ライフサイエンスコーパス: N-acetylcysteine

1 f the phenotype by the antioxidant action of N-acetylcysteine.

2 ress program were blocked by the antioxidant N-acetylcysteine.

3 od and can be prevented with the antioxidant N-acetylcysteine.

4 lasmid that was prevented by the addition of N-acetylcysteine.

5 okine signaling 3), and antioxidants such as N-acetylcysteine.

6 n of glutamate, alphaKG, or nucleobases with N-acetylcysteine.

7 eroxide, and these effects were inhibited by N-acetylcysteine.

8 substantially reduced in mice that received N-acetylcysteine.

9 She was treated with N-acetylcysteine.

10 the NOX subunit NOX2 and by the antioxidant N-acetylcysteine.

11 chronic treatment with the cystine prodrug, N-acetylcysteine.

12 ed HBEC and did not occur in the presence of N-acetylcysteine.

13 uld be partially reversed by the antioxidant N-acetylcysteine.

14 processes were reversed by the antioxidant, N-acetylcysteine.

15 revented by the antioxidants glutathione and N-acetylcysteine.

16 subgroup heterogeneity was present only for N-acetylcysteine.

17 roduction, which was quenched by addition of N-acetylcysteine.

18 ked by the addition of the thiol-antioxidant N-acetylcysteine.

19 ells with the clinically important reductant N-acetylcysteine.

20 rolonged therapeutic efficacy as compared to N-acetylcysteine.

21 ated by capsazepine, and by the antioxidant, N-acetylcysteine.

22 es in uterine arteries, which was blocked by N-acetylcysteine.

23 y CD4 T cells is improved by the antioxidant N-acetylcysteine.

24 espiratory epithelium integrity with EGTA or N-acetylcysteine.

25 bunit, which was restored in the presence of N-acetylcysteine.

26 3988, and oxidative stress was attenuated by N-acetylcysteine.

27 mediated relaxations, which were reversed by N-acetylcysteine.

28 ssure-dependent tone, which were annulled by N-acetylcysteine.

29 Another set of mice received the antioxidant N-acetylcysteine.

30 n of LKB1 and by incubation with antioxidant N-acetylcysteine.

31 sm of action, the reference thiols cysteine, N-acetylcysteine, 2-mercaptoethanesulfonic acid, mercapt

32 N-acetylcysteine (3.3%) decreased biofilm biomass and ki

33 ) were observed, as well as increased use of N-acetylcysteine (48.9% vs. 69.3% overall; 15.8% vs. 49.

34 cysteamine bitartrate (60 mg/kg per day) and N-acetylcysteine (60 mg/kg per day) and were assessed ev

35 Group 2 received N-acetylcysteine 600 mg orally twice a day, from preoper

36 r studying the biochemical transformation of N-acetylcysteine, a commonly prescribed Cys supplement d

37 was performed for several small peptides and N-acetylcysteine, a drug administered intravenously to t

38 Supplementation of N-acetylcysteine, a glutathione precursor, conferred a p

39 ed cell death was rescued in the presence of N-acetylcysteine, a glutathione precursor.

40 el gating, and was attenuated by antioxidant N-acetylcysteine, a known scavenger of acrolein.

41 and (2) use the EAAC1(-/-) mouse to evaluate N-acetylcysteine, a membrane-permeable cysteine pro-drug

42 Antioxidant N-acetylcysteine, a precursor for glutathione synthesis,

43 We posit that treatment with N-acetylcysteine, a precursor of glutathione, the larges

44 Treatment with N-acetylcysteine, a safe prodrug against oxidation, reve

45 Perioperative fenoldopam and N-acetylcysteine abrogate the early postoperative declin

46 ncurrent administration of the ROS inhibitor N-acetylcysteine abrogated beta-catenin/HIF pathway acti

47 N-acetylcysteine accelerates amputation stump healing in

48 Although N-acetylcysteine administered before cocaine did not alt

49 ion of N-acetylcysteine, we examined whether N-acetylcysteine administered before daily cocaine also

50 the toxin, whereas replenishing GSH level by N-acetylcysteine administration or activation of nuclear

