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Methylglyoxal

About: Methylglyoxal is a research topic. Over the lifetime, 2844 publications have been published within this topic receiving 102037 citations. The topic is also known as: acetylformaldehyde & pyruvaldehyde.


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Journal ArticleDOI
TL;DR: S-p-Nitrobenzoxycarbonylglutathione was a potent competitive inhibitor of glyoxalase II with a Ki value of 1.20 +/- 0.21 microM, and the hemithioacetal formed non-enzymically from the reaction of methylglyoxal with reduced glutathionewas a weak competitive inhibitor with a ki value of 834 +/- 98 microM.
Abstract: Glyoxalase II was purified from human red blood cells. The purification factor was 83 300 and the yield was 24% or 1.7 μg/ml red blood cells. The purified protein was a monomer with a molecular mass of 29 200 Da and an isoelectric point of 8.3. The rate of hydrolysis of S-D-lactoylglutathione to reduced glutathione and D-lactate, catalysed by glyoxalase II, followed Michaelis-Menten kinetics where the Km and kcat values where 146 ± 9 μM and 727 ± 16 s−1, respectively in 50 mM Tris/HCl, pH 7.4 at 37 °C. Other S-2-hydroxyacylglutathione derivatives were also acceptable substrates. S-p-Nitrobenzoxycarbonylglutathione was a potent competitive inhibitor of glyoxalase II with a Ki value of 1.20 ± 0.21 μM, and the hemithioacetal formed non-enzymically from the reaction of methylglyoxal with reduced glutathione was a weak competitive inhibitor with a Ki value of 834 ± 98 μM.

55 citations

Journal ArticleDOI
TL;DR: Findings suggest that monascin acts as an anti-diabetic and anti-oxidative stress agent to a greater degree than rosiglitazone and thus may have therapeutic potential for the prevention of diabetes.

55 citations

Journal ArticleDOI
TL;DR: It is demonstrated that blunting glycative stress prevents the long‐term impact of endothelial dysfunction on vascular aging, and systemically overexpressing glyoxalase I (GLO1) reduced age‐related endothelial glycative and oxidative stress, altered phohphorylation of eNOS, and attenuated endotheric dysfunction.
Abstract: Endothelial dysfunction is a major contributor to cardiovascular disease (CVD), particularly in elderly people Studies have demonstrated the role of glycation in endothelial dysfunction in nonphysiological models, but the physiological role of glycation in age-related endothelial dysfunction has been poorly addressed Here, to investigate how vascular glycation affects age-related endothelial function, we employed rats systemically overexpressing glyoxalase I (GLO1), which detoxifies methylglyoxal (MG), a representative precursor of glycation Four groups of rats were examined, namely young (13 weeks old), mid-age (53 weeks old) wild-type, and GLO1 transgenic (WT/GLO1 Tg) rats Age-related acceleration in glycation was attenuated in GLO1 Tg rats, together with lower aortic carboxymethyllysine (CML) and urinary 8-hydroxydeoxyguanosine (8-OHdG) levels Age-related impairment of endothelium-dependent vasorelaxation was attenuated in GLO1 Tg rats, whereas endothelium-independent vasorelaxation was not different between WT and GLO1 Tg rats Nitric oxide (NO) production was decreased in mid-age WT rats, but not in mid-age GLO1 Tg rats Age-related inactivation of endothelial NO synthase (eNOS) due to phosphorylation of eNOS on Thr495 and dephosphorylation on Ser1177 was ameliorated in GLO1 Tg rats In vitro, MG increased phosphorylation of eNOS (Thr495) in primary human aortic endothelial cells (HAECs), and overexpression of GLO1 decreased glycative stress and phosphorylation of eNOS (Thr495) Together, GLO1 reduced age-related endothelial glycative and oxidative stress, altered phohphorylation of eNOS, and attenuated endothelial dysfunction As a molecular mechanism, GLO1 lessened inhibitory phosphorylation of eNOS (Thr495) by reducing glycative stress Our study demonstrates that blunting glycative stress prevents the long-term impact of endothelial dysfunction on vascular aging

55 citations

Journal ArticleDOI
TL;DR: The results suggest that tenuigenin displays antiapoptotic and antioxidative activity in hippocampal neurons due to scavenging of intracellular reactive oxygen species, regulating Bcl-2 family and suppressing caspase-3 activity induced by methylglyoxal, which might explain at least in part the beneficial effects of tenUigenin against degenerative disorders involving diabetic cognitive impairment.

55 citations

Journal ArticleDOI
TL;DR: In this article, the anticancer effect of methylglyoxal plus ascorbic acid was further augmented with the addition of creatine and there was no visible sign of tumor.
Abstract: The creatine/creatine kinase (CK) system plays a key role in cellular energy buffering and transport. In vertebrates, CK has four isoforms expressed in a tissue-specific manner. In the process of creatine biosynthesis several other important metabolites are formed. The anticancer effect of creatine had been reported in the past, and recent literature has reported low creatine content in several types of malignant cells. Furthermore, creatine can protect cardiac mitochondria from the deleterious effects of some anticancer compounds. Previous work from our laboratory showed progressive decrease of phosphocreatine, creatine and CK upon transformation of skeletal muscle into sarcoma. It was convincingly demonstrated that prominent expression of creatine-synthesizing enzymes l-arginine: glycine amidinotransferase and N-guanidinoacetate methyltransferase occurs in sarcoma, Ehrlich ascites carcinoma and sarcoma 180 cells; whereas, both these enzymes are virtually undetectable in skeletal muscle. Creatine transporter also remained unaltered in malignant cells. The anticancer effect of methylglyoxal had been known for a long time. The present work shows that this anticancer effect of methylglyoxal is significantly augmented in presence of creatine. On creatine supplementation the effect of methylglyoxal plus ascorbic acid was further augmented and there was no visible sign of tumor. Moreover, creatine and CK, which were very low in sarcoma tissue, were significantly elevated with the concomitant regression of tumor.

55 citations


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Performance
Metrics
No. of papers in the topic in previous years
YearPapers
2023112
2022306
2021173
2020156
2019153
2018128