ライフサイエンスコーパス: nitroso

1 e donors (such as 1-propamine 3-(2-hydroxy-2-nitroso-1-propylhydrazine (PAPA) NONOate and diethylamin

2 amine [SNAP] or PAPA NONOATE, 3-[2-Hydroxy-2-nitroso-1-propythdrazinol]-1-propanamine], NOC-15 [PAPA-

3 study of the use of the Fe(III)/3-hydroxy-4-nitroso-2,7-naphthalenedisulfonic acid (NRS) complexes o

4 othiazolidine-4-carboxylic acid (NTCA) and N-nitroso-2-methyl-thiazolidine-4-carboxylic acid (NMTCA)

5 Reactions between 1-nitroso-2-naphthols and alpha-functionalized ketones suc

6 e (MNPZ), nitrosodiethanolamine (NDELA), and nitroso-(2-hydroxyethyl) glycine (NHeGly) were measured

7 in the initial formation of MNX (hexahydro-1-nitroso-3,5-dinitro-1,3,5-triazine).

8 The 1-nitroso-5,6-dihydrouracil induced mutant ant30-310 had o

9 ino-9H-pyrido[2,3-b]indole (HONH-AalphaC), 2-nitroso-9H-pyrido[2,3-b]indole (NO-AalphaC), N-acetyloxy

10 ll in the tandem cycloaddition to afford the nitroso acetal 38a in 77% yield.

11 In addition, the highly functionalized nitroso acetal products can be hydrogenolyzed selectivel

12 be density functional theory calculations on nitroso acetal-to-aminal rearrangements reported by Denm

13 novel dyotropic rearrangement that converts nitroso acetals into tetracyclic aminals was discovered.

14 cycloadditions to form highly functionalized nitroso acetals.

15 m to increasing concentrations of NO donor S-nitroso acetyl penicillamine (SNAP).

16 incorporating the nitric oxide (NO) donor S-nitroso-acetylpenicillamine (SNAP) and silicone oil in c

17 modify tissue constituents, forming S- and N-nitroso adducts and metal nitrosyls implicated in NO sig

18 ArN=O (Ar = 3,5-Me(2)C(6)H(3), Ph) to give C-nitroso adducts that exhibit three different modes of bo

19 ference in S-nitroso-hemoglobin (SNOHb) or S-nitroso-albumin (SNOAlb) using the tri-iodide method and

20 vitro NO donor treatment of human plasma, S-nitroso-albumin did not form with NO exposure <2 microM,

21 is involved in the sequential process, the N-nitroso aldol reaction, followed by Michael addition.

22 1,2-oxazines from phosphinyl- and phosphonyl-nitroso alkenes has been developed.

23 enol ethers to 4-phosphinyl or 4-phosphonyl nitroso alkenes mediated by water itself.

24 (4)(2-), S(2)O(3)(2-) and Co(CN)(6)(3-), and nitroso-amino-pyrimidine receptors in water suggested th

25 er between the Cu center and the coordinated nitroso and diene units.

26 evations resulted in: (1) rapid formation of nitroso and nitrosyl species; (2) moderate short-term ch

27 icantly higher myocardial levels of nitrite, nitroso, and nitrosyl-heme, and displayed a 48% reductio

28 other N-oxidases involved in hydroxylamino-, nitroso-, and/or nitrosugar formation.

29 S-nitroso-AS content is regulated by cellular glutathione

30 kyl-substituted allenes to dienes, and final nitroso/butadiene [4 + 2] cycloadditions.

31 t of small molecules and discovered aromatic nitroso, carboxylate, sulfonamide, and arylstibonic acid

32 further advances in the evergreen field of C-nitroso chemistry, including the discovery of new ways t

33 t (heretofore unknown) that is mediated by S-nitroso-CoA (SNO-CoA).

