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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

57 3-Mercaptopropionate-, N-acetyl-L-cysteine-, and dithiothreitol-dependent deacy

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

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

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

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

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

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

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

65 -1 and ERK-2 phosphorylation, whereas DPI or N-acetyl-l-cysteine blocked such activation.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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