51 Mice in posttreatment were treated with N-acetylcysteine after folic acid.

52 e JNK inhibitor SP600125, or the antioxidant N-acetylcysteine alleviated insulin resistance, demonstr

53 induced glutamatergic adaptations by chronic N-acetylcysteine also caused enduring inhibition of coca

54 Furthermore, the administration of N-acetylcysteine also prevented NF-kappaB activation, ne

55 lternative antioxidants (vitamin C, DTT, and N-acetylcysteine) also enhanced the chemotactic activity

56 Chemical chaperones or the antioxidant N-acetylcysteine ameliorated glucose tolerance and insul

57 Consistently, treatment with anti-oxidant N-acetylcysteine ameliorates muscle necrosis in Stra13-/

58 ent study sought to evaluate the efficacy of N-acetylcysteine amide (NACA) eye drops in reversing the

59 r endothelial (HBMVEC) cells to test whether N-acetylcysteine amide (NACA), a novel antioxidant, prev

60 hypothesized that a novel thiol antioxidant, N-acetylcysteine amide (NACA), might ameliorate cellular

61 N-acetylcysteine amide eye drops were administered begin

62 raperitoneally on postpartum day 10, whereas N-acetylcysteine amide was injected intraperitoneally on

63 re randomly divided into a control group, an N-acetylcysteine amide-only group, a sodium selenite-ind

64 N-acetylcysteine, an amino acid, seems to restore the ex

65 ponsible for changes in DICER, we found that N-acetylcysteine, an antioxidant and anti-aldehyde, prot

66 N-Acetylcysteine, an antioxidant and GSH precursor, sign

67 air, and to pretreatment with antioxidants (N-acetylcysteine and ascorbate) and placebo.

68 e effects could be reverted or aggravated by N-acetylcysteine and buthionine sulfoximine, respectivel

69 reatment of DCs or CSE with the antioxidants N-acetylcysteine and catalase.

70 the astroglial glutamate transporter GLT-1 (N-acetylcysteine and ceftriaxone) can decrease measures

71 Both N-acetylcysteine and glutathione (GSH) supplementation a

72 The antioxidants N-acetylcysteine and glutathione monoethyl ester inhibit

73 from modulation studies of glutathione using N-acetylcysteine and L-buthionine-sulfoximine indicate t

74 N-acetylcysteine and phosphoinositide 3-kinase (PI3K) in

75 All patients received a high dose of N-acetylcysteine and sodium bicarbonate solution.

76 pileptogenesis by a transient treatment with N-acetylcysteine and sulforaphane, which act to increase

77 ce for the potential roles of bortezomib and N-acetylcysteine, and explore new therapeutic approaches

78 Group 3 received both fenoldopam and N-acetylcysteine, and group 4 patients served as control

79 C (PKC) inhibitor GF109203X, the antioxidant N-acetylcysteine, and the reduced form of glutathione.

80 uperior regenerability by each of ascorbate, N-acetylcysteine, and urate when compared to alpha-TOH.

81 In this work, water-dispersible N-acetylcysteine- and l-cysteine-stabilized palladium na

82 er/chlorobenzene two-phase system containing N-acetylcysteine as a reducing agent in the aqueous phas

83 Reactions conducted with ascorbate or N-acetylcysteine as a reductant under aerobic conditions

84 -phase peroxidation system containing excess N-acetylcysteine as a stoichiometric thiol reducing agen

85 ing preclinical data and supports the use of N-acetylcysteine as a treatment for cocaine dependence.

86 ed suppressor cells, whereas the antioxidant N-acetylcysteine attenuates the inhibitory effects of ph

87 ce in pre- + posttreatment were treated with N-acetylcysteine before folic acid and after folic acid.

88 ere treated with a subcutaneous injection of N-acetylcysteine before the folic acid injection.