34 es to conjugated dienes in the presence of a nitroso compound (additive) was studied quantum mechanic

35 Calculated results reveal that the unbound nitroso compound acts as a better proton transferring ag

36 ar hetero-Diels-Alder cycloadduct of an acyl nitroso compound and a 9,10-dimethyl anthracene derivati

37 We report a method of S-nitroso compound detection using cavity ring-down measur

38 Several pathways, involving the nitroso compound in a free or bound state to the gold-al

39 ncludes the observed nitroxide radical and C-nitroso compound intermediates has been forwarded to exp

40 g-down detection allows the measurement of S-nitroso compound levels from pico- to nanomole amounts.

41 t appeared that the moderate basicity of the nitroso compound plays a crucial role to reduce the acti

42 A resin-bound nitroso compound sequestered a single unexpected compone

43 ree radicals, consists of using a nitrone or nitroso compound to "trap" an unstable free radical as a

44 The lower rate of conversion of the (C7-R)-nitroso compound to the corresponding oximes compared wi

45 The conversion of the (C8-S)-nitroso compound to the E/Z-oximes was approximately 8 t

46 leophilic addition of the protein thiol to a nitroso compound to yield an N-hydroxysulfenamide, which

47 EPR spectroscopic evidence showed that the nitroso compound trapped other transient intermediates t

48 everse isomerization from the oxime to the C-nitroso compound was observed.

49 addition of nitrile oxide to form a bicyclic nitroso compound, followed by a retro-ene reaction of th

50 e structure of the acyl group of the acyloxy nitroso compound.

51 Aromatic C-nitroso compounds (Ar-N horizontal lineO) and related sp

52 Nitrite (NO2(-)) and nitroso compounds (E-NO, E = RS, RO, and R2N) in mammali

53 iron, heterocyclic amines, and endogenous N-nitroso compounds (NOC) are proposed to explain this eff

54 a precursor in the endogenous formation of N-nitroso compounds (NOC), which are possible bladder carc

55 Humans are exposed to preformed N-nitroso compounds (NOCs) and endogenous NOCs.

56 been linked to the formation of genotoxic N-nitroso compounds (NOCs) and lipid peroxidation products

57 Metabolic activation of some N-nitroso compounds (NOCs), an important class of DNA dama

58 e exposed to both endogenous and exogenous N-nitroso compounds (NOCs), and many NOCs can be metabolic

59 , heterocyclic aromatic amines (HAAs), and N-nitroso compounds (NOCs).

60 rates of addition of radicals to nitrones or nitroso compounds (spin traps; STs).

61 , we report that appropriately substituted C-nitroso compounds act solely as donors of neutral nitric

62 Dietary N-nitroso compounds and endogenous nitrosation are importa

63 Cured meat increased nitroso compounds and lipoperoxidation in human stools (

64 lative DNA damage rates of three mutagenic N-nitroso compounds and styrene.

65 ction of nitroaromatics to the corresponding nitroso compounds and, subsequently, to hydroxylamine pr

66 ay increase cancer risk as HCAs, PAHs, and N-nitroso compounds are carcinogenic in animal models.

67 After metabolic activation, many N-nitroso compounds are converted into a diazoacetate inte

68 C-Nitroso compounds are sources of biologically active neu

69 Together, these results identify acyloxy nitroso compounds as a new class of HNO donors.

70 stry of nitrile oxides, oximes, oxazete, and nitroso compounds as well as S(N)Vin reactions.

71 Many N-nitroso compounds can be metabolically activated to give

72 Some N-nitroso compounds can be metabolically activated to yiel

73 These results suggest that nitroso compounds form a general class of thiol-modifyin

74 Humans are exposed to N-nitroso compounds from both endogenous and exogenous sou

75 cient condensation of sulfinic acid and aryl nitroso compounds has been transformed into a chemoselec

76 Various N-nitroso compounds have been associated with neural tube

77 S-Nitroso compounds have received much attention in biolog

78 approximately 5 pmol of S(15)NO groups for S-nitroso compounds in aqueous solutions.

