ライフサイエンスコーパス: nitrosothiol

1 of nitric oxide metabolites (ie, nitrite and nitrosothiols).

2 ion that converts a protein Cys thiol to a S-nitrosothiol.

3 m exposure to free *NO but not from cellular nitrosothiol.

4 intracellular reactive oxygen species and S-nitrosothiol.

5 ependent conformational change, to form an S-nitrosothiol.

6 logical response to this biologically active nitrosothiol.

7 th a second NO molecule to produce HNO and a nitrosothiol.

8 teine thiol (or thiolate anion) to form an S-nitrosothiol.

9 form thionitrous acid (HSNO), the smallest S-nitrosothiol.

10 ite versus chemical intermediates, such as S-nitrosothiols.

11 s encompassing the cellular homeostasis of S-nitrosothiols.

12 s release occurs due to NO liberation from S-nitrosothiols.

13 erate high levels of intracellular protein S-nitrosothiols.

14 al effects of nitric oxide are mediated by S-nitrosothiols.

15 be involved in the regulation of cellular S-nitrosothiols.

16 cellular activity of small molecular weight nitrosothiols.

17 es and the instability of cellular protein S-nitrosothiols.

18 beta subunit (cysbeta-93) to form bioactive nitrosothiols.

19 ult in decreased rates of decomposition of S-nitrosothiols.

20 intracellular glutathione and formation of S-nitrosothiols.

21 and the subsequent formation of NO-donating nitrosothiols.

22 that NO reacts with ---SH groups, forming S-nitrosothiols.

23 species and related modifications such as S-nitrosothiols.

24 anion, the nitric oxide free radical, and S-nitrosothiols.

25 of enzymatic control of cellular thiols and nitrosothiols.

26 from reaction of copper(II) thiolates with S-nitrosothiols.

27 ducts, with a decrease in the formation of S-nitrosothiols.

28 e presence of nitrite to form N(2)O(3) and S-nitrosothiols.

29 can be achieved through rational design of S-nitrosothiols.

30 gnificantly higher concentrations of total S-nitrosothiols (11.1+/-2.9 nmol/mL) than normal pregnancy

31 The nitrosothiol 2 was prepared via direct S-nitrosation of

32 ation, did not change total red blood cell S-nitrosothiol abundance but did shift S-nitrosothiol dist

33 manually curated data set of proteins with S-nitrosothiols, accounting for a variety of biochemical f

34 ion of NO provides the fully characterized S-nitrosothiol adduct [Cu(I)](kappa(1)-N(O)SR), which reve

35 s can react with thiols of proteins and form nitrosothiol adducts.

36 S-Nitrosothiol and iron-nitrosyl-protein adducts did not a

37 currently used to quantify putative protein nitrosothiol and N-nitrosamine derivatives.

38 We tested the hypothesis that total S-nitrosothiol and S-nitrosoalbumin concentrations are inc

39 Further reaction of HNO with the remaining S-nitrosothiol and thiol results in the generation of othe

40 this is a NO-containing factor such as an S-nitrosothiol and/or a dinitrosyl-iron (II) cysteine comp

41 Due to combined increases in nitrosothiols and decreases in protein, the preeclampsia

42 Dietary nitrate increased plasma S-nitrosothiols and nitrite, enhanced revascularization, i

43 f apparent total N-nitroso compounds (ATNC), nitrosothiols and nitrosyl iron compounds (FeNO) were an

44 Nitric oxide, S-nitrosothiols and peroxynitrite are reported to variousl

45 For S-nitrosothiols and peroxynitrite to interfere with the ac

46 actor for the interaction of the enzyme with nitrosothiols and peroxynitrite.

47 f complex I was susceptible to inhibition by nitrosothiols and peroxynitrite.

48 could facilitate nitric oxide release from S-nitrosothiols and represents a potential physiological m

49 The role of circulating S-nitrosothiols and SNO-Hb in the regulation of basal vasc

50 hrough exposure to cell membrane-permeable S-nitrosothiols and that sGC is S-nitrosylated and desensi

51 r ascorbate leads to the generation of NO or nitrosothiols and thus stimulates the activation of sGC.