89 orylation and activity, whereas antioxidants N-acetylcysteine, beta-naphthoflavone, and tertiary buty

90 In addition, the potent antioxidant N-acetylcysteine blocked EMT and expression of HIF-1alph

91 The antioxidant compound N-acetylcysteine blocked the curcumin-induced increased

92 eration of reactive oxygen species (ROS), as N-acetylcysteine blocked the induction of death receptor

93 New drugs including N-acetylcysteine, bortezomib, recombinant ADAMTS13, and

94 o neuritogenesis were blocked by antioxidant N-acetylcysteine (both L and D-forms) and by a variety o

95 as rescued by treatment with the antioxidant N-acetylcysteine but not by p53 inactivation.

96 sed by the reactive oxygen species scavenger N-acetylcysteine but not by reducing agents or NO pathwa

97 although treatable by timely application of N-acetylcysteine, can be fatal.

98 thiols, including cysteine, dithiothreitol, N-acetylcysteine, captopril, bovine and human serum albu

99 N-Acetylcysteine, catalase, and l-N(G)-monomethyl argini

100 not controls) with the glutathione precursor N-acetylcysteine caused a marked increase in I(Ca,L).

101 showed considerably reduced reactivity with N-acetylcysteine compared to the prototypical derivative

102 Pre-treatment with N-acetylcysteine completely reversed BSO+AUR-induced cel

103 Treatment with N-acetylcysteine could slow the progression of, but not

104 ntioxidants (vitamins C and E, selenium, and N-acetylcysteine) countered the oxidative stress but did

105 ibitable by pretreating the lymphocytes with N-acetylcysteine, cyclosporin A, or bongkrekic acid, emp

106 Pretreatment with N-acetylcysteine decreases phosphorylation of p53 in cit

107 he treatment of trichotillomania, found that N-acetylcysteine demonstrated statistically significant

108 OS scavenger dimethylthiourea or antioxidant N-acetylcysteine did not alleviate caspase-3 production.

109 N-Acetylcysteine did not prevent ethanol-induced mortali

110 JAK2V617F-mutant cells with the antioxidant N-acetylcysteine diminished reactive oxygen species (ROS

111 Treatment of mice with the antioxidant N-acetylcysteine diminishes PGC-1alpha variation observe

112 N-acetylcysteine, diphenyleneiodonium, and apocynin bloc

113 R, or HIF-1 and by oxamate, apocynin, U0126, N-acetylcysteine, dithioerythritol, and antibodies to VE

114 rted protection in the context of suboptimal N-acetylcysteine dosing.

115 N-acetylcysteine (dosing range, 1200-2400 mg/d) or place

116 N-acetylcysteine (dosing range, 1200-3000 mg/d) or place

117 he ability of the equine clinical treatments N-acetylcysteine, EDTA, and hydrogen peroxide to disrupt

118 The reducing agent N-acetylcysteine eliminated the effects of selenium on E

119 temperatures indicate that the -SH group of N-acetylcysteine enhances the rate of its hydrolysis by

120 combined with treatment with the antioxidant N-acetylcysteine, establishing that reactive oxygen spec

121 Treatment with N-acetylcysteine from gestation on normalized most neuro

122 NPs: pharmacological (rescue with trolox and N-acetylcysteine), genetic (analysis of metal-sensitive

123 No adverse events occurred in the N-acetylcysteine group, and N-acetylcysteine was well to

124 Patients who received N-acetylcysteine had an incidence of acute renal failure

125 nding EGF-like growth factor and antioxidant N-acetylcysteine had beneficial effects on epithelial wo

126 altered myocyte properties, the antioxidant N-acetylcysteine had broader effects in limiting glucose

127 Patients assigned to receive N-acetylcysteine had significantly greater reductions in

128 ture possible therapeutic approaches include N-acetylcysteine, hypothermia, liver assist devices, and

129 High-dose antioxidant treatment with N-acetylcysteine improved airspace caliber and attenuate

130 nd are often steatotic, although addition of N-acetylcysteine improves the quality of the cells obtai

131 ere is controversy regarding the benefits of N-acetylcysteine in acute kidney injury.

132 The NACIAM trial (N-acetylcysteine in Acute Myocardial Infarction) examine

133 mpletely abolished the protective effects of N-acetylcysteine in Met-KO hepatocytes.