79 ondary or tertiary amines and amides, form N-nitroso compounds in the presence of nitrite.

80 These acyloxy nitroso compounds inhibit glyceraldehyde 3-phosphate deh

81 ethod for the synthesis of gem-difluorinated nitroso compounds is described.

82 The most common method to assay biological S-nitroso compounds is to chemically or photochemically re

83 These results suggest that N-nitroso compounds may influence the risk of ESCC in men,

84 N-nitroso compounds represent a common type of environment

85 exposure may also lead to the formation of N-nitroso compounds that can act as alkylating agents.

86 agents and highly acidic conditions, form N-nitroso compounds that have been found to be teratogenic

87 Humans are exposed to N-nitroso compounds through environmental exposure and end

88 Addition of these acyloxy nitroso compounds to AhpC C165S yields a sulfinic acid a

89 yzed radical addition with in situ-generated nitroso compounds to prepare sterically hindered amines

90 amines, polycyclic aromatic hydrocarbons, N-nitroso compounds, and heme iron.

91 combined forming the corresponding nitro and nitroso compounds, and the most reactive cis/syn isomer

92 N-Nitroso compounds, known animal carcinogens, are formed

93 Nitrate and nitrite are precursors of N-nitroso compounds, which induce tumors of the pancreas i

94 he acidic medium of stomach to form N- and C-nitroso compounds.

95 nous production of mutagenic aldehydes and N-nitroso compounds.

96 ma by reducing the endogenous formation of N-nitroso compounds.

97 excess carboxylic acid gives various acyloxy nitroso compounds.

98 Processed meats contain N-nitroso compounds.

99 ites because of the increased formation of N-nitroso compounds.

100 ngs and the azo linkage was formed via amine/nitroso condensation; protected forms of three other Abc

101 ed with organic solvent in the presence of a nitroso-containing resin.

102 [reaction: see text] Acyl nitroso cycloadducts of the alkaloid thebaine undergo an

103 y-alpha,beta-d-glucopyranose-2-)-N2-acetyl-S-nitroso-d,l-penicillaminami de (glycol-SNAP-2) were also

104 NAP-1 (N-(beta-D-glucopyranosyl)-N2-acetyl-S-nitroso-D,L-penicillaminamide) or the type 5 phosphosdie

105 NO)(5-MeIm)](+) generates a mixture of the C-nitroso derivative (OEP)Fe(PhNO)(5-MeIm) and (OEP)Fe(Ph)

106 Structures of complexes with the BTZ-derived nitroso derivative CT325 reveal the mode of inhibitor bi

107 ding oximes compared with that of the (C8-S)-nitroso derivative is attributed to the fact that the ac

108 NO or N2O3 as well as the formation of the S-nitroso derivative of hemoglobin, which has also been re

109 e conversion of either the (C7-R)- or (C8-S)-nitroso derivative to the corresponding E/Z-oximes.

110 er (at 40 degrees C) than that of the (C7-R)-nitroso derivative.

111 When we incubated RDX and its nitroso derivatives with XplA, we found that successive

112 es, but could nevertheless degrade all three nitroso derivatives, demonstrating the potential for com

113 e-7- and -8-oximes and their corresponding C-nitroso derivatives, which are the key intermediates for

114 ticonvulsant drugs, or drugs that may form N-nitroso derivatives.

115 eo- and highly enantioselective synthesis of nitroso Diels-Alder-type bicycloketones using dienamine.

116 troso species in situ, which were trapped in nitroso-Diels-Alder (NDA) reactions with various dienes

117 n accomplished through the one-pot oxidative nitroso-Diels-Alder reaction of N-arylhydroxylamines wit

118 Chiral phosphoric acid-catalyzed asymmetric nitroso-Diels-Alder reaction of nitrosoarenes with carba

119 rse the regioselectivity of the noncatalyzed nitroso-Diels-Alder reaction.

