine.

18 y chronic p.o. administration of antioxidant N-acetyl-L-cysteine.

19 an cancer cells treated with the antioxidant N-acetyl-L-cysteine.

20 ertonic treatment and were both prevented by N-acetyl-l-cysteine.

21 The general antioxidant N-acetyl-l-cysteine (6 mM), and the superoxide dismutase

22 Scavenging of vanadate-induced H(2)O(2) by N-acetyl-l-cysteine (a general antioxidant) or catalase

23 Inclusion of N-acetyl-L-cysteine, a known antioxidant and NF-kappaB i

24 N-Acetyl-L-cysteine, a known oxidant scavenger, inhibite

25 Treatment with N-acetyl-l-cysteine, a potent antioxidant, abolished lip

26 vels, which was inhibited by the antioxidant N-acetyl-L-cysteine, a precursor of glutathione, but not

27 nt of cells with intracellular ROS scavenger N-acetyl-l-cysteine also inhibits AGP-induced activation

28 d AQP3 and NOTCH1 expression, and the use of N-acetyl-L-cysteine altered NOTCH1 expression, suggestin

29 N-acetyl-L-cysteine, an ROS inhibitor, rescued p21-induc

30 poptosis, whereas water-soluble antioxidants N-acetyl L-cysteine and glutathione had little effect.

31 activation was sensitive to the antioxidants N-acetyl L-cysteine and pyrrolidine dithiocarbamate, as

32 The ROS scavenger N-acetyl L-cysteine and the mitochondrial antioxidant Mi

33 atory signaling pathways, as the antioxidant N-acetyl-l-cysteine and a Syk inhibitor differentially b

34 Among the various thiol supplements studied, N-acetyl-L-cysteine and alpha-lipoic acid hold the most

35 enced by the lack of effects of antioxidants N-acetyl-L-cysteine and ascorbic acid.

36 monomethyl-L-arginine or by the antioxidants N-acetyl-L-cysteine and ascorbic acid.

37 of caspases YVAD and zVAD, the antioxidants N-acetyl-l-cysteine and butylated hydroxyanisole, or an

38 Pretreatment with N-acetyl-l-cysteine and catalase expression ameliorated

39 upporting this, combinatorial treatment with N-acetyl-l-cysteine and catalase substantially inhibited

40 Similarly, combined N-acetyl-l-cysteine and catalase treatment also suppress

41 N-acetyl-L-cysteine and cyclosporine A, blocked ethanol

42 ression could be blocked by the antioxidants N-acetyl-L-cysteine and dimethyl sulfoxide at both the p

43 s such as reduced glutathione, L-cysteine or N-acetyl-L-cysteine and fully reduced by dithiothreitol

44 ROS contributed to cell death because both N-acetyl-L-cysteine and glutathione in its reduced form

45 e, ascorbate 2-phosphate, alpha-lipoic acid, N-acetyl-L-cysteine and glutathione increased phosphatas

46 blocked by pretreatment with the antioxidant N-acetyl-L-cysteine and GSH but not with cysteine.

47 by the common antioxidants alpha-tocopherol, N-acetyl-l-cysteine and GSH, but not by the nonspecific

48 CDDO-induced apoptosis is also abrogated by N-acetyl-L-cysteine and GSH.

49 se AlpJ, can generate these metabolites from N-acetyl-l-cysteine and l-cysteine, respectively, and th

50 N-acetyl-l-cysteine and mito-TEMPO blocked the induction

51 old nanoparticles protected by monolayers of N-acetyl-l-cysteine and of tiopronin ligands.

52 ntrate, Lipid Mixture 1, Gelatin Peptone N3, N-Acetyl-L-Cysteine and Pluronic F-68) were assayed in o

53 inhibitor genistein and by the antioxidants N-acetyl-L-cysteine and pyrrolidinedithiocarbamate, sugg

54 In contrast, N-acetyl-l-cysteine and reduced glutathione are much les

55 and diethyl maleate) nor reducing compounds (N-acetyl-l-cysteine and reducing glutathione) could disr

56 in undergoes spontaneous hydrolysis to yield N-acetyl-L-cysteine and the inactive lactacystin analog,

57 hosphorylation is blocked by the antioxidant N-acetyl-L-cysteine and the NADPH oxidase inhibitor, DPI

58 Antioxidants (N-acetyl-L-cysteine and Tiron) and inhibitors of mitocho

59 by the ability of ROS inhibitors, including N-acetyl-L-cysteine and Tiron, to block this killing eff

60 he enzyme was highly active with l-cysteine, N-acetyl-l-cysteine, and allyl mercaptan.