134 The salutary effects of N-acetylcysteine in this mouse model provide an impetus

135 icipants (31 randomized to placebo and 35 to N-acetylcysteine) included in the analysis, 59 (89%) wer

136 n(III) tetrakis(4-benzoic acid)porphyrin and N-acetylcysteine increased the ratio of Akt to ERK phosp

137 by addition of nontoxic copper chelators or N-acetylcysteine, indicating a role for copper and react

138 nt fatty acid beta-oxidation, with S-nitroso-N-acetylcysteine induced site-specific S-nitrosylation o

139 ative stress was blocked by exposing mice to N-acetylcysteine, induction of liver UGT1A1 and CYP2B10

140 The cytoprotective antioxidant N-acetylcysteine inhibited Dp44mT-induced autophagosome

141 t dye CM-H(2)DCF-DA), whereas treatment with N-acetylcysteine inhibited EGCG-stimulated phosphorylati

142 s treatment with the free radical scavenger, N-acetylcysteine, inhibited this effect.

143 Animal models suggest that N-acetylcysteine inhibits cocaine-seeking.

144 In this study we show that the ROS scavenger N-acetylcysteine inhibits CSR.

145 However, three different N-acetylcysteine interventions neither significantly imp

146 echanism in RYR1-related myopathies and that N-acetylcysteine is a successful treatment modality ex v

147 N-acetylcysteine is an antioxidant and anti-inflammatory

148 ation therapy with cysteamine bitartrate and N-acetylcysteine is associated with delay of isoelectric

149 ombination of oral cysteamine bitartrate and N-acetylcysteine is beneficial for patients with neurona

150 N-acetylcysteine is more renoprotective than hydration a

151 Oral acetylcysteine (also known as N-acetylcysteine) is used with pirfenidone to treat idio

152 r agents (eg, riluzole, ketamine, memantine, N-acetylcysteine, lamotrigine, celecoxib, ondansetron) e

153 More importantly, the antioxidant, oral N-acetylcysteine led to amelioration of the muscle atrop

154 tates, reducing reactive oxygen species with N-acetylcysteine lessened protein aggregation and decrea

155 Treatment with the redox-active pharmaceutic N-acetylcysteine lowers gastric mucosal neutrophil infil

156 N-acetylcysteine may be protective against DILI while ta

157 olume, presence of diabetes mellitus, use of N-acetylcysteine, mean baseline SCr, and estimated glome

158 eviously reported that phosphocysteamine and N-acetylcysteine mediate ceroid depletion in cultured ce

159 Timely administration of N-acetylcysteine (N-Ac) prevents the progression of seri

160 eived an infusion of sodium bicarbonate plus N-acetylcysteine (N-AC) started just before contrast inj

161 dministration of the free radical scavenger, N-acetylcysteine (NAC 150 mg kg(-1) intraperitoneal); co

162 imicked the effects of nicotine on AMPK, and N-acetylcysteine (NAC) abolished nicotine-enhanced AMPK

163 ) were treated in the presence or absence of N-acetylcysteine (NAC) administered 24 hours and 1 hour

164 Pretreatment with the antioxidant N-acetylcysteine (NAC) and expression of MT1 in the Ikkb

165 of two structurally unrelated antioxidants: N-acetylcysteine (NAC) and melatonin.

166 roprobes after pharmacologic challenges with N-acetylcysteine (NAc) and MK-801.

167 We used the pharmaceutical antioxidant N-acetylcysteine (NAC) as a bait reactant to measure NO

168 such as glutathione ethyl ester (GSH-EE); or N-acetylcysteine (NAC) attenuate 15d-PGJ(2)-induced plat

169 tment with antioxidants alpha-tocopherol and N-acetylcysteine (NAC) attenuated paraquat-induced impla

170 cently, it was reported that the antioxidant N-acetylcysteine (NAC) decreased DMXAA-induced TNF-alpha

171 ting Nkx3.1 mutant mice with the antioxidant N-acetylcysteine (NAC) for 13 weeks post-weaning.

