ライフサイエンスコーパス: methylglyoxal

1 bitors (beta-glucoside, D-fucose, valine and methylglyoxal).

2 tution reaction was studied in the past with methylglyoxal.

3 with elevated levels of the toxic catabolite methylglyoxal.

4 erial survival upon exposure to diacetyl and methylglyoxal.

5 rted to the toxic molecules aminoacetone and methylglyoxal.

6 y incubating native albumin with glucose and methylglyoxal.

7 muM(-)(1) were achieved for the detection of methylglyoxal.

8 r levels of the growth-inhibitory metabolite methylglyoxal.

9 the advanced glycated end product precursor methylglyoxal.

10 atalysis of the elimination reaction to give methylglyoxal.

11 its alpha-oxoaldehyde decomposition product methylglyoxal.

12 be significantly increased by treatment with methylglyoxal.

13 ulation and excretion of the glycating agent methylglyoxal.

14 F1alpha by the glyoxalase 1 (GLO1) substrate methylglyoxal.

15 be significantly increased by treatment with methylglyoxal.

16 ot to acrolein, crotonaldehyde, glyoxal, and methylglyoxal.

17 xonil treatment triggered elevated cytosolic methylglyoxal.

18 f dimer decomposition and hence formation of methylglyoxal.

19 es), consistent with previous experiments on methylglyoxal.

20 , and reactive dicarbonyl compounds - mainly methylglyoxal.

21 mediate) with glycolysis metabolites such as methylglyoxal.

22 )-(2)H]DHAP (23%), [2(R)-(2)H]GAP (31%), and methylglyoxal (18%) from an enzyme-catalyzed elimination

23 Methylglyoxal (2-oxopropanal) is a compound known to con

24 Methylglyoxal, 3-DG, and glyoxal were the predominant 1,

25 The adduct derived from methylglyoxal-3-(2'-deoxyribosyl)-6,7-dihydro-6,7-dihydr

26 of Glo1 (27%, P < 0.05) and decreased plasma methylglyoxal (-37%, P < 0.05) and total body methylglyo

27 etabolites containing reactive groups (e.g., methylglyoxal, 4-hydroxynonenal, and glutaconyl-CoA), or

28 d detoxification of the atherogenic compound methylglyoxal (+54%, P = 0.008).

29 inhibits the apoptotic response of a cell to methylglyoxal, a by-product of glycolysis.

30 scular basement membrane type IV collagen by methylglyoxal, a dicarbonyl glycating agent with increas

31 n embryonic kidney cells upon treatment with methylglyoxal, a glycolysis byproduct that is present at

32 also affected the extent of modifications by methylglyoxal, a highly reactive metabolite that can be

33 products released by A2E photodegradation is methylglyoxal, a low molecular weight reactive dicarbony

34 cytoplasmic microcompartment for disposal of methylglyoxal, a toxic byproduct of glycolysis, as 1-pro

35 formation of brown carbon was observed upon methylglyoxal addition, detected as an increase in water

36 nd degradation of acetaldehyde, glyoxal, and methylglyoxal along with spatiotemporal variations in th

37 Methylglyoxal also increased spontaneous Ca(2+) release

38 additional reactants were required, although methylglyoxal, ammonia, and formaldehyde also participat

39 that remains constant with reaction time for methylglyoxal-ammonium sulfate systems.

40 e interactions between a mixture of glyoxal, methylglyoxal and 2,3-butanedione and the digestive enzy

41 onyl compounds (alpha-DCs), such as glyoxal, methylglyoxal and 2,3-butanedione, are highly reactive s

42 This detailed analysis showed that methylglyoxal and a fructose-1-P- or fructose-1,6-bisP-d

43 Metabolism of methylglyoxal and AGE accumulation were studied in human

44 cosone, 5-hydroxymethyl-2-furfural, glyoxal, methylglyoxal and diacetyl concentrations were determine

45 rmation was predominant from glucosone while methylglyoxal and diacetyl originated from 1-deoxyglucos

46 Known manuka markers, methylglyoxal and dihydroxyacetone, have been characteri

47 Methylglyoxal and dimethylglyoxal were mainly formed fro

48 Thus, increased formation of methylglyoxal and ECM glycation in hyperglycemia impairs

49 urface uptake of isoprene-generated glyoxal, methylglyoxal and epoxydiol accounts for approximately 8