52 s to be more susceptible to NO (especially S-nitrosothiols) and subsequent necrotic cell death.

53 to stain for NADPH diaphorase were rich in S-nitrosothiols, and (7) procedures that accelerate decomp

54 ate (NO(3) (-)), nitrosyl-metal complexes, S-nitrosothiols, and 3-nitrotyrosine.

55 to the anaerobic regulon protected against S-nitrosothiols, and anaerobic growth of E. coli lacking O

56 acellular-reduced glutathione (GSH), protein nitrosothiols, and the activation of the transcription f

57 erin (GTN) and nitric oxide donors such as S-nitrosothiols are clinically vasoactive through stimulat

58 S-Nitrosothiols are known as reagents for NO storage and t

59 Because S-nitrosothiols are known to modify enzymes containing rea

60 studied, the response elements specific to S-nitrosothiols are less clear.

61 Nitrosothiols are ubiquitous molecules that comprise an

62 chanism of inactivation was reported using S-nitrosothiols as the NO donor.

63 to those reported for low-molecular-weight S-nitrosothiols, as well as from nitrite.

64 ndicates that hypoxic vasodilation entails S-nitrosothiol-based (SNO-based) vasoactivity (rather than

65 exploited in the evolutionary development of nitrosothiol-based innate immunity and may provide an av

66 Our results suggest that an S-nitrosothiol-based signal originating from RBCs mediates

67 These observations suggest that S-nitrosothiol biochemistry is of central importance to th

68 cus is on oxidized nitrogen in the form of S-nitrosothiol bond-containing species, which are now appr

69 d was evaluated as a fluorescence probe of S-nitrosothiol-bound NO transfer in human umbilical vein e

70 irst gel-based method to identify not only S-nitrosothiols but also other labile NO-based modificatio

71 y of ascorbate to generate a thiol from an S-nitrosothiol, but not from alternatively S-oxidized thio

72 A fraction (25%) was exported as S-nitrosothiol, but this fraction was not increased at low

73 Findings indicate that nitrate, nitrite and nitrosothiols, but not NO or iron nitrosyl species (FeNO

74 We have investigated the breakdown of S-nitrosothiols by wild-type (WT) SOD and two common FALS

75 Nitric oxide and S-nitrosothiols can be metabolized by bacteria, but only a

76 howed that exposure to nitric oxide and to S-nitrosothiols causes S-nitrosylation of sGC, which direc

77 m accounts for several unexplained facets of nitrosothiol chemistry in solution, including the observ

78 y binding to cysteine residues and forming S-nitrosothiol complexes.

79 10(-1) microM) and accurate means to measure nitrosothiol concentration in biologic samples.

80 e conclude that S-nitrosoalbumin and total S-nitrosothiol concentrations are significantly increased

81 re pronounced effect of protecting against S-nitrosothiols, confirms this finding.

82 Erythrocyte S-nitrosothiol content (reflecting mainly S-nitrosohemoglo

83 Compared to similar measurements of total S-nitrosothiol content in bulk solution, use of the microf

84 ys a key role in cellular redox homeostasis, nitrosothiol content in cells, and antiapoptotic signali

85 1+/-25 pmol/mg protein, respectively) when S-nitrosothiol content was expressed per milligram protein

86 lcysteine (SNOAC), decreasing erythrocytic S-nitrosothiol content, both during whole-blood deoxygenat

87 ccurs in tandem with increased erythrocyte S-nitrosothiol content, EM, and O2 unloading.

88 IPC and GSNO both significantly increased S-nitrosothiol contents and S-nitrosylation levels of the

89 atment with NO donors (increasing cellular S-nitrosothiol contents) substantially enhanced the initia

90 e fluorescence intensity of dansyl-labeled S-nitrosothiols could be enhanced up to 30-fold.

91 We now report that (1) S-nitrosothiols covalently modify both NBT and TNBT, but o

92 tutive NOS activity and generation of NO via nitrosothiol degradation within the first hour.