120 N-Nitroso-dimethylamine was detected in all examined produ

121 The NDA and nitroso-ene reaction pathways of nitroso intermediates w

122 h involves the formation of a C-N bond via a nitroso-ene reaction.

123 ay, 2-nitrosobenzonitrile undergoes a tandem nitroso-ene/intramolecular cyclization to form benzo[c]i

124 Experimental evidence further suggests that nitroso formation occurs substantially by means of oxida

125 e effect of cystine on the transfer of the S-nitroso functional group from the extracellular to the i

126 hanisms by which an S-nitrosothiol (or the S-nitroso functional group) is transferred across cell mem

127 tion between the resulting hydroxylamine and nitroso functional groups.

128 further by increased expression of GFAP by S-nitroso glutathione (GSNO), an NO donor.

129 n of guanylate cyclase but was mimicked by S-nitroso-glutathione (GSNO; an S-nitrosylating agent).

130 ations, GSNO and the constitutively active S-nitroso-glutathione diethyl ester stimulate CFTR transcr

131 d only glyphosate is prone to nitrosation, n-nitroso glyphosate and glufosinate were used as template

132 rotamers with reversed orientation of the 5-nitroso group are observed for compounds with two differ

133 ubstituents; however, the orientation of the nitroso group does not have any influence on the positio

134 The 5-nitroso group is able to form strong intramolecular hydr

135 The Cys 69 nitroso group is also protected but requires a higher pH

136 Surprisingly, the Cys 62 nitroso group is completely buried and pointing to the p

137 rotamers differing in the orientation of the nitroso group were observed in the NMR spectra of the co

138 To establish the unique influence of the S-nitroso group, our study describes high resolution three

139 an inert nitro group replacing the reactive nitroso group.

140 hat NH2Cl is the source of the N atom of the nitroso group.

141 2e-, 2H+ oxidation of the hydroxylamine to a nitroso group.

142 X-ray crystallographic analysis reveals the nitroso groups possess a "nitroxyl-like" bent configurat

143 and amplification of the N-Methyl-N'-nitro-N-nitroso-guanidine (MNNG) HOS transforming gene (MET) onc

144 Using N-methyl-N-nitro-N-nitroso-guanidine mutagenesis and selection, a mutant st

145 r the complete carcinogen 1-methyl-3-nitro-1-nitroso-guanidine or two-stage initiation and promotion

146 P activation in lungs of N-methyl-N'-nitro-N-nitroso-guanidine-treated mice or H(2)O(2)-treated cells

147 agens, 5-azacytidine and N-methyl-N'-nitro-N-nitroso-guanidine.

148 axation is inhibited by prior depletion of S-nitroso-Hb, potentiated by low-molecular-weight thiols,

149 Quantitatively there was no difference in S-nitroso-hemoglobin (SNOHb) or S-nitroso-albumin (SNOAlb)

150 ylated hemoglobin and, to a lesser extent, S-nitroso-hemoglobin.

151 ic oxidant in the final oxidation of an aryl-nitroso intermediate to the aryl-nitro product.

152 sent in these compounds to the corresponding nitroso intermediates by addition at the unsubstituted e

153 Research has shown that the nitroso intermediates of BTZs that are generated in vivo

154 The NDA and nitroso-ene reaction pathways of nitroso intermediates with dienes were mapped by DFT com

155 r similar to the von Richter reaction to the nitroso intermediates, to initiate the inhibition of Dpr

156 oarenes to nitroarenes via hydroxylamine and nitroso intermediates.

