ライフサイエンスコーパス: methylglyoxal

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

2 es), consistent with previous experiments on methylglyoxal.

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

4 r levels of the growth-inhibitory metabolite methylglyoxal.

5 the advanced glycated end product precursor methylglyoxal.

6 , and reactive dicarbonyl compounds - mainly methylglyoxal.

7 atalysis of the elimination reaction to give methylglyoxal.

8 its alpha-oxoaldehyde decomposition product methylglyoxal.

9 be significantly increased by treatment with methylglyoxal.

10 ulation and excretion of the glycating agent methylglyoxal.

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

12 be significantly increased by treatment with methylglyoxal.

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

14 r H2O2-producing activity in the presence of methylglyoxal.

15 mediate) with glycolysis metabolites such as methylglyoxal.

16 f the cytoplasm protects E. coli DNA against methylglyoxal.

17 cells to the inhibitory effects of exogenous methylglyoxal.

18 with elevated levels of the toxic catabolite methylglyoxal.

19 rted to the toxic molecules aminoacetone and methylglyoxal.

20 y incubating native albumin with glucose and methylglyoxal.

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

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

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

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

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

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

27 ng protein involved in the detoxification of methylglyoxal, a by-product of glycolysis.

28 HAGH functions in a pathway to detoxify methylglyoxal, a compound present in coffee and alcoholi

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

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

31 osttranslational modification of proteins by methylglyoxal, a highly reactive compound derived from g

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 Methylglyoxal also increased spontaneous Ca(2+) release

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

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

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

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

41 Metabolism of methylglyoxal and AGE accumulation were studied in human

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

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

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

45 Methylglyoxal and dimethylglyoxal were mainly formed fro

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

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

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

49 he conversion of the hemithioacetal of toxic methylglyoxal and glutathione to nontoxic (S)-D-lactoylg

50 atically produced hemimercaptal of cytotoxic methylglyoxal and glutathione to nontoxic S-D-lactoylglu

51 onversion of the thiohemiacetal, formed from methylglyoxal and glutathione, to S-D-lactoylglutathione

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 sium channels protects E. coli cells against methylglyoxal and limits the amount of DNA damage.

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

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

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

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

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

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

61 mutations in Tpi lead to an accumulation of methylglyoxal and the consequent enhanced production of

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

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

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

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

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

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

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

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

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

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

72 .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

73 Glyoxal and methylglyoxal are reactive dicarbonyl metabolites formed

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

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

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 cal for accumulation of the polyamine analog methylglyoxal bis(guanylhydrazone) (MGBG) that induces a

81 se complexed with the competitive inhibitors methylglyoxal bis(guanylhydrazone) and 4-amidinoindan-1-

82 UV spectroscopic studies show that methylglyoxal bis(guanylhydrazone) binds as the dication

83 The competitive inhibitor methylglyoxal bis(guanylhydrazone) binds at a single sit

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

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

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

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

88 ubation with fructose, hydrogen peroxide and methylglyoxal (compounds that have been implicated in di

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

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

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

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

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

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

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

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

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

98 ored for N(epsilon)-carboxymethyl-lysine and methylglyoxal derivatives by enzyme-linked immunosorbent

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

100 of N(epsilon)-carboxymethyllysine (CML) and methylglyoxal-derivatives (MG) (L-AGE).

101 or N(epsilon)-carboxymethyl-lysine (CML) and methylglyoxal-derivatives (MG).

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

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

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

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

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

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

108 Modification by methylglyoxal destabilized Tyr-411 and increased the pK(

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

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

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

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

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

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

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

116 Methylglyoxal enhancements were three to six times highe

117 required for the degradation of the DNA upon methylglyoxal exposure.

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

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

120 Methylglyoxal forms stable adducts primarily with argini

121 Methylglyoxal forms stable adducts primarily with argini

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

123 kinetic parameters for the GLOX oxidation of methylglyoxal, glyceraldehyde, dihydroxyacetone, glycola

124 Glyoxal, methylglyoxal, glycolaldehyde, and hydroxyacetone form N

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

126 e-arginine cross-links derived from glucose, methylglyoxal, glyoxal, and 3-deoxyglucosone, i.e. gluco

127 der oxidative conditions, DL-glyceraldehyde, methylglyoxal, glyoxal, nor glycolaldehyde, are precurso

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

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

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

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

132 Glyoxyl hydroimidazolone and methylglyoxal hydroimidazolone correlated negatively wit

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

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

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

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

137 This enol then tautomerizes to methylglyoxal in solution.

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

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

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

141 Human serum albumin is modified by methylglyoxal in vivo.

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

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

144 ells deficient in GLX2 are hypersensitive to methylglyoxal-induced apoptosis.

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

146 ults suggest this event is not essential for methylglyoxal-induced death.