93 RT externalization occurred together in an S-nitrosothiol-dependent and caspase-independent manner.

94 We observed that PDI catalyzes the S-nitrosothiol-dependent oxidation of the heme group of my

95 enitrosylated RBCs than during infusion of S-nitrosothiol-depleted RBCs, and this difference in coron

96 S-nitrosohemoglobin and plasma S-nitrosothiols did not change with NO inhalation.

97 alpha-NADP did not produce diformazan, (5) S-nitrosothiols did not promote NADPH-dependent reduction

98 ell S-nitrosothiol abundance but did shift S-nitrosothiol distribution to lower molecular weight spec

99 within endothelial cells from an exogenous S-nitrosothiol donor or from endogenous production of NO b

100 human monocytes as a model, we observed that nitrosothiol donors S-nitrosoglutathione and S-nitroso-N

101 onse in proportion to the concentration of S-nitrosothiols (e.g., nitrosocysteine, nitrosoglutathione

102 siological levels of nitric oxide (NO) and S-nitrosothiols (e.g., S-nitrosoglutathione, GSNO) and ari

103 Nitrosothiol esters of diclofenac comprise a novel class

104 sine monophosphate (cGMP) generation after S-nitrosothiol exposure (65.4 +/- 26.7% reduction compared

105 thiols modified using nitric oxide, termed S-nitrosothiols, facilitate the hypersensitive response in

106 The selective S-nitrosothiol formation at Cys-81 led to a doubling of th

107 nvolved both S- and N-nitrosation, and RBC S-nitrosothiol formation emerged as a sensitive indicator

108 r, is much less effective at intracellular S-nitrosothiol formation in the presence of L-cystine or L

109 Nitrosothiol formation in vivo depends not only on the a

110 desensitization and find that heme-assisted nitrosothiol formation of beta1Cys-78 and beta1Cys-122 c

111 GSNO is a low molecular weight SNO (S-nitrosothiol) formed during oxidation of NO.

112 ver, a subsequent incubation of the cells in nitrosothiol-free medium resulted in reconstitution of t

113 atively transferring the thiol groups into S-nitrosothiol functionalities.

114 lytic Cu(II)/(I)-mediated decomposition of S-nitrosothiols generates NO(g) in the thin polymeric film

115 or microsome-associated thiols led to NO or nitrosothiol generation and thus stimulated the activati

116 a NO reaction with cysteine residues to form nitrosothiol groups.

117 ors (including a.NO donor [DeaNonoate], an S-nitrosothiol [GSNO], and the nitroxyl anion donor, Angel

118 Transnitrosation between thiols and S-nitrosothiols has been suggested to be a mechanism of si

119 tanding the biosynthesis and catabolism of S-nitrosothiols has proven to be difficult, in part becaus

120 S-nitrosothiols have been implicated as intermediary trans

121 S-nitrosothiols have been suggested to play an important r

122 rofluidic sensor to facilitate photolysis of nitrosothiols (i.e., S-nitrosoglutathione, S-nitrosocyst

123 ve, and specific methods for quantitation of nitrosothiols in biological samples.

124 ) enhanced the therapeutic actions of oral S-nitrosothiols in mouse models of C. difficile infection.

125 trol samples and 53.7% and 56.8% of plasma S-nitrosothiols in normal pregnancy and preeclampsia, resp

126 but not SNP or SIN-1, increased levels of S-nitrosothiols in SN56 proteins, consistent with the tran

127 n fraction contained 49.4% of total plasma S-nitrosothiols in the control samples and 53.7% and 56.8%

128 ,we obtained evidence for the formation of S-nitrosothiols in the ER molecule.

129 gnificant increases in nitrite, nitrate, and nitrosothiols in the heart, plasma, and liver.

130 tely accounted for the increased levels of S-nitrosothiols in total plasma.

131 n and storage of NO metabolites (nitrite and nitrosothiols) in the heart.