61 lated antioxidants butylated hydroxyanisole, N-acetyl-L-cysteine, and pyrrolidine dithiocarbamate, or

62 3-Mercaptopropionate-, N-acetyl-L-cysteine-, and dithiothreitol-dependent deacy

63 over, the thiol-antioxidants glutathione and N-acetyl-L-cysteine antagonized the Cpd 5-induced Cdk4 t

64 Pretreatment with antioxidant N-acetyl-l-cysteine, apoptosis signal-regulating kinase

65 In addition, the free radical scavenger N-acetyl-L-cysteine attenuated ROS generation and apopto

66 The antioxidant N-acetyl-L-cysteine attenuated the down-regulatory effec

67 Pretreatment of A549 cells with N-acetyl-l-cysteine attenuated the oxidant-mediated redu

68 antioxidants pyrrolidinedithiocarbamate and N-acetyl-l-cysteine attenuated this response, as well as

69 Conversely, N-acetyl L-cysteine blocked apoptosis induced by Bay/HDA

70 -1 and ERK-2 phosphorylation, whereas DPI or N-acetyl-l-cysteine blocked such activation.

71 N-acetyl-L-cysteine blocked the EGFR activation and redu

72 Treatment of MM cells with an antioxidant N-acetyl-L-cysteine blocks 2ME2, but not Dex-induced apo

73 polyethylene glycol-superoxide dismutase and N-acetyl-L-cysteine but not by inhibitors of protein kin

74 tion of ROS was prevented by the antioxidant N-acetyl-l-cysteine but not by the NADPH oxidase inhibit

75 ffectively blocked by the thiol antioxidant, N-acetyl-L-cysteine, but not by androgen, a powerful sur

76 oresponsive composite material consisting of N-acetyl-L-cysteine capped CdAgTe quantum dots (NAC-CdAg

77 Antioxidants such as N-acetyl-L-cysteine, catalase, and 1, 2-dihydroxy-benzen

78 ipolysis, whereas the free radical scavenger N-acetyl-l-cysteine completely inhibited the effect.

79 N-acetyl-L-cysteine conferred protection, but N-acetyl-D

80 Pretreatment of neutrophils with N-acetyl-L-cysteine, cytochalasin D, or cyclosporin A si

81 in combination with one of a series of FSDs (N-acetyl-L-cysteine, D-penicillamine, captopril, L-cyste

82 ngers of ROS, such as catalase, aspirin, and N-acetyl-L-cysteine, decreased Cr(VI)-induced apoptosis,

83 ction/TOF-MS coupled with o-phthaldialdehyde/N-acetyl-L-cysteine derivatization.

84 The antioxidant N-acetyl-L-cysteine diminished G-CSF-induced ROS product

85 stingly, pretreatment with the antioxidants, N-acetyl-L-cysteine, dithiothreitol, and glutathione, im

86 Following liquefaction of the sputa by using N-acetyl-L-cysteine, DNA was isolated and analyzed by PC

87 strongly inhibited by S-(2,4-dinitrophenyl)-N-acetyl-L-cysteine (DNP-NAC) and by all other mercaptur

88 To break the stalemate, N-acetyl-L-cysteine functionalized chitosan copolymer (C

89 Pretreatment with N-acetyl-L-cysteine, glutathione, or vitamin E attenuate

90 Pretreatment with an antioxidant, N-acetyl-L-cysteine, had no effects on PEITC activation

91 )O(2) and was prevented with the antioxidant N-acetyl-L-cysteine, indicating that reactive oxygen spe

