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.

Formaldehyde and Acetaldehyde Increase Aqueous-Phase Production of Imidazoles in Methylglyoxal/Amine Mixtures: Quantifying a Secondary Organic Aerosol Formation Mechanism

Abstract: Formaldehyde and acetaldehyde are commonly found in cloud droplets because of reversible partitioning and hydration reactions. An SOA formation pathway was recently identified in which these common aldehydes are irreversibly incorporated into imidazole derivatives formed by reaction with dicarbonyl species and ammonium salts or amine species. Here we use ultraviolet–visible and nuclear magnetic resonance kinetic measurements to determine the influence of formaldehyde and acetaldehyde on aqueous methylglyoxal chemistry. The presence of formaldehyde increases imidazole product formation rates by factors of 2 and ≥5 in reactions with ammonium sulfate and amines, respectively, and increases imidazole product yields in methylglyoxal + amine reactions by more than an order of magnitude. Acetaldehyde is less likely to be incorporated into imidazole products and increases formation rates and yields only in reactions involving amines. We estimate that aqueous formation of imidazoles could generate as much as 1.05 ...

Methylglyoxal activates the human transient receptor potential ankyrin 1 channel

Abstract: Methylglyoxal (MG) is an endogenous carbonyl compound that is produced in large quantity under hyperglycemic conditions, which are believed to contribute to the development of diabetic neuropathy. However, the mechanism by which this occurs and the molecular targets of MG are unclear. In the present study, we investigated the effect of MG on transient receptor potential ankyrin 1 (TRPA1) activation in human TRPA1-expressing HEK293 cells. MG activated TRPA1-expressing HEK293 cells, but failed to activate human capsaicin-sensitive transient receptor potential vanilloid 1 (TRPV1)-expressing HEK293 cells or mock-transfected HEK293 cells. MG also induced calcium (Ca(2+)) influx in a concentration-dependent manner, and the concentration-response curve indicates that the effect of MG has an EC(50) of 343.1 ± 17.3 µM. Interestingly, the time course in the intracellular Ca(2+) concentration ([Ca(2+)](i)) in human TRPA1-expressing HEK293 showed considerable differences in response to MG and cinnamaldehyde. Furthermore, we examined four endogenous carbonyl compounds, including MG, glyceraldehyde, glycolaldehyde, and glyoxal; only MG notably activated TRPA1-expressing HEK293 cells. These results may provide insight into the TRPA1-mediated effects of MG on diabetic neuropathy.

Formation of methylglyoxal by bacteria isolated from human faeces.

Abstract: Bacteria present in the human gut may produce methylglyoxal—a cytotoxic substance in mammals. This was investigated by studying the activity of methylglyoxal synthase, which produces methylglyoxal from dihydroxyacetone phosphate, and methylglyoxal concentration in growth medium of various bacteria isolated from human faeces. Facultative and strictly anaerobic bacteria isolated from faeces were able to produce methylglyoxal in both defined and complex media. Proteus spp. produced large amounts of methylglyoxal and had the greatest methylglyoxal synthase activity. Supplementing defined medium for facultative anaerobes with glucose 1% w/v did not significantly alter enzyme activity or methylglyoxal production. Inclusion of short chain fatty acids or bile acids in the medium reduced methylglyoxal synthase activity and methylglyoxal production by Proteus spp. None of the organisms examined had amine oxidase activity which could have contributed to methylglyoxal production from aminoacetone.

Edaravone Protected Human Brain Microvascular Endothelial Cells from Methylglyoxal-Induced Injury by Inhibiting AGEs/RAGE/Oxidative Stress

Abstract: Subjects with diabetes experience an increased risk of cerebrovascular disease and stroke compared with nondiabetic age-matched individuals. Increased formation of reactive physiological dicarbonyl compound methylglyoxal (MGO) seems to be implicated in the development of diabetic vascular complication due to its protein glycation and oxidative stress effect. Edaravone, a novel radical scavenger, has been reported to display the advantageous effects on ischemic stroke both in animals and clinical trials; however, little is known about whether edaravone has protective effects on diabetic cerebrovascular injury. Using cultured human brain microvascular endothelial cells (HBMEC), protective effects of edaravone on MGO and MGO enhancing oxygen-glucose deprivation (OGD) induced injury were investigated. Cell injury was measured by 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) formation, cell account, lactate dehydrogenase (LDH) release and Rhodamine 123 staining. Advanced glycation end-products (AGEs) formation and receptor for advanced glycation end-products (RAGE) expression were measured by western blotting. Cellular oxidative stress was measured by reactive oxygen species (ROS) release. Treatment of MGO for 24 h significantly induced HBMEC injury, which was inhibited by pretreatment of edaravone from 10–100 µmol/l. What’s more, treatment of MGO enhanced AGEs accumulation, RAGE expression and ROS release in the cultured HBMEC, which were inhibited by 100 µmol/l edaravone. Finally, treatment of MGO for 24 h and then followed by 3 h OGD insult significantly enhanced cell injury when compared with OGD insult only, which was also protected by 100 µmol/l edaravone. Thus, edaravone protected HBMEC from MGO and MGO enhancing OGD-induced injury by inhibiting AGEs/RAGE/oxidative stress.