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Methylglyoxal

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Methylglyoxal
Skeletal formula
Skeletal formula
Ball-and-stick model of methylglyoxal
Names
IUPAC name
2-Oxopropanal
Other names
Pyruvaldehyde
Identifiers
3D model (JSmol)
ChEBI
ChEMBL
ChemSpider
DrugBank
ECHA InfoCard 100.001.059 Edit this at Wikidata
KEGG
MeSH Methylglyoxal
UNII
  • InChI=1S/C3H4O2/c1-3(5)2-4/h2H,1H3 checkY
    Key: AIJULSRZWUXGPQ-UHFFFAOYSA-N checkY
  • InChI=1/C3H4O2/c1-3(5)2-4/h2H,1H3
    Key: AIJULSRZWUXGPQ-UHFFFAOYAZ
  • CC(=O)C=O
Properties
C3H4O2
Molar mass 72.063 g·mol−1
Appearance Yellow liquid
Density 1.046 g/cm3
Boiling point 72 °C (162 °F; 345 K)
Related compounds
glyoxal
propionaldehyde
propanedial
acetone
diacetyl
acetylacetone
Related compounds
 glyoxylic acid
pyruvic acid
acetoacetic acid
Except where otherwise noted, data are given for materials in their standard state (at 25 °C [77 °F], 100 kPa).
☒N verify (what is checkY☒N ?)

Methylglyoxal, also called pyruvaldehyde or 2-oxopropanal, is the organic compound with the formula CH3C(O)CHO. Gaseous methylglyoxal has two carbonyl groups, an aldehyde and a ketone but in the presence of water, it exists as hydrates and oligomers.[1] It is a reduced derivative of pyruvic acid.

Industrial production and use

Methylglyoxal is produced industrially by degradation of saccharides using overexpressed methylglyoxal synthase.[2]

Biochemistry

In organisms, methylglyoxal is formed as a side-product of several metabolic pathways.[3