92 N-acetyl-L-cysteine inhibited BPEx-induced eosinophilic

93 ngers, including cell permeable catalase and N-acetyl-L-cysteine, inhibited glucose-stimulated H2O2 a

94 N-acetyl-L-cysteine (L-NAC) is a proposed therapeutic fo

95 and treatment with the antioxidant compound, N-acetyl-l-cysteine (l-NAC), blocked both the early and

96 Like reduced glutathione, N-acetyl-L-cysteine, L-cysteine methyl ester, and L-cyst

97 d nucleolar retention of NS mutants, whereas N-acetyl-L-cysteine largely prevented the effects of MG1

98 Interestingly, the antioxidant N-acetyl-L-cysteine markedly reversed these changes.

99 Accumulation of GSH in these cells using N-acetyl-L-cysteine mimicked the effect of ATRA on MDSC

100 f Glutathione (GSH) and we demonstrated that N-acetyl L-cysteine (NAC), a precursor to GSH, protected

101 as reduced by increasing the thiol pool with N-acetyl L-cysteine (NAC), while NAC had little effect o

102 xidants [pyrrolidine dithiocarbamate (PDTC), N-acetyl l-cysteine (NAC)] or Ca2+ chelators (EGTA-AM, T

103 Neutralization of ROS by N-acetyl-l-cysteine (NAC) abrogated the phosphorylation

104 ermination that involves derivatization with N-acetyl-l-cysteine (NAC) and separation by HPLC was dev

105 ne (DFO), everolimus (Eve), metformin (Met), N-acetyl-l-cysteine (NAC) and topoisomerase I (TOPO), wh

106 Pretreatment with N-acetyl-L-cysteine (NAC) and vitamin E (Trolox) were us

107 N-Acetyl-l-cysteine (NAC) but not other antioxidants, su

108 Sulforaphane (SFN) and its N-acetyl-L-cysteine (NAC) conjugate are effective inhibi

109 N-acetyl-l-cysteine (NAC) exhibits protective properties

110 ogenic prodrug named TPA-NAC, by introducing N-acetyl-l-cysteine (NAC) into a conjugated acceptor ske

111 tation with the thiol-containing antioxidant N-acetyl-l-cysteine (NAC) on levels of oxidative DNA dam

112 M glucose with and without the antioxidants, N-acetyl-L-cysteine (NAC) or aminoguanidine (AG).

113 enylene iodonium (DPI), and by antioxidants, N-acetyl-L-cysteine (NAC) or pyrrolidine dithiocarbamate

114 nsitive RPMI 8226 cells with the antioxidant N-acetyl-L-cysteine (NAC) protects cells against these e

115 The ROS scavengers edaravone (EDA) and N-acetyl-L-cysteine (NAC) reduced ROS level, downregulat

116 from LPS-treated mothers, while antioxidant N-acetyl-L-cysteine (NAC) reversed these changes togethe

117 The antioxidant N-acetyl-l-cysteine (NAC) significantly reduces the cyto

118 In contrast, N-acetyl-L-cysteine (NAC) treatment in H9c2 cells, or ov

119 ser exposure, whereas similar treatment with N-acetyl-L-cysteine (NAC) was less effective.

120 In murine embryonic fibroblasts, N-acetyl-L-cysteine (NAC), a GSH generating agent, enhan

121 The presence of N-acetyl-L-cysteine (NAC), a GSH precursor, mitigated bo

122 synthetic glucocorticoid, and treatment with N-acetyl-L-cysteine (NAC), a thiol antioxidant, inhibits

123 On the other hand, treatment with N-acetyl-l-cysteine (NAC), an oxygen free radical scaven

124 treatment (1 to 5 days) with 1 to 10 mmol/L N-acetyl-L-cysteine (NAC), an ROS scavenger, decreased n

125 ence of four reductants, namely, GSH, l-Cys, N-acetyl-l-cysteine (NAC), and ascorbic acid.