172 N-acetylcysteine (NAC) has anti-atherosclerotic effect w

173 Systemic N-acetylcysteine (NAC) has been shown to restore glutama

174 N-acetylcysteine (NAC) has been suggested to prevent rel

175 combination of prednisone, azathioprine, and N-acetylcysteine (NAC) has been widely used as a treatme

176 N-Acetylcysteine (NAC) has been widely used in cell cult

177 rmalities were all rescued by treatment with N-acetylcysteine (NAC) in diabetic females during gestat

178 taneous treatment with the thiol antioxidant N-acetylcysteine (NAC) inhibited parameters indicative o

179 N-acetylcysteine (NAC) is an antioxidant with reactive o

180 N-acetylcysteine (NAC) is an FDA-approved drug that has

181 N-acetylcysteine (NAC) is known to promote endothelial c

182 The glutathione (GSH) precursor N-acetylcysteine (NAC) is used to treat patients with AP

183 ypes, the in vivo effects of the antioxidant N-acetylcysteine (NAC) on two mouse models for NPC1 dise

184 nistration of anti-inflammatory drugs, i.e., N-acetylcysteine (NAC) or mitoquinone-Q (mito-Q) in low

185 ong administration of the potent antioxidant N-acetylcysteine (NAC) prevented acetaminophen-induced l

186 nvestigate whether a donor pretreatment with N-acetylcysteine (NAC) reduces the incidence of DGF in a

187 atment of HMVEC-d cells with the antioxidant N-acetylcysteine (NAC) significantly inhibited KSHV entr

188 engers pyrrolidinedithiocarbamate (PDTC) and N-acetylcysteine (NAC) significantly inhibited ROS produ

189 ctric barrier discharge (DBD) plasma treated N-Acetylcysteine (NAC) solution against planktonic and b

190 Significant interaction was observed between N-acetylcysteine (NAC) therapy and rs3750920 within TOLL

191 We calibrated and applied an N-acetylcysteine (NAC) thiol reactivity assay as a surro

192 N-acetylcysteine (NAC) treatment prevents relapse in ani

193 N-acetylcysteine (NAC) was found to improve transplantat

194 The antioxidant N-acetylcysteine (NAC) was used to decrease ROS in both

195 ogether with 1 of 4 prophylactic regimes (1) N-acetylcysteine (NAC), (2) sodium bicarbonate (NaHCO3)

196 was to assess the feasibility of using oral N-acetylcysteine (NAC), a glutamatergic modulator and an

197 In rodents, N-acetylcysteine (NAC), a stimulator of the cystine-glut

198 N-acetylcysteine (NAC), a thiol-containing antioxidant,

199 N-acetylcysteine (NAC), an antidote for acetaminophen po

200 Furthermore, N-acetylcysteine (NAC), an antioxidant and ROS scavenger

201 eiodonium (DPI), a flavoenzyme inhibitor, or N-acetylcysteine (NAC), an antioxidant.

202 N-acetylcysteine (NAC), an FDA-approved anti-mucolytic a

203 y zerumbone was abolished by glutathione and N-acetylcysteine (NAC), and this correlated with decreas

204 The only available treatment, N-acetylcysteine (NAC), has a limited time window of eff

205 into four groups for daily treatment: HBOT, N-acetylcysteine (NAC), HBO and NAC, and control (normox

206 vestigate the effect of a thiol antioxidant, N-acetylcysteine (NAC), in SSc.

207 ously showed that the glutathione precursor, N-acetylcysteine (NAC), prevented hypoglycemia-associate

208 ng a total of 10 strategies: saline, statin, N-acetylcysteine (NAC), sodium bicarbonate (NaHCO3), NAC

209 suggest that the over-the-counter supplement N-acetylcysteine (NAC), via glutamate modulation in the

210 tolerance, and efficacy of the GSH precursor N-acetylcysteine (NAC).

211 hed by the antioxidant L-cysteine derivative N-acetylcysteine (NAC).

212 window of the only current treatment option, N-acetylcysteine (NAC).

213 on of ISO with the current standard of care, N-acetylcysteine (NAC).