157 sport of amino acid-based S-nitrosothiols (S-nitroso-L-cysteine and S-nitrosohomocysteine) occurs via

158 Using S-nitroso-L-cysteine-ethyl ester (SNCEE) and S-nitrosoglut

159 By using S-nitroso-l-cysteine-ethyl-ester, an intracellular NO dono

160 d bovine endothelial cells with NO donors, S-nitroso-L-glutathione (GSNO) and S-nitroso-N-penicillami

161 on, whereas exposure of RAW 264.7 cells to S-nitroso-l-glutathione, a NO donor, triggered LKB1 S-nitr

162 n vitro by the nitric oxide donor compound S-nitroso-L-glutathione, failed to exhibit glucose-induced

163 st, DDAH-1 is sensitive to inactivation by S-nitroso-L-homocysteine (3.79 M(-1) s(-1)).

164 nhibition by L-homocysteine, H(2)O(2), and S-nitroso-L-homocysteine is quantified.

165 e maintenance of steady-state tissue nitrite/nitroso levels and illustrate the consequences of nitrit

166 terminal NO(2) group, probably to form a Ti-nitroso linkage between NAB and Ti.

167 ctive in the oxygenation of p-anisidine to 4-nitroso-methoxybenzene.

168 S-Nitroso modifications of cysteines 62 and 69 are clearly

169 s by others showed that administration of 4-(nitroso)-N-(5-methyl-1,2-oxazol-3-yl)benzenesulfonamide

170 of a series of differentially O-protected N-nitroso-N-acetyl sialyl glycosides and of isotopic label

171 hanism of the oxidative deamination of the N-nitroso-N-acetyl sialyl glycosides leading with overall

172 , with an excess of NO(g) or NO-generators S-nitroso-N-acetyl-D,L-pencillamine and diethylamine NONOa

173 oduction fell with both AI and addition of S-nitroso-N-acetyl-d,l-penicillamine (a NO donor) but was

174 EMP levels by 3-fold, whereas the NO donor S-nitroso-N-acetyl-D,L-penicillamine (SNAP) decreased it.

175 S-nitroso-N-acetyl-D,L-penicillamine (SNAP), a NO donor, w

176 o acetylcholine and the nitric oxide donor S-nitroso-N-acetyl-D,L-penicillamine that were restored by

177 lled release vehicles for NO, the NO donor S-nitroso-N-acetyl-D-penicillamine (SNAP) was encapsulated

178 ctive agents, S-nitrosoglutathione (GSNO), S-nitroso-N-acetyl-dl-penacillamine, and sodium nitropruss

179 e migraine trigger NTG or another NO donor S-nitroso-N-acetyl-DL-penicillamine (SNAP) at doses releva

180 The NO donor S-nitroso-N-acetyl-DL-penicillamine (SNAP) rapidly reduced

181 SN56) following exposure to the NO donors S-nitroso-N-acetyl-dl-penicillamine (SNAP), 3-morpholinosy

182 nhibition of HDAC activity, since GSNO and S-nitroso-N-acetyl-dl-penicillamine significantly and reve

183 The NO donor SNAP (S-nitroso-N-acetyl-DL-penicillamine) and a soluble guanyly

184 sensory neurons from the TG the NO donor, S-nitroso-N-acetyl-dl-penicillamine, inhibited M-current.

185 Bath application of the NO donor, S-nitroso-N-acetyl-penicillamine (SNAP), reproducibly incr

186 with either vehicle or nitric oxide donor (S-nitroso-N-acetyl-penicillamine [SNAP] or PAPA NONOATE, 3

187 NAC was converted to S-nitroso-N-acetylcysteine (SNOAC), decreasing erythrocyti

188 deficient fatty acid beta-oxidation, with S-nitroso-N-acetylcysteine induced site-specific S-nitrosy

189 e.g., nitrosocysteine, nitrosoglutathione, S-nitroso-N-acetylcysteine, S-nitrosoalbumin) present in t

190 cGMP-elevating agents such as the NO donor S-nitroso-N-acetylpenicillamine (SNAP) and C-type natriure

191 not higher (100-500 mum), concentration of S-nitroso-N-acetylpenicillamine (SNAP) can reverse the eff