132 approximately 50% reduction in perfusate [S-nitrosothiol], in association with an increase in perfus

133 couple NAD(P)H oxidation with reduction of S-nitrosothiols, including protein and low-molecular-weigh

134 of dynamin2 or treatment with the NO donor S-nitrosothiols increases, whereas targeted reduction of e

135 nstituted domain peptides demonstrate that S-nitrosothiols indeed release zinc from both the alpha- a

136 The nitrosothiol intermediate reacts further with RSH to pro

137 lts suggest that inactivation of papain by S-nitrosothiols is due to a direct attack of the highly re

138 tudy, we demonstrate that the transport of S-nitrosothiols is essential for these compounds to affect

139 ay responsible for the cellular effects of S-nitrosothiols is specific for S-nitrosocysteine (CSNO),

140 Thionitrous acid (HSNO), the smallest S-nitrosothiol, is emerging as a potential key intermediat

141 se to exposure to both free nitric oxide and nitrosothiols (k (inact)/K(I) >= 5 m(-1) s(-1)), which i

142 whereas the BJR responses elicited by the S-nitrosothiol, L-S-nitrosocysteine (5 micromol/kg, i.v.),

143 mutated thioredoxin reductase denitrosate S-nitrosothiols less efficiently.

144 thiol uptake, increasing the intracellular S-nitrosothiol level from approximately 60 pmol/mg of prot

145 nitrate, nitrite, and low-molecular-weight S-nitrosothiol levels by chemiluminescence.

146 uction of NO was paralleled by a decrease in nitrosothiol levels for 2 hour, suggesting that immediat

147 lysis, this device was used to measure basal nitrosothiol levels from the vasculature of a healthy po

148 ovide new insight into the determinants of S-nitrosothiol levels in subcellular compartments.

149 ne biosynthesis pathway and an increase in S-nitrosothiol levels suggest S-nitrosylation to be a cons

150 estored intracardiac nitrite and increased S-nitrosothiol levels, decreased pathological cardiac mito

151 was accompanied by an increase in cellular S-nitrosothiol levels, modification of cysteines residues,

152 t resulting in 100-fold higher intracellular nitrosothiol levels.

153 c oxide synthase expression, and nitrite and nitrosothiol levels.

154 In parallel, S-nitrosothiol-linked probes enable enrichment and detecti

155 the detection of other low-molecular weight nitrosothiols (LMW-RSNOs) in biological samples.

156 rocedures that accelerate decomposition of S-nitrosothiols, markedly reduced NADPH diaphorase stainin

157 cordingly, mutation of Cys 890 compromised S-nitrosothiol-mediated control of AtRBOHD activity, pertu

158 nts a potential physiological mechanism of S-nitrosothiol metabolism.

159 Importantly, S-nitrosothiol-MIF formation was measured both in vitro an

160 This decrease was paralleled by a S-nitrosothiol-MIF- but not Cys81 serine (Ser)-MIF mutant-

161 the catalytic site and that nitric oxide (or nitrosothiols) might act as a negative regulator of V-AT

162 versies surrounding the proposal that this S-nitrosothiol modulates blood flow in vivo.

163 cubated with cysteine, suggesting that these nitrosothiols must react with cysteine to form CSNO, whi

164 bioactivation, nitrite was reduced to NO, S-nitrosothiols, N-nitros-amines, and iron-nitrosylated he

165 one marrow-derived CD31(+)/CD45(-), plasma S-nitrosothiols, nitrite, and skeletal tissue cGMP levels

166 isulfide acts as a source of nitrosonium for nitrosothiol nitrosation, completing the catalytic cycle

167 ulated by redox reactions involving NO and S-nitrosothiols (nitrosative stress), emphasizing a versat

168 mass spectrometry, we found that NO forms S-nitrosothiols on Cys67 and Cys95 of HIV-PR which directl

169 d method for analyzing protein and peptide S-nitrosothiols on gels using the fluorescent probes 4,5-d

170 of NBT after modification, (2) addition of S-nitrosothiols or beta- or alpha-NADPH to solutions of NB

171 gical event when NO-dependent formation of S-nitrosothiols or peroxynitrite structurally modifies com

172 However, the mechanisms by which an S-nitrosothiol (or the S-nitroso functional group) is tran

173 e data demonstrate for the first time that S-nitrosothiols oxidatively modify PTEN, leading to revers

174 Plasma nitrite (P = 0.01), S-nitrosothiols (P = 0.03) and total red blood cell NO (P

175 ption and corresponding delivery of plasma S-nitrosothiols (P>0.05).

176 y effected by NO(g) with the use of trityl-S-nitrosothiol (Ph3CSNO) as the nitric oxide source.