214 N-Acetylcysteine (NAC, a clinically approved mucolytic d

215 ntions (corticosteroids, pentoxifylline, and N-acetylcysteine [NAC], alone or in combination) with ea

216 C-5 non-cancerous cells with the antioxidant N-acetylcysteine or 2,2,6,6-tetramethylpiperidine-1-oxyl

217 plemented HCT 116 cells with the antioxidant N-acetylcysteine or 2,2,6,6-tetramethylpiperidine-1-oxyl

218 rtrophy and preserved systolic function with N-acetylcysteine or a placebo for 12 months (n=10 per gr

219 ttenuated by the addition of the antioxidant N-acetylcysteine or ascorbate to the D medium.

220 ment of CSE-knockout mice with NaHS, but not N-acetylcysteine or ezetimibe, inhibited the accelerated

221 armacological treatment with the antioxidant N-acetylcysteine or genetic disruption of the DNA damage

222 ntrast, reduction of adipose DNA damage with N-acetylcysteine or metformin ameliorated cellular senes

223 ibition of Th17 induction with ROS scavenger N-acetylcysteine or mitoquinone, a specific inhibitor fo

224 induced apoptosis was blocked by antioxidant N-acetylcysteine or NF-kappaB inhibitor via down-regulat

225 o-controlled trial, 15 participants received N-acetylcysteine or placebo during a 3-day hospitalizati

226 Patients were randomized to receive either N-acetylcysteine or placebo for 7 days, in addition to s

227 ary end points between patients treated with N-acetylcysteine or placebo.

228 We focused on use of N-acetylcysteine or sodium bicarbonate for the preventio

229 of KB cells with antioxidants vitamin C and N-acetylcysteine or the pharmacological inhibitor PD1683

230 N-Acetylcysteine or tris(2-carboxylethyl)phosphine as co

231 ellular level, the presence of antioxidants (N-acetylcysteine or vitamin E) significantly reduced the

232 Administration of an antioxidant chemical, N-acetylcysteine, or ectopically overexpressing a reacti

233 d medication (serotonin reuptake inhibitors, N-acetylcysteine, or naltrexone).

234 of RhoA-deficient mice with a ROS scavenger N-acetylcysteine partially restored thymocyte developmen

235 While taking N-acetylcysteine, participants reported less desire to u

236 They randomly received N-acetylcysteine, physiologic saline, or sodium bicarbon

237 The greatest reduction in CIN was seen with N-acetylcysteine plus IV saline in patients receiving LO

238 atients receiving LOCM and with statins plus N-acetylcysteine plus IV saline.

239 However, N-acetylcysteine posttreatment worsened folic acid toxic

240 Glutathione levels did not increase in N-acetylcysteine posttreatment.

241 Glutathione levels decreased less in N-acetylcysteine pretreatment but also increased beginni

242 The survival rates in N-acetylcysteine pretreatment mice were significantly be

243 Interestingly, N-acetylcysteine pretreatment prevented cocaine-induced

244 N-acetylcysteine pretreatment was effective in reducing

245 hen assessed at least 3 weeks after the last N-acetylcysteine pretreatment.

246 N-acetylcysteine produced these changes by inducing an e

247 Our data support the administration of N-acetylcysteine prophylaxis, particularly in high-risk

248 Chronic treatment with N-acetylcysteine protects against mitochondrial oxidativ

249 Both CV-3988 and N-acetylcysteine reduced MS-WF-stimulated pneumococcal a

250 Exposure to the antioxidant N-acetylcysteine reduced oxidative stress and improved s

251 Treating mice in vivo with N-acetylcysteine reduces ROS levels, rescues HSC cycling

252 We propose that N-acetylcysteine represents the first potential therapeu

253 Intraperitoneal injection of the antioxidant N-acetylcysteine rescued defective follicle and oocyte d

254 Nurr1 in HEK293T cells, and the antioxidant N-acetylcysteine rescued from this effect.

255 tment of Paf(-/-) mice with the anti-oxidant N-acetylcysteine restored lymphoid progenitor numbers to

256 Treatment with N-acetylcysteine restored oxidized to total glutathione

257 thways of BCR-derived ROS with the scavenger N-acetylcysteine resulted in impaired in vitro BCR-induc

258 natal treatment of mice with the antioxidant N-acetylcysteine reversed the pollutant-induced increase

259 The antioxidant N-acetylcysteine reversed this phenotype, reducing both

260 retreated with vitamin E or sulforaphane and N-acetylcysteine; samples included A2E-free cells.