192 The NO donor S-nitroso-N-acetylpenicillamine (SNAP) induced apoptosis w

193 As a consequence, the NO donor S-nitroso-N-acetylpenicillamine (SNAP) inhibits lipopolysa

194 e (CSNO), S-nitrosoglutathione (GSNO), and S-nitroso-N-acetylpenicillamine (SNAP) reversibly oxidized

195 The vasodilation elicited by the NO donor S-nitroso-N-acetylpenicillamine (SNAP) was inhibited by OD

196 death and nitrite levels at 24 h caused by S-nitroso-N-acetylpenicillamine (SNAP), a direct nitric ox

197 reatment with the nitric oxide (NO) donor, S-nitroso-N-acetylpenicillamine (SNAP), and the phosphodie

198 The NO donor S-nitroso-N-acetylpenicillamine (SNAP), at all concentrati

199 rons (CGNs) by treatment with the NO donor S-nitroso-N-acetylpenicillamine (SNAP), for short (6 h) or

200 ly enhanced TH17 cell differentiation, and S-nitroso-N-acetylpenicillamine (SNAP), the NO donor, dose

201 NTG or the spontaneous nitric oxide donor S-nitroso-N-acetylpenicillamine (SNAP).

202 In the resting state, NO donors S-nitroso-N-acetylpenicillamine (SNAP; 50 microM) and sodi

203 f primary cultured RCECs with an NO donor, S-nitroso-N-acetylpenicillamine (SNAP; N-acetyl-3-(nitroso

204 were exposed to combinations of NO donors (S-nitroso-N-acetylpenicillamine [SNAP] and others), a cGMP

205 iolate (NOC-18), S-nitrosoglutathione, and S-nitroso-N-acetylpenicillamine also suppressed CYP2B prot

206 However, treatment with the NO donors S-nitroso-N-acetylpenicillamine and spermine NONOate [N-(-

207 The NO donor S-nitroso-N-acetylpenicillamine decreases ceramide-induced

208 Moreover, S-nitrosoglutathione and S-nitroso-N-acetylpenicillamine directly blocked the activ

209 La and COS-7 cells, the nitric oxide donor S-nitroso-N-acetylpenicillamine increased the activity of

210 promoter, in which the nitric oxide donor S-nitroso-N-acetylpenicillamine reduces urea transporter-A

211 Increasing levels of nitric oxide using S-nitroso-N-acetylpenicillamine resulted in a decrease in

212 trosothiol donors S-nitrosoglutathione and S-nitroso-N-acetylpenicillamine suppressed caspase-9 and c

213 erated by the addition of 400 microM SNAP (S-nitroso-N-acetylpenicillamine) caused a 10-fold increase

214 enhances M1 macrophage polarization while S-nitroso-N-acetylpenicillamine, a NO donor, suppresses M1

215 ced response, the vasodilation elicited by S-nitroso-N-acetylpenicillamine, an NO donor that activate

216 onophore ionomycin, the nitric oxide donor S-nitroso-N-acetylpenicillamine, and the protein kinase G

217 erestingly, treatment of EC with NO donor, S-nitroso-N-acetylpenicillamine, did not activate SREBP, s

218 When FLS were cultured with S-nitroso-N-acetylpenicillamine, the pattern of MMR expres

219 Through the use of S-nitroso-N-acetylpenicillamine, which releases NO upon ex

220 nic conditions with the nitric oxide donor S-nitroso-N-acetylpenicillamine.

221 al tissues and incubated with the NO donor S-nitroso-N-acetylpenicillamine.

222 ted the relaxation induced by the NO donor S-nitroso-N-acetylpenicillamine.

223 ains to the prototypical alkylating agent, N-nitroso-N-ethylurea (ENU).