126 tate was modulated with a thiol-antioxidant, N-acetyl-L-cysteine (NAC), and cell cycle progression wa

127 Thiol antioxidants, including N-acetyl-L-cysteine (NAC), are widely used as modulators

128 Pretreatment with the antioxidants N-acetyl-L-cysteine (NAC), ascorbic acid or vitamin E, b

129 tment with an oxygen free radical scavenger, N-acetyl-l-cysteine (NAC), attenuated the FoxO1 inhibiti

130 N-acetyl-L-cysteine (NAC), but not caspase inhibitors, b

131 uced cell growth was reduced by antioxidants N-acetyl-L-cysteine (NAC), catalase, and the glutathione

132 se inhibitor LY294002, glutathione precursor N-acetyl-L-cysteine (NAC), curcumin, epigallocatechin-3

133 phorylation was inhibited by the addition of N-acetyl-l-cysteine (NAC), indicating that free radical-

134 of the reactions of these thiol esters with N-acetyl-l-cysteine (NAC), N-acetylcysteamine, and N(2)-

135 ed the efficacy of a weak organic acid drug, N-acetyl-L-cysteine (NAC), on the eradication of biofilm

136 cetate (NaOAc) buffer containing 5 mg.mL(-1) n-acetyl-l-cysteine (NAC), or 0.25 M NaOAc containing 5

137 an inhibitor of ROS production, antioxidant N-acetyl-L-cysteine (NAC), or an inhibitor of NO, 1,400W

138 nducing cigarette smoke extract, antioxidant N-acetyl-l-cysteine (NAC), or both.

139 mined using the antioxidants glutathione and N-acetyl-L-cysteine (NAC).

140 in response to reduced glutathione (GSH) or N-acetyl-L-cysteine (NAC).

141 Thiol antioxidants (N-acetyl-l-cysteine [NAC] and N-acystelyn, carbocysteine

142 tor PD98059 (10 micromol/L), the antioxidant N-acetyl-l-cysteine, NAC (30 mmol/L), and the NADPH oxid

143 in, MbetaCD) and oxidative stress inhibitor (N-acetyl-L-cysteine, NAC) slightly rescued the viability

144 A standard procedure using N-acetyl-L-cysteine (NALC) and NaOH has been widely adop

145 ce of the USP method to that of the standard N-acetyl-L-cysteine-NaOH (NALC) method for conventional

146 osis complex organisms from cultures or from N-acetyl-l-cysteine-NaOH-treated, smear-positive specime

147 The antioxidant N-acetyl-L-cysteine normalized ROS levels and restored I

148 Administration of N-acetyl L-cysteine or a chimeric superoxide dismutase (

149 s, blockade of XO activity by pharmacologic (N-acetyl-L-cysteine or allopurinol) or molecular (by sma

150 acheally and injected with the antioxidants, N-acetyl-L-cysteine or dimethylthiourea, prior to sensit

151 d by pretreating cells with the antioxidants N-acetyl-L-cysteine or dithiothreitol.

152 Quenching of these ROS by the antioxidant N-acetyl-l-cysteine or inhibition of the mitochondrial d

153 suppressed by treatment with an antioxidant, N-acetyl-L-cysteine or overexpressing TRX.

154 s prevented by general antioxidants, such as N-acetyl-l-cysteine or Tiron.

155 NF kappa B (pyrrolidine dithiocarbamate and N-acetyl-l-cysteine) or PI 3-kinase (LY294002) inhibited

156 s inhibitor ferrostatin-1, antioxidants like N-acetyl-L-cysteine, or by the iron scavenger deferoxami

157 on, which was attenuated by the antioxidant, N-acetyl-L-cysteine, or Cu sequestration.

158 with l-2-oxo-4-thiazolidinecarboxylic acid, N-acetyl-l-cysteine, or d,l-buthionine-S,R-sulfoximine.