177 ripheral circulation, and (iii) SNO-Hb and S-nitrosothiols play a minimal role in the regulation of b

178 l concentrations of nitrite and deoxyHb, a S-nitrosothiol precursor is formed within seconds and prod

179 onic chain mechanism in which nitrosation of nitrosothiol produces a nitrosated cation that, in turn,

180 Here we demonstrate that sulfinic acids and nitrosothiols react to form a stable thiosulfonate bond,

181 emical mechanism by which nitric oxide and S-nitrosothiols react with cysteine residues in ornithine

182 Exogenous NO, nitrite and nitrosothiols react with placental homogenates to form i

183 m normal placentas, and that NO, nitrite and nitrosothiols react with placental homogenates to form i

184 vivo Using this approach, called SNOxICAT (S-nitrosothiol redox isotope-coded affinity tag), we found

185 can be preserved in a more stable form of S-nitrosothiols (RS-NO).

186 N) that leads to S-nitrosation to give the S-nitrosothiol RSNO and copper(II) hydroxide [Cu(II)]-OH.

187 study, we examined the chemical pathways of nitrosothiol (RSNO) production at low micromolar concent

188 itric oxide (NO) delivery is achieved from S-nitrosothiol (RSNO) type NO donor doped silicone rubber

189 The decomposition of S-nitrosothiols (RSNO) in solution under oxidative conditi

190 oxidation leads to formation of vasoactive S-nitrosothiols (RSNO) in vitro and in vivo as detected el

191 Nitrosothiols (RSNO), formed from thiols and metabolites

192 metabolites with thiols and metals to form S-nitrosothiols (RSNOs) and metal nitrosyls.

193 S-Nitrosothiols (RSNOs) are carriers of nitric oxide (NO)

194 S-Nitrosothiols (RSNOs) are important exogenous and endoge

195 Amperometric detection of S-nitrosothiols (RSNOs) at submicromolar levels in blood s

196 Although S-nitrosothiols (RSNOs) have been frequently implicated in

197 Nitrosothiols (RSNOs) have been proposed as important in

198 dely used methodology for the detection of S-nitrosothiols (RSNOs) in biological samples.

199 S-Nitrosothiols (RSNOs) serve as air-stable reservoirs for

200 S-nitrosothiols (RSNOs) serve as ready sources of biologic

201 The concentration of S-nitrosothiols (RSNOs), endogenous transporters of the si

202 with the low molecular mass cell-permeable S-nitrosothiol S-nitrosocysteine ethyl ester (SNCEE).

203 nd inhibited by the physiologically relevant nitrosothiol S-nitrosoglutathione.

204 ein S-nitrosylation, the colocalization of S-nitrosothiol (S-NO) and protein-tyrosine phosphatase 1B

205 ing protein and low-molecular-weight (LMW) S-nitrosothiols (S-nitroso-GSH (GSNO) and S-nitroso-CoA (S

206 the specific transport of amino acid-based S-nitrosothiols (S-nitroso-L-cysteine and S-nitrosohomocys

207 /K(I) analyses, we quantified the ability of nitrosothiols (S-nitrosoglutathione and S-nitroso-N-acet

208 ries of novel diclofenac esters containing a nitrosothiol (-S-NO) moiety as a NO donor functionality

209 dues in ornithine decarboxylase to form an S-nitrosothiol(s) on the protein.

210 GGT also metabolizes the naturally occurring nitrosothiol, S-nitrosoglutathione (GSNO).

211 te activation and is the precursor of NO and nitrosothiols, serving as the link between organic nitra

212 ransformation and is the precursor of NO and nitrosothiols, serving as the link between organic nitra

213 te that zinc thiolate bonds are targets of S-nitrosothiol signaling and further indicate that MT-III

214 b) on HPV, expired NO (eNO), and perfusate S-nitrosothiol (SNO) concentration in isolated, perfused r

215 idney injury (AKI), double knockout (-/-), S-nitrosothiol (SNO) condition at a nitrosylation level of

216 ses the rate at which low-molecular-weight S-nitrosothiol (SNO) decomposes in vitro.