224 A three-generation ENU (N-Nitroso-N-ethylurea)-based forward genetic screen was pe

225 eased sensitivity to DNA damage induced by N-nitroso-N-ethylurea, ionizing radiation, or UV radiation

226 c(Min/+) or Apc(Min/+)Smad4(+/-) mice with N-Nitroso-N-Methyl Urea (NMU) results in abnormal foci in

227 Experiments with deuterated N-nitroso-N-methyl-N-ethylamine demonstrated that the lowe

228 ur nitrosamines (N-nitrosodiphenylamine 1, N-nitroso-N-methylaniline 2, N-butyl-N-(4-hydroxybutyl)nit

229 lated crops such as maize, we conducted an N-nitroso-N-methylurea (NMU) mutagenesis of S. viridis and

230 lever rats (n = 20 per group) treated with N-nitroso-N-methylurea and testosterone to induce prostate

231 precedes the NAD(+) depletion in N-methyl-N-nitroso-N-nitroguanidine (MNNG)-treated cortical neurons

232 donors, S-nitroso-L-glutathione (GSNO) and S-nitroso-N-penicillamine (SNAP).

233 myotubes treated with nitric oxide donors, S-nitroso-N-penicillamine (SNAP, 25 muM) or diethylenetria

234 rosomorpholine by hydroxylation alpha to the nitroso nitrogen can result in the deposition of a metas

235 mes (ORFs) in in vitro-cultivated 1-methyl-3-nitroso-nitroguanidine (MNNG)-treated and untreated spir

236 ring the ischemic phase, with an increase in nitroso/nitrosyl products in the heart.

237 Neither the (C7-R)-nitroso- nor (C8-S)-nitrosobicycloheptane system require

238 itrosamino)-1-(3-pyridinyl)-1-butanone and N-nitroso nornicotine were also detected.

239 tures, the nitrene reacts with O2 to produce nitroso O-oxide mainly in its syn conformation.

240 dation of 1a, whereas transformations of the nitroso oxide isomers derived from 1b led to a set of st

241 Upon visible light irradiation (450 nm), the nitroso oxide rapidly rearranges to nitrobenzene.

242 e DFT simulation and kinetic modeling of the nitroso oxide transformations as well as the product ana

243 onds and asymmetric molecule structure these nitroso oxides exist as four conformers (cis/syn, cis/an

244 larities of the consumption of corresponding nitroso oxides, which are the reaction intermediates, we

245 ramolecular cycloaddition of an asymmetric P-nitroso phosphine oxide (19) for the first time produces

246 Benzyl phenyl P-nitroso phosphine oxide (5) reacts as an N-O heterodieno

247 ese results suggest the reactions of these P-nitroso phosphine oxides and 1,3-cyclopentadiene occur t

248 converts o-aminophenols to the corresponding nitroso product (hydroxyanilinase activity).

249 NOS) expression, nitrate/nitrite production, nitroso product formation, peroxynitrite accumulation, a

250 orates were converted into the corresponding nitroso products in good to excellent yields.

251 luding plasma and red blood cell nitrate and nitroso proteins and plasma nitrite, but lower concentra

252 The 29 S-nitroso proteins identified are all enzymes, mostly serv

253 the emission of nitric oxide (NO) and the S-nitroso-proteome of IE and non-isoprene-emitting (NE) gr

254 their S-nitrosylation pattern, the in vivo S-nitroso-proteome of the NE genotype was more susceptible

255 rimidines and the stability of the resulting nitroso radical cations, the structures of which are det

256 The tert-butyl N-hydroxycarbamate-derived nitroso reagent 1 reacted with N-Cbz-protected spirocycl

257 then undertaken to exploit the hydroxylamine/nitroso redox couple using LC-DED detection for the meas

258 lmonary bypass and reperfusion on myocardial nitroso-redox balance in patients undergoing cardiac sur

259 valuated excitation-contraction coupling and nitroso-redox balance in spontaneously hypertensive hear

260 dative stress), and that therapies restoring nitroso-redox balance in the heart could prevent sudden

261 ntrol both the redox- and NO-based pathways (nitroso-redox homeostasis), which subserve innate and ce

262 Together these findings demonstrate that nitroso-redox imbalance causes RyR2 oxidation, hyponitro

263 Finally, we show that nitroso-redox imbalance due to decreased NOS1 activity s

264 Our findings suggest that nitroso-redox imbalance is an important mechanism of ven

265 , patient-derived CS cells displayed greater nitroso-redox imbalance than UV(S)S cells.