50 period of 48 h for ternary solutions of both methylglyoxal and formaldehyde in aqueous ammonium sulfa

51 ll wall, and by causing over-accumulation of methylglyoxal and glycerol, which in turn impacts NO det

52 In addition, methylglyoxal and glyoxal produced more light-absorbing

53 damage induced by reactive carbonyls (mainly methylglyoxal and glyoxal), called DNA glycation, is qua

54 using various cytotoxic aldehydes including methylglyoxal and malondialdehyde as substrates and the

55 Enzymes in the glycolytic, sorbitol, methylglyoxal and mitochondrial pathways were elevated i

56 The addition of methylglyoxal and NADH, NADPH, F 420H 2, or DTT to a M.

57 ioxidant defense system utilized to detoxify methylglyoxal and neutralize free radicals.

58 on of enzymes dedicated to detoxification of methylglyoxal and other reactive electrophiles.

59 lements the function of Hsp31 by suppressing methylglyoxal and oxidative stress, thus signifying the

60 The biochemical routes for the metabolism of methylglyoxal and the formation of lactaldehyde and hydr

61 ns between the alpha-dicarbonyls glyoxal and methylglyoxal and the primary amines glycine and methyla

62 tion of acetaldehyde, pyruvic acid, acetoin, methylglyoxal, and alpha-ketoglutaric acid in wine with

63 hylglyoxal, elevated levels of intracellular methylglyoxal, and carbon source-dependent growth defect

64 action mixtures of small aldehydes (glyoxal, methylglyoxal, and glycolaldehyde) with ammonium sulfate

65 (SOAS) to compare the potential of glyoxal, methylglyoxal, and IEPOX to partition to ALW, as the ini

66 Acetol was generated in hearts perfused with methylglyoxal, and its formation was increased in akr1b4

67 Thus, it can be concluded that the levels of methylglyoxal, and therefore the antimicrobial effect of

68 man DJ-1 is a protein deglycase that repairs methylglyoxal- and glyoxal-glycated amino acids and prot

69 homologs Hsp31, YhbO, and YajL could repair methylglyoxal- and glyoxal-glycated nucleotides and nucl

70 .4-1.0 mg L(-1) glyoxal and 0.8-1.3 mg L(-1) methylglyoxal; and between 0.8-3.0 mg L(-1) and 0.5-1.8

71 Glyoxal and methylglyoxal are reactive dicarbonyl metabolites formed

72 ospheric concentrations, whereas glyoxal and methylglyoxal are significantly undersaturated.

73 Isoprene epoxydiol (IEPOX), glyoxal, and methylglyoxal are ubiquitous water-soluble organic gases

74 al approach for the quantitative analysis of methylglyoxal as a biomarker in human plasma has been de

75 Our results identify the dicarbonyl methylglyoxal as a marker metabolite for MDSCs that medi

76 ication of p300 by the dicarbonyl metabolite methylglyoxal as being responsible for this decreased as

77 llowed for the identification of glyoxal and methylglyoxal as key browning intermediates in apple jui

78 ubated for 24 hours with control solution or methylglyoxal at concentrations of 0.001%, 0.01%, 0.10%,

79 ubated for 24 hours with control solution or methylglyoxal at concentrations of 0.01%, 0.10%, and 1.0

80 to a toxic polyamine biosynthesis inhibitor methylglyoxal bis-(guanylhydrazone) (MGBG), but the mole

81 Here we demonstrate that methylglyoxal-bis-guanylhydrazone (MGBG), a polyamine an

82 eraldehyde-3-P (Ga-P-3), which converts into methylglyoxal by a 2,3-elimination of phosphate.

83 In addition, the modification by methylglyoxal causes the antibody to elute earlier in th

84 d from the reaction of ammonium sulfate with methylglyoxal changes under photolytic aging by UVA radi

85 ety of conditions associated with changes in methylglyoxal concentration, including cancer and diabet

86 olute consistently decreased with increasing methylglyoxal concentration, indicating diffusion impeda

87 olute consistently decreased with increasing methylglyoxal concentration, indicating diffusion impeda

88 Higher glyoxal and methylglyoxal concentrations were observed in biological

89 Administration of deferoxamine abrogated methylglyoxal conjugation, normalizing both HIF-1alpha/p

90 A linear relationship was found between methylglyoxal content (279-1755 mg/kg) in Leptospermum p

91 ve tool for honey antibacterial activity and methylglyoxal content was assessed.