217 The role of S-nitrosothiol (SNO) formation and turnover in governing N

218 S-nitrosothiol (SNO) formation was increased in isoprotere

219 Disruption of S-nitrosothiol (SNO) homeostasis may result not only from

220 Here we utilize antibodies specific for the nitrosothiol (SNO) moiety to provide an immunohistochemi

221 Further, this Trx S-nitrosothiol (SNO) reductase activity was potentiated fo

222 zinc finger transcription factor (ZF-TF), S-nitrosothiol (SNO) Regulated 1 (SRG1), is a central targ

223 in human erythrocytes haemoglobin-derived S-nitrosothiol (SNO), generated from imported NO, is assoc

224 etaCys93) that has been assigned a role in S-nitrosothiol (SNO)-based hypoxic vasodilation by RBCs.

225 S-nitrosothiol (SNO)-deficient RBCs produce impaired vasod

226 ic vasodilation is recapitulated by native S-nitrosothiol (SNO)-replete RBCs and by SNO-Hb itself, wh

227 tein cysteine (Cys) thiol (-SH) to form an S-nitrosothiol (SNO).

228 ety to a protein cysteine thiol forming an S-nitrosothiol (SNO).

229 ety to a protein cysteine thiol to form an S-nitrosothiol (SNO).

230 steine thiol by an NO group to generate an S-nitrosothiol (SNO).

231 10(-4) at 3 h vs. 6.5 x 10(-4) (fresh) mol S-nitrosothiol (SNO)/mol Hb tetramer (P = 0.032, mercuric-

232 ed 1,276 S-nitrosylated cysteine residues [S-nitrosothiol (SNO)] on 491 proteins in resting hearts fr

233 We demonstrate here that S-nitrosothiols (SNO) caused a dose-dependent inhibition o

234 mical reaction products [nitrite, nitrate, S-nitrosothiols (SNO), and nitrotyrosine] before, immediat

235 achment of NO to cysteine residues to form S-nitrosothiols (SNO).

236 n (iron nitrosyl, FeNO) to cysteine thiol (S-nitrosothiol, SNO) that subserves bioactivation, and in

237 a family of NO-related molecules and that S-nitrosothiols (SNOs) are central to signal transduction

238 Nitric oxide (NO) and/or S-nitrosothiols (SNOs) can prevent the loss of beta-AR sig

239 ereas treatments favoring stabilization of S-nitrosothiols (SNOs) decreased its cytotoxic potency.

240 e that nitric oxide (NO) and/or endogenous S-nitrosothiols (SNOs) exert protective effects in a varie

241 emical data demonstrate a pivotal role for S-nitrosothiols (SNOs) in mediating the actions of nitric

242 lation reflects dynamic equilibria between S-nitrosothiols (SNOs) in proteins and small molecules (lo

243 ly through protein S-nitrosylation to form S-nitrosothiols (SNOs) in target proteins, operates coordi

244 ehydrogenase involved in the regulation of S-nitrosothiols (SNOs) in vivo.

245 rd nitric oxide (NO) leads to formation of S-nitrosothiols (SNOs) that play important roles in pathog

246 S-nitrosothiols (SNOs), formed by nitric oxide (NO)-mediat

247 dified the biotin switch assay for protein S-nitrosothiols (SNOs), using resin-assisted capture (SNO-

248 NO bioactivity is packaged in the form of S-nitrosothiols (SNOs), which are relatively resistant to

249 synthase (NOS), superoxide dismutase, and S-nitrosothiols (SNOs), which have recently been identifie

250 reductase (GSNOR) and are depleted of lung S-nitrosothiols (SNOs).

251 r of NO from Hb to form other (vasoactive) S-nitrosothiols (SNOs).

252 ) is signalled by deoxyhaemoglobin-derived S-nitrosothiols (SNOs).

253 ative modification of Cys residues to form S-nitrosothiols (SNOs).

254 activity in mammals is largely mediated by S-nitrosothiols (SNOs).

255 sylation by biologically relevant low-mass S-nitrosothiols (SNOs).

256 The direct amperometric detection of S-nitrosothiol species (RSNOs) is realized by modifying a

257 source of this NO is the already available S-nitrosothiol store rather than de novo synthesis by NOS.

258 through intracellular NO by modulation of S-nitrosothiol stores and stimulation of NOS activity.

