Methylglyoxal | |
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2-oxopropanal |
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Identifiers | |
CAS number | 78-98-8 |
PubChem | 880 |
ChemSpider | 857 |
UNII | 722KLD7415 |
DrugBank | DB03587 |
KEGG | C00546 |
MeSH | Methylglyoxal |
ChEBI | CHEBI:17158 |
ChEMBL | CHEMBL170721 |
Jmol-3D images | Image 1 |
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Properties | |
Molecular formula | C3H4O2 |
Molar mass | 72.0627 |
Related compounds | |
Related ketones, aldehydes | glyoxal propionaldehyde propanedial acetone diacetyl acetylacetone |
Related compounds | glyoxylic acid pyruvic acid acetoacetic acid |
(verify) (what is: / ?) Except where noted otherwise, data are given for materials in their standard state (at 25 °C, 100 kPa) |
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Infobox references |
Methylglyoxal, also called pyruvaldehyde or 2-oxopropanal (CH3-CO-CH=O or C3H4O2) is the aldehyde form of pyruvic acid. It has two carbonyl groups, so it is a dicarbonyl compound. Methylglyoxal is both an aldehyde and a ketone.
In organisms, methylglyoxal is formed as a side-product of several metabolic pathways.[1] It may form from 3-amino acetone, which is an intermediate of threonine catabolism, as well as through lipid peroxidation. However, the most important source is glycolysis. Here, methylglyoxal arises from nonenzymatic phosphate elimination from glyceraldehyde phosphate and dihydroxyacetone phosphate, two intermediates of glycolysis. Since methylglyoxal is highly cytotoxic, the body developed several detoxification mechanisms. One of these is the glyoxalase system. Methylglyoxal reacts with glutathione to form a hemithioacetal. This is converted into S-D-lactoyl-glutathione by glyoxalase I,[2] and then further metabolised into D-lactate by glyoxalase II.[3]
Why methylglyoxal is produced remains unknown, but several articles indicate it is involved in the formation of advanced glycation endproducts (AGEs). In fact, methylglyoxal is proven to be the most important glycation agent (forming AGEs).[4] In this process, methylglyoxal reacts with free amino groups of lysine and arginine and with thiol groups of cysteine, forming AGEs. Recent research has identified heat shock protein 27 (Hsp27) as a specific target of posttranslational modification by methylglyoxal in human metastatic melanoma cells.[5] Other glycation agents include the reducing sugars:
Due to increased blood glucose levels, methylglyoxal has higher concentrations in diabetics, and has been linked to arterial atherogenesis. Damage by methylglyoxal to low-density lipoprotein though glycation causes a fourfold increase of atherogenesis in diabetics.[6]