261 N-acetylcysteine seems to be beneficial for patients wit

262 These findings indicate that N-acetylcysteine selectively alters plasticity-dependent

263 The antioxidant N-acetylcysteine significantly inhibited ROS generation,

264 NAC was converted to S-nitroso-N-acetylcysteine (SNOAC), decreasing erythrocytic S-nitr

265 ntion (statin therapy, acetylsalicylic acid, N-acetylcysteine, sodium bicarbonate, off-pump coronary

266 Administration of N-acetylcysteine, sodium bicarbonate, or physiologic sal

267 N-acetylcysteine, sodium bicarbonate, statins, and ascor

268 ex I inhibitor-induced miR-663 expression by N-acetylcysteine suggested that reactive oxygen species

269 d a more general cytoprotective profile than N-acetylcysteine, suggesting a mechanism of action that

270 hat APAP-induced autophagy was suppressed by N-acetylcysteine, suggesting APAP mitochondrial protein

271 ide intermediate formed a stable adduct with N-acetylcysteine, suggesting that oxidative transformati

272 ndent inflammatory response was inhibited by N-acetylcysteine, suggesting that PRC may contribute to

273 versed by its product lactate or antioxidant N-acetylcysteine, suggesting that Y10 phosphorylation-me

274 tion and beta-oxidation products, as well as N-acetylcysteine, taurine and sulfo-conjugates in both r

275 minophen-induced liver injury at a time when N-acetylcysteine, the standard therapy, has no efficacy.

276 N-Acetylcysteine, theophylline, and other agents have sh

277 Among patients receiving N-acetylcysteine, there were trends toward reduced incid

278 NA lesions was abrogated by the anti-oxidant N-acetylcysteine, this treatment did not alter the accum

279 Fourteen healthy animals were given N-acetylcysteine to evaluate for toxicity and the other

280 infected murine macrophages, the addition of N-acetylcysteine to isoniazid treatment potentiated the

281 Addition of GSH or N-acetylcysteine to PBMCs selectively restored IL-12 and

282 for CRH5 but not AB12, MM cells, and in vivo N-acetylcysteine treatment eliminated these effects.

283 N-acetylcysteine treatment resulted in significant reduc

284 In addition, the N-acetylcysteine treatment significantly increased BKCa

285 Compared with placebo, N-acetylcysteine treatment was associated with significa

286 and demonstrate beneficial effects of early N-acetylcysteine treatment.

287 nical trial of prednisone, azathioprine, and N-acetylcysteine underwent HRCT at study start and finis

288 f patients "much or very much improved" with N-acetylcysteine use compared with 16% taking placebo (P

289 N-Acetylcysteine use was limited in this group, presumab

290 plain the variation from clinical studies of N-acetylcysteine use.

291 To test this, the cysteine prodrug N-acetylcysteine was administered before daily cocaine t

292 The substrate activity of propionyl-s- N-acetylcysteine was found to be negligible and that of

293 occurred in the N-acetylcysteine group, and N-acetylcysteine was well tolerated.

294 t even 2-3 weeks after the last injection of N-acetylcysteine, we examined whether N-acetylcysteine a

295 hen H(2)S-releasing compounds L-cysteine and N-acetylcysteine were added to the cell culture, the amo

296 and EAAC1(-/-) mice chronically treated with N-acetylcysteine were evaluated at serial time points fo

297 y, 15 of the 32 participants (47%) receiving N-acetylcysteine were much or very much improved compare

298 xidant and redox regulator compounds such as N-acetylcysteine, which could be used preventively in yo

299 perone 4-phenyl butyric acid and antioxidant N-acetylcysteine, which significantly attenuate lewisite

300 The present pilot study evaluated whether N-acetylcysteine would suppress reactivity to cocaine-re