259 nction as a generator for the formation of S-nitrosothiols such as S-nitrosoglutathione and, as such,

260 Other nitrosothiols such as S-nitrosoglutathione are not subst

261 to cause vasodilation as compared to other S-nitrosothiols suggests potential application in biologic

262 data provide evidence for a physiological S-nitrosothiol synthase activity of tetrameric Hb that dep

263 NO can be converted into nitrite or nitrosothiols that are stable until cleaved by UV to rel

264 We hypothesized that nitrosothiols that promote protein S-nitrosylation would

265 thiols was used to explore the kinetics of S-nitrosothiol/thiol transnitrosation and was evaluated as

266 that a single sulfinic acid can react with a nitrosothiol to form a thiosulfonate linkage.

267 d cation that, in turn, reacts with a second nitrosothiol to produce nitrosated disulfide and the NO

268 in the enzyme active site on the sulfur of S-nitrosothiols to form a mixed disulfide between the inac

269 Here, we report that H(2)S reacts with S-nitrosothiols to form thionitrous acid (HSNO), the small

270 luded ultraviolet-induced decomposition of S-nitrosothiols to liberate NO captured by a florigenic re

271 did not elicit diformazan, (3) addition of S-nitrosothiols to solutions of NBT plus beta- or alpha-NA

272 sence of paraformaldehyde, (4) addition of S-nitrosothiols to solutions of NBT plus beta- or alpha-NA

273 This reaction converts unstable primary S-nitrosothiols to stable disulfide-iminophosphorane produ

274 mational changes in the toxin enabled host S-nitrosothiols to transnitrosylate the toxin catalytic cy

275 However, the mechanisms by which S-nitrosothiols transduce their activity across cell membr

276 to be incompatible with life were all the S-nitrosothiols transformed into bioactive equivalents dur

277 this study, we have examined the effect of S-nitrosothiol transport on intracellular thiol status and

278 -20x improvement in sensitivity depending on nitrosothiol type).

279 sence of L-cystine enhanced GSNO-dependent S-nitrosothiol uptake, increasing the intracellular S-nitr

280 A bis-ligation reaction of S-nitrosothiols using triaryl substituted phosphine-thioes

281 The resultant protein-S-nitrosothiol was found to be unstable and to decompose s

282 The inhibition of papain by S-nitrosothiol was rapidly reversed by dithiothreitol, but

283 Intracellular accumulation of S-nitrosothiols was observed with 2a but not with 2b.

284 ed by yeast flavohemoglobin against NO and S-nitrosothiols was seen under both anaerobic and aerobic

285 In addition, one of the dansyl-labeled S-nitrosothiols was used to explore the kinetics of S-nitr

286 kground nitrite and stabilizes erythrocyte S-nitrosothiols, we find the levels of SNO-Hb in the basal

287 nitrate, nitrite, and low-molecular-weight S-nitrosothiol were in the normal range; however, enhanced

288 S-Nitrosothiols were barely detectable.

289 Moreover, a variety of additional S-nitrosothiols were catabolized more readily by A4V SOD t

290 Surprisingly, when concentrations of S-nitrosothiols were high, nitric oxide function also gove

291 A series of fluorophore-labeled S-nitrosothiols were synthesized, and their fluorescence e

292 We found that low-molecular-weight S-nitrosothiols were undetectable and S-nitroso-albumin le

293 ficantly more reactive than MT-I/II toward S-nitrosothiols, whereas the reactivity of all three isofo

294 lium induces a precipitous decline in cell S-nitrosothiol, which depends upon enhanced Trx activity a

295 is reflected in the level of intracellular S-nitrosothiols, which are constitutively metabolized.

296 wed by reductive generation of thiols from S-nitrosothiols, which are then labeled with either a biot

297 nism, we here investigate the reactions of S-nitrosothiols with different isoforms of MT.

298 and thiols, furnishing iron nitrosyls and S-nitrosothiols with wide-ranging stabilities and reactivi

299 nges that occur after exposure of cells to S-nitrosothiol, with respect to thiol chemistry, are disti

300 g reactive cysteines, we hypothesized that S-nitrosothiols would oxidize PTEN and inhibit its phospha