92 ty based on percentage inhibition as well as methylglyoxal content.

93 inhibition is needed to 'value' honeys with methylglyoxal contents in excess of 200mg/kg.

94 rate oxidation (glycolaldehyde, glyoxal, and methylglyoxal) covalently modify lipid-free apoA-I and i

95 L. major and human enzymes were active with methylglyoxal derivatives of several thiols, but showed

96 ible nitric oxide synthase upregulation, and methylglyoxal-derived advanced glycation end product, ni

97 hyl lysine (CE-OVA), pyrraline (Pyr-OVA), or methylglyoxal-derived arginine derivatives (MGO-OVA).

98 CML), N(euro)-(carboxyethyl)lysin (CEL), and methylglyoxal-derived hydroimadazolidine (MG-H1) were me

99 The methylglyoxal-derived hydroimidazolones (MG-Hs) comprise

100 ived imidazolinone derivative in addition to methylglyoxal-derived hydroimidazolones.

101 of the advanced glycation end product (AGE) methylglyoxal-derived imidazolium crosslink (MODIC).

102 Unexpectedly, the DNA content of methylglyoxal-derived imidazopurinone and oxidative mark

103 f HSA with sugars revealed 9 glyoxal- and 14 methylglyoxal-derived modification sites.

104 Ablation of the methylglyoxal detoxification enzyme glyoxalase I (Glo1)

105 Somatic gene transfer of the methylglyoxal detoxification enzyme, glyoxalase-1, resto

106 In Leishmania major, the first step in methylglyoxal detoxification is performed by a trypanoth

107 at lactoylglutathione (LGSH), a byproduct of methylglyoxal detoxification, is elevated in both human

108 impairments of the gamma-glutamyl cycle and methylglyoxal detoxification.

109 LmAQP1 is also permeable to water, glycerol, methylglyoxal, dihydroxyacetone and sugar alcohols.

110 rendered them permeable to water, glycerol, methylglyoxal, dihydroxyacetone and sugar alcohols.

111 oxyglucosone, 3,4-dideoxyglucosone, glyoxal, methylglyoxal, dimethylglyoxal, and 5-hydroxymethylfurfu

112 this study, we spectroscopically identified methylglyoxal diol (MGD) and obtained the gas-phase part

113 ensitivity to millimolar levels of exogenous methylglyoxal, elevated levels of intracellular methylgl

114 Methylglyoxal enhancements were three to six times highe

115 We have measured KS of glyoxal and methylglyoxal for the atmospherically relevant salts (NH

116 d to measure interfacial tension of reacting methylglyoxal, formaldehyde, and ammonium sulfate aqueou

117 Methylglyoxal forms stable adducts primarily with argini

118 This work is the first report of methylglyoxal functioning in central metabolism.

119 ified accumulation of the dicarbonyl radical methylglyoxal, generated by semicarbazide-sensitive amin

120 Glyoxal, methylglyoxal, glycolaldehyde, and hydroxyacetone form N

121 nds (glucosone, 3-deoxyglucosone, threosone, methylglyoxal, glyoxal) and 5-hydroxymethylfurfural in a

122 d endogenous reducing sugars or dicarbonyls (methylglyoxal, glyoxal) that results in protein inactiva

123 s, asparagine, acrylamide, 3-deoxyglucosone, methylglyoxal, glyoxal, and 5-hydroxymethylfurfural were

124 deoxythreosone, 3-deoxythreosone, threosone, methylglyoxal, glyoxal; the alpha-keto-carboxylic acids

125 tures, product absorbance followed the order methylglyoxal > glyoxal > glycolaldehyde > hydroxyaceton

126 umidification experiments followed the order methylglyoxal > glyoxal > glycolaldehyde = hydroxyaceton

127 azard ratio [HR] 1.60 [95% CI 1.08-2.37]) or methylglyoxal hydroimidazolone (HR 1.30 [95% CI 1.02-1.6

128 Glyoxyl hydroimidazolone and methylglyoxal hydroimidazolone correlated negatively wit

129 rboxyethyl lysine, carboxymethyl lysine, and methylglyoxal hydroimidazolone correlated positively wit

130 o sulfoxides was dramatically increased, but methylglyoxal hydroimidazolones levels that are GSH/glyo

131 nsitive for the analysis of plasma levels of methylglyoxal in healthy volunteer and diabetic patients

132 ined results revealed high concentrations of methylglyoxal in HFASs (average 102 +/- 91 mg/kg, range

133 days of incubation with the glycation agent methylglyoxal in the absence or presence of the glycatio

134 e the blood-brain barrier, elevate levels of methylglyoxal in the brain, and reduce depression-like b

135 d less accumulation of the toxic metabolite, methylglyoxal in the transgenic lines under non-stress a

136 r damage caused by oxidants, xenobiotics and methylglyoxal in the trypanosomatid parasites, which cau

137 inhibited TPI and also caused it to release methylglyoxal in vitro.

138 n of alpha-dicarbonyl compounds, glyoxal and methylglyoxal, in "Ribera del Guadiana" monovarietal win

139 The prototype RCS methylglyoxal increased and then decreased the RyR2 open

140 nd QW (50-200 muM) showed protection against methylglyoxal-induced cell deaths in human umbilical vei

141 (100 muM) showed protective effects against methylglyoxal-induced human umbilical vein endothelial c

142 virtually no 2-AAA formed in the presence of methylglyoxal instead of ascorbate.

143 Methylglyoxal is a cytotoxic reactive carbonyl compound

144 Methylglyoxal is a highly reactive alpha-ketoaldehyde th

145 Methylglyoxal is a highly reactive dicarbonyl degradatio

146 Methylglyoxal is a reactive metabolite byproduct of glyc

147 Methylglyoxal is already known to be generated by carboh

148 bon electrode for the sensitive detection of methylglyoxal is delineated for the first time using squ

149 Methylglyoxal is detoxified by the Glyoxalase system, co

150 Given that methylglyoxal is frequently generated under both physiol

151 Methylglyoxal is predicted to be a minor contributor.

152 Modifications of arginine residues by methylglyoxal lead to two adducts (dihydroxyimidazolidin

153 s, including arsenite, 4-hydroxynonenal, and methylglyoxal, led to decreased GSIS.

154 lation by shRNA caused a 40% increase in the methylglyoxal level, which was completely prevented by g

155 m of reactive metabolite and glycating agent methylglyoxal-may improve metabolic and vascular health.

156 d maintained angiogenesis, and inhibition of methylglyoxal metabolism with a cell permeable glyoxalas

157 acid (FA) synthesis, translation processes, methylglyoxal metabolism, DNA repair and recombination,

158 ors for glyoxal-methylamine (19% by vol) and methylglyoxal-methylamine (8% by vol) aerosol, indicatin

159 Glyoxal- and methylglyoxal-methylamine aerosol particles shattered in

160 that two ubiquitous atmospheric trace gases, methylglyoxal (MG) and acetaldehyde, known to be surface

161 oward aerobic glycolysis unavoidably favours methylglyoxal (MG) and advanced glycation end products (

162 BrC components produced through reactions of methylglyoxal (MG) and ammonium sulfate (AS), both of wh

163 The accumulation of dicarbonyl compounds, methylglyoxal (MG) and glyoxal (G), has been observed in

164 Methylglyoxal (MG) can accumulate and promote inflammati

165 Methylglyoxal (MG) elicits activation of K(+) efflux sys

166 Aqueous-phase processing of methylglyoxal (MG) has been suggested to play a key role

167 Survival of exposure to methylglyoxal (MG) in Gram-negative pathogens is largely

168 We investigate the hydration of methylglyoxal (MG) in the gas phase, a process not previ

169 Methylglyoxal (MG) is a common byproduct of the ubiquito

170 Methylglyoxal (MG) is a cytotoxic by-product of glycolys

171 Methylglyoxal (MG) is a key signaling molecule resulting

172 Methylglyoxal (MG) is a predominant precursor for advanc

173 Methylglyoxal (MG) is a reactive metabolic intermediate

174 Methylglyoxal (MG) is a reactive metabolite that forms a

175 Methylglyoxal (MG) is a toxic by-product of glycolysis t

176 Methylglyoxal (MG) is a toxic metabolite that is elevate

177 However, methylglyoxal (MG) is evolving as a diabetes marker sinc

178 ents and small dicarbonyls (glyoxal (GO) and methylglyoxal (MG)), we investigated RPE lipofuscin as a

179 Methylglyoxal (MG), a by-product of DHAP, also accumulat

180 GLO1 increases anxiety by reducing levels of methylglyoxal (MG), a GABAA receptor agonist.

181 Methylglyoxal (MG), an arginine-directed glycating agent

182 es where increased reactive glycating agent, methylglyoxal (MG), is involved.

183 by the glycolysis-derived alpha-oxoaldehyde, methylglyoxal (MG), prevents hyperglycemia-induced oxida

184 r generates the dicarbonyls glyoxal (GO) and methylglyoxal (MG), that are known to modify proteins by

185 thod for the detection and quantification of methylglyoxal (MG), the major physiological substrate of

186 d metabolism is the highly reactive compound methylglyoxal (MG), which accumulates in all cells, in p

187 formation of the highly reactive dicarbonyl methylglyoxal (MG), yet the early consequences of MG for

188 outer nuclear layer thinning, and increased methylglyoxal (MG)-adducted protein.

189 bolites, including reactive dicarbonyls like methylglyoxal (MG).

190 rapid in vitro glycation of COLI and FN used methylglyoxal (MG).

191 phosphate isomerase (TPI) causing release of methylglyoxal (MG).

192 e detoxification of the glycolytic byproduct methylglyoxal (MG).

193 oxification of dicarbonyl species, primarily methylglyoxal (MG).

194 ., glucosepane [GSPNE], hydroimidazolones of methylglyoxal [MG-H1] and glyoxal, and carboxyethyl-lysi

195 11 mg/kg, 0.10mg/kg, 0.09 mg/kg for glyoxal, methylglyoxal (MGo) and diacetyl, respectively.

196 Methylglyoxal (MGO) and glyoxal (GO) are toxic reactive

197 Methylglyoxal (MGO) and glyoxal (GO), known as reactive

198 Methylglyoxal (MGO) and its precursor dihydroxyacetone (

199 with lysine, arginine and histidine to bind methylglyoxal (MGO) and reducing the formation of advanc

200 athways related to the glycolytic by-product methylglyoxal (MGO) are rewired in Alkbh7(-/-) mice, alo

201 Glycolysis generates methylglyoxal (MGO) as an unavoidable, cytotoxic by-prod

202 a GSH-independent glyoxalase that detoxifies methylglyoxal (MGO) by converting it into lactate.

203 ), 3-deoxyglucosone (3-DG), glyoxal (GO) and methylglyoxal (MGO) during simulated gastrointestinal di

204 h these new probes we found that, similar to methylglyoxal (MGO) glycation, ribose glycation specific

205 Although the glucose-derived product methylglyoxal (MGO) has been detected in periodontal les

206 ration reaction of dihydroxyacetone (DHA) to methylglyoxal (MGO) in a honey model system has been exa

207 the conversion of dihydroxyacetone (DHA) to methylglyoxal (MGO) in honey is proposed; a building blo

208 the conversion of dihydroxyacetone (DHA) to methylglyoxal (MGO) in maturing New Zealand manuka honey

209 Methylglyoxal (MGO) is a highly reactive a-dicarbonyl co

210 Methylglyoxal (MGO) is a reactive dicarbonyl metabolite

211 Methylglyoxal (MGO) is one of the highly reactive dicarb

212 Methylglyoxal (MGO) is one type of reactive aldehyde tha

213 Preincubating with the RCS, methylglyoxal (MGO) likewise reduced SERCA2a activity.

214 ted previously that the pathogenicity of RCS methylglyoxal (MGO) may be due to modification of critic

215 gical levels of either the carbonyl compound methylglyoxal (MGO) or glucose resulted in modification

216 We recently showed that glycation of aSyn by methylglyoxal (MGO) potentiates its oligomerization and

217 the conversion of dihydroxyacetone (DHA) to methylglyoxal (MGO) was examined in New Zealand manuka h

218 ported herein, an unexpected modification by methylglyoxal (MGO) was identified, for the first time,

219 atrol, apigenin, kaempferol and fisetin) and methylglyoxal (MGO) were determined at pH 7.4 and 37 deg

220 RPCs, RPCs pre-incubated in high glucose or methylglyoxal (MGO) were evaluated using the T cell prol

221 s of conversion of dihydroxyacetone (DHA) to methylglyoxal (MGO) were investigated in manuka honeys a

222 es of the dicarbonyl compounds glyoxal (GO), methylglyoxal (MGO), 3-deoxyglucosone (3-DG) were assess

223 Methylglyoxal (MGO), a dicarbonyl metabolite produced by

224 Methylglyoxal (MGO), a major precursor for advanced glyc

225 Reactive alpha-dicarbonyls (alpha-DCs), like methylglyoxal (MGO), accumulate with age and have been i

226 Glyoxal (GO), methylglyoxal (MGO), diacetyl (DA) and 3-deoxyglucosone

227 with the added advantage that it can measure methylglyoxal (MGO), dihydroxyacetone (DHA) and leptospe

228 ystallin by a metabolic dicarbonyl compound, methylglyoxal (MGO), enhances its chaperone-like functio

229 of this study was to analyze the dicarbonyls methylglyoxal (MGO), glyoxal (GO), and 3-deoxyglucosone

230 Plasma concentrations of dicarbonyls methylglyoxal (MGO), glyoxal (GO), and 3-deoxyglucosone

231 glucose-derived dicarbonyl metabolites like methylglyoxal (MGO), glyoxal (GO), and 3-deoxyglucosone

232 The alpha-oxoaldehyde, methylglyoxal (MGO), has been implicated as a cause of c

233 tly, we found that histones are subjected to methylglyoxal (MGO)-induced glycation on nucleophilic si

234 hesis and protective effect against H2O2 and methylglyoxal (MGO)-induced stress in epithelial gastric

235 m composed of bovine serum albumin (BSA) and methylglyoxal (MGO).

236 Methylglyoxal modification of mSin3A results in increase

237 Methylglyoxal modification of mSin3A results in increase

238 thelial cells, high glucose causes increased methylglyoxal modification of the corepressor mSin3A.

239 , increased glycolytic flux causes increased methylglyoxal modification of the corepressor mSin3A.

240 A similar mechanism involving methylglyoxal-modification of other coregulator proteins

241 f mouse tubule epithelial cells treated with methylglyoxal-modified albumin.

242 es demonstrate a specific mechanism by which methylglyoxal modifies a transcriptional corepressor to

243 o determine the interactions between glyoxal/methylglyoxal monohydrate with Cl(-), NO3(-), SO4(2-), N

244 -3.1, -10.3, -7.91, 6.11, and 1.6 kJ/mol for methylglyoxal monohydrate with uncertainties of 8 kJ/mol

245 generated either by the NAD(P)H reduction of methylglyoxal or by the aldol cleavage of fuculose-1-pho

246 Major dicarbonyl compounds such as methylglyoxal or glyoxal are found to be the main precur

247 glyoxal, followed by similar production from methylglyoxal or hydroxyacetone.

248 glycated by incubation with sugars (glucose, methylglyoxal or ribose) +/-5-15 mg/mL of aged and fresh

249 Pharmacological scavenging of methylglyoxal prevented anoikis and maintained angiogene

250 approach to determine secondary glyoxal and methylglyoxal produced by oxidation of isoprene and othe

251 herein that glycation of DNA by glyoxal and methylglyoxal produces a quantitatively important class

252 ethylglyoxal (-37%, P < 0.05) and total body methylglyoxal-protein glycation (-14%, P < 0.01).

253 A good prediction of methylglyoxal (R(2) 0.75) content in honey was achieved

254 One millimolar glucose or 1 mM methylglyoxal raised ATP in the DeltaatpD knockout cells

255 Under dry, particle-free conditions, methylglyoxal reacted (presumably on chamber walls) with

256 endence (Angstrom coefficients) observed for methylglyoxal reaction mixtures, the lack of surface act

257 HIF1alpha modification by methylglyoxal reduced heterodimer formation and HIF1alph

258 Independently of AGER, methylglyoxal reduced the release of endothelial CSF-1 (

259 the other Mrr1-regulated genes are putative methylglyoxal reductases.

260 We report enhancements of glyoxal and methylglyoxal relative to carbon monoxide and formaldehy

261 se metabolism enzymes and a reduction in the methylglyoxal removal enzyme GLO1 in both C9orf72 and sp

262 Detoxification of methylglyoxal requires reduced glutathione (GSH), which

263 mg L(-1) and 0.5-1.8 mg L(-1) of glyoxal and methylglyoxal respectively, in red wines.

264 .8 nmol L(-1) for acetaldehyde, glyoxal, and methylglyoxal, respectively.

265 l L(-1) h(-1) for acetaldehyde, glyoxal, and methylglyoxal, respectively.

266 .065, -0.1 molality(-1), respectively) while methylglyoxal "salts-out" (KS of +0.16, +0.075, +0.02, +

267 ation enzyme glyoxalase I (Glo1) potentiates methylglyoxal sensitivity and reduces tumor growth in mi

268 imate could not be determined for glyoxal or methylglyoxal, since several processes have not been qua

269 Methylglyoxal slowly photodegraded in seawater (~0.001-0

270 B1 deacetylase are encoded in an operon with methylglyoxal synthase.

271 well as their interactions with glyoxal and methylglyoxal that lead to an increase in browning.

272 alpha-TCsNe inhibited ergosterol synthesis, methylglyoxal (the aflatoxin enhancer) content and enhan

273 as the rate-determining step in formation of methylglyoxal, the bioactive component in manuka honey.

274 This effect is mediated by ROS-induced methylglyoxal, the major substrate of glyoxalase 1.

275 Dedicated glyoxalases convert methylglyoxal to d-lactate using multiple catalytic stra

276 atalyzed the F 420H 2-dependent reduction of methylglyoxal to lactaldehyde, a precursor of the lactat

277 acts, producing sufficient concentrations of methylglyoxal to support the reaction.

278 hemithioacetal, formed from glutathione and methylglyoxal, to a lactic acid thioester.

279 ndent reductase activity toward diacetyl and methylglyoxal, toxic electrophilic dicarbonyls.

280 a catabolite repression, possibly to prevent methylglyoxal toxicity.

281 This study found that flavonoid treatment in methylglyoxal treated cerebellar neurons increased the f

282 Acetol formation in methylglyoxal-treated HUVECs was prevented by the aldose

283 Methylglyoxal treatment effectively increased nonenzymat

284 In particular, we found that methylglyoxal treatment gave rise to altered expression

285 Likewise, methylglyoxal treatment of Drk1-expressing yeast phenoco

286 , exposure of cells to oxidants H(2)O(2) and methylglyoxal up-regulated MIOX expression and its phosp

287 The effects of methylglyoxal uptake on the physical and optical propert

288 An unexpectedly high amount of methylglyoxal was found in mire and forest honeys.

289 [1,3,3,3- (2)H 4]-Methylglyoxal was incorporated into lactaldehyde and hyd

290 a well-defined reduction peak in response to methylglyoxal was observed.

291 on treating cells with increasing amounts of methylglyoxal, we found that the levels of Hsp27 decreas

292 C (PKC) pathway, and increased formation of methylglyoxal were assessed.

293 Glyoxal and methylglyoxal were measured using broadband cavity enhan

294 by the reactions between 5-A-RU and glyoxal/methylglyoxal were simple adducts, 5-(2-oxoethylideneami

295 ns with small molecules, such as glyoxal and methylglyoxal, which are derived from other metabolic pa

296 tive carbonyl species (RCS) glyoxal (GO) and methylglyoxal while nonoxidative glucose adduction to th

297 derived enzyme catalyzes the condensation of methylglyoxal with a dihydroxyacetone-P fragment, which

298 AqSOA was made from the dark reactions of methylglyoxal with methylamine in simulated evaporated c

299 ydroxymethylfurfural, furfural, glyoxal, and methylglyoxal, with l-alanine were analyzed with Fourier

300 The hydroxyacetone was derived directly from methylglyoxal, with the hydrogen for the reduction being