266 Ca(2+) cycling and contractility impaired by nitroso-redox imbalance, and NTG enhanced contractile ef

267 We used two models of nitroso-redox imbalance, neuronal NO synthase-deficient

268 yponitrosylated in heart failure, because of nitroso-redox imbalance.

269 of reactive nitrogen species, a situation of nitroso-redox imbalance.

270 Hence, rescuing the nitroso-redox levels is a potential therapeutic strategy

271 ontractile function in myocytes with altered nitroso-redox levels.

272 myocytes experiencing an imbalance of their nitroso-redox levels.

273 The nitroso resin selectively sequestered a single compound,

274 ack-transformation to SMX was observed for 4-nitroso-SMX, indicating that this metabolite may serve a

275 orin heme, but it can also be stored as an S-nitroso (SNO) conjugate of the proximal heme cysteine (C

276 Evidence for the pivotal role of S-nitroso (SNO) hemoglobin in mediating this response is d

277 in which we demonstrate the production of S-nitroso (SNO)-Hb through a heme-Fe(III)NO intermediate.

278 We conclude that intravascular nitroso species and nitrite both have the potential to r

279 s (B3LYP/6-31G*), which showed that the acyl nitroso species are super-reactive and that activation e

280 s considered to result from reduction of the nitroso species back to the hydroxylamine species.

281 pping studies indicate the intermediacy of a nitroso species during this reaction.

282 intermediacy of a nitroxide radical and a C-nitroso species during this reaction.

283 nd 2-ethyl-2-oxazoline in methanol gave acyl nitroso species in situ, which were trapped in nitroso-D

284 ow, the main decomposition pathway for the S-nitroso species leads to formation of nitric oxide.

285 hot5 null alleles show increased nitrate and nitroso species levels, and the heat sensitivity of both

286 form the nitroso species, hydrolysis of this nitroso species to produce nitroxyl, and reductive nitro

287 ation of hydroxyurea by catalase to form the nitroso species, hydrolysis of this nitroso species to p

288 ogical samples also contained mercury-stable nitroso species, indicating the additional involvement o

289 reacted with H(2)O(2) in the presence of the nitroso spin trap 2-methyl-2-nitrosopropane (MNP), yield

290 (TDP)-l-epi-vancosamine to the corresponding nitroso sugar.

291 e four-electron oxidation of amino sugars to nitroso sugars.

292 hus, we have used a T cell-priming assay and nitroso sulfamethoxazole (SMX-NO) as a model Ag to inves

293 zole, sulfamethoxazole beta-D-glucuronide, 4-nitroso sulfamethoxazole, and 4-nitro sulfamethoxazole w

294 llin, and dicloxacillin, but not abacavir or nitroso sulfamethoxazole.

295 te formation appears to be linked to N --> O nitroso transfer between the N-benzyl-N-nitrosoamides an

296 Benzo(a)pyrene [B(a)P] and N-nitroso-tris-chloroethylurea (NTCU) were used to induce

297 ight different inbred strains of mice with N-nitroso-tris-chloroethylurea by skin painting and found

298 ces in susceptibility to Lscc induction by N-nitroso-tris-chloroethylurea with NIH Swiss, A/J, and SW

299 in the presence of iron, large amounts of N-nitroso-tryptophan can be formed even at neutral pH, as

300 guanine (O6BG) and N,N'-bis(2-chloroethyl)-N-nitroso-urea (BCNU) stably increased the percentage of t