147 In mutants lacking KefB and KefC, methylglyoxal-induced DNA damage was reduced by incubati

148 (100 muM) showed protective effects against methylglyoxal-induced human umbilical vein endothelial c

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

150 Methylglyoxal is a cytotoxic reactive carbonyl compound

151 Methylglyoxal is a highly reactive alpha-ketoaldehyde th

152 Methylglyoxal is a highly reactive dicarbonyl degradatio

153 Methylglyoxal is a highly reactive dicarbonyl degradatio

154 Methylglyoxal is a potent glycating agent under physiolo

155 Methylglyoxal is already known to be generated by carboh

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

157 Methylglyoxal is detoxified by the Glyoxalase system, co

158 Given that methylglyoxal is frequently generated under both physiol

159 ine decomposition of the triosephosphates to methylglyoxal is now observed by UV and (1)H NMR spectro

160 Methylglyoxal is predicted to be a minor contributor.

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

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

163 dine, N(epsilon)-(1-carboxyethyl)lysine, and methylglyoxal lysine dimer.

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

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

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

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

168 Glyoxal- and methylglyoxal-methylamine aerosol particles shattered in

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

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

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

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

173 Methylglyoxal (MG) can accumulate and promote inflammati

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

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

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

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

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

179 Methylglyoxal (MG) is a key signaling molecule resulting

180 Methylglyoxal (MG) is a predominant precursor for advanc

181 Methylglyoxal (MG) is a reactive alpha-dicarbonyl that i

182 Methylglyoxal (MG) is a reactive metabolic intermediate

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

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

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

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

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

188 Methylglyoxal (MG), an alpha-dicarbonyl compound, can be

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

190 y a physiological alpha-dicarbonyl compound, methylglyoxal (MG), enhances its chaperone function.

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

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

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

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

195 Methylglyoxal (MG), which forms MG-derived AGE, is eleva

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

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

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

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

200 ction: dihydroxyacetone-P --> P(i) + ePY --> methylglyoxal (MG).

201 ing (epsilon)N-carboxymethyllysine (CML) and methylglyoxal (MG).

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

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

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

205 11 mg/kg, 0.10mg/kg, 0.09 mg/kg for glyoxal, methylglyoxal (MGo) and diacetyl, respectively.

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

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

208 er normal fibronectin (FN) or FN modified by methylglyoxal (MGO) and glyoxal (GO).

209 Methylglyoxal (MGO) and its precursor dihydroxyacetone (

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

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

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

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

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

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

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

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

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

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

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

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

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

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

224 Methylglyoxal (MGO), a dicarbonyl metabolite produced by

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

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

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

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

229 ort that the circulating glucose metabolite, methylglyoxal (MGO), enhances cisplatin-induced apoptosi

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

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

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

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

234 structural and functional changes induced by methylglyoxal modification have not been fully disclosed

235 Methylglyoxal modification of critical arginine residues

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 Methylglyoxal modifies arginine within the human lens, a

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

245 -3.1, -10.3, -7.91, 6.11, and 1.6 kJ/mol for methylglyoxal monohydrate with uncertainties of 8 kJ/mol

246 The effect of the toxic metabolite methylglyoxal on the DNA of Escherichia coli cells has b

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

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

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

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

251 Pharmacological scavenging of methylglyoxal prevented anoikis and maintained angiogene

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

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

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

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

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

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

258 Methylglyoxal reacted with human serum albumin under phy

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

260 HIF1alpha modification by methylglyoxal reduced heterodimer formation and HIF1alph

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

262 Exposure of E. coli cells to methylglyoxal reduces the transformability of plasmid DN

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

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

265 t evidence that exposure of E. coli cells to methylglyoxal results in DNA degradation, our results su

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

267 Methylglyoxal synthase (MGS) and triosephosphate isomera

268 e analogue 2-phosphoglycolate (2PG) bound to methylglyoxal synthase (MGS) is presented at a resolutio

269 ave been proposed to explain the activity of methylglyoxal synthase (MGS), a homohexameric allosteric

270 ities of triosephosphate isomerase (TIM) and methylglyoxal synthase (MGS).

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

272 spectroscopy as the immediate product of the methylglyoxal synthetase (MGS) reaction: dihydroxyaceton

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

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

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

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

277 argpyrimidine, a modification of arginine by methylglyoxal, to establish how argpyrimidine content re

278 a catabolite repression, possibly to prevent methylglyoxal toxicity.

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

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

281 Methylglyoxal treatment effectively increased nonenzymat

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

283 an serum albumin was modified minimally with methylglyoxal, tryptic peptide mapping indicated a hotsp

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

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

286 With this coupled reaction, for each mol of methylglyoxal, veratryl alcohol (a lignin peroxidase sub

287 Modification of Arg-410 by methylglyoxal was found in albumin glycated in vivo.

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

292 Glyoxal and methylglyoxal were measured using broadband cavity enhan

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

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

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

296 s enediolic intermediate to form the enol of methylglyoxal, while TIM catalyzes proton donation to C2

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

298 es, the best is the extracellular metabolite methylglyoxal with a Km of 0.64 mM an apparent rate of c

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

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