159 Treatment with antioxidants, N-ACETYL-L-CYSTEINE, or dimethylsulfoxide, failed to att

160 A thiol antioxidant, N-acetyl-l-cysteine, or overexpression of an H(2)O(2) sc

161 ethyl-l-arginine, the free radical scavenger N-acetyl-l-cysteine, or the NOS substrate l-arginine par

162 D(P)H oxidase inhibitor DPI, the antioxidant N-acetyl-L-cysteine, or the superoxide scavenger Tiron,

163 releases the biologically active persulfide (N-acetyl l-cysteine persulfide, NAC-SSH) in a spatiotemp

164 2) S), hydrogen persulfide (H(2) S(2) ), and N-acetyl-l-cysteine persulfide (N-CysSSH), we examined t

165 N-acetyl-L-cysteine pretreatment, which blocks CD40-medi

166 The antioxidant N-acetyl-l-cysteine prevented mitochondrial inhibitors f

167 Pretreatment with the antioxidant N-acetyl-L-cysteine prevented ouabain-stimulated Na/K-AT

168 of iron-overloaded mice with the antioxidant N-acetyl-L-cysteine prevented the development of trabecu

169 ROS scavengers butylated hydroxyanisole, and N-acetyl-L-cysteine prevented the luteolin-induced suppr

170 Pretreatment with the antioxidant N-acetyl-L-cysteine protected embryos with activated hyp

171 is phenomenon was blocked by the antioxidant N-acetyl-L-cysteine, pyrrolidine dithiocarbamate, and th

172 Treatment with N-acetyl-l-cysteine reduced both the basal and inducible

173 N-Acetyl-l-cysteine reduced oxidative stress, prevented

174 s with the reactive oxygen species scavenger N-acetyl-l-cysteine reduced the levels of interleukin-6,

175 In addition the thiol antioxidant, N-acetyl-L-cysteine, rescued cells from glucose deprivat

176 (MAPK)/ERK inhibitor PD98059 and antioxidant N-acetyl-l-cysteine restored normal proliferation of Atm

177 vivo treatment with the antioxidative agent N-acetyl-L-cysteine resulted in reversion of the FoxO-de

178 the Src inhibitor, PP2, and the antioxidant N-acetyl-L-cysteine revealed critical roles for Src and

179 Accordingly, treatment with the antioxidant N-acetyl-l-cysteine reversed the phenotype, normalizing

180 Also, the cell-permeable thiol N-acetyl l-cysteine, reverses DMF inhibition of the NFka

181 Mercapturic acids are N-acetyl-L-cysteine S-conjugates that are formed from a

182 ocked by addition of a reducing agent DTT or N-acetyl-L-cysteine, showing that process of oxidation i

183 The precipitate forms during N-acetyl-L-cysteine-sodium hydroxide (NALC-NaOH) deconta

184 gated included chemical decontamination with N-acetyl-l-cysteine-sodium hydroxide (NALC-NaOH), alone

185 ch depends on initial sample processing with N-acetyl-l-cysteine-sodium hydroxide (NALC-NaOH), chemic

186 N-Acetyl-l-cysteine-sodium hydroxide (NALC-NaOH)-deconta

187 s MTB results for detection of MTBC DNA from N-acetyl-l-cysteine-sodium hydroxide (NALC-NaOH)-treated

188 The antioxidant N-acetyl-l-cysteine somewhat reduced 4-HPR cytotoxicity

189 receptor activity by asbestos is blocked by N-acetyl-l-cysteine, suggesting that it is an initial re

190 ed by the antioxidants 2-mercaptoethanol and N-acetyl-L-cysteine, suggesting that the death signaling

191 Pretreatment with the ROS scavenger N-acetyl-L-cysteine, the ERK1/2 inhibitor UO126, or ERK1

192 N-acetyl-L-cysteine therapy has been used in clinical st

193 his study, we explore the effect of low dose N-acetyl-L-cysteine therapy, delivered using a targeted,

194 ndergo nonenzymatic nucleophilic addition by N-acetyl-l-cysteine to generate the C-S bond leading dir

195 Addition of N-acetyl-l-cysteine to the culture medium reduced the in

196 Finally, administration of the antioxidant N-acetyl-l-cysteine to Ucp2(-/-) pregnant mice alleviate

197 th the antioxidant and glutathione precursor N-acetyl-L-Cysteine treatment (NAC).

198 dase inhibitor MDL-75275 and the antioxidant N-acetyl-L-cysteine, which when used in combination with

199 The standard technique was N-acetyl-L-cysteine with sodium hydroxide (NALC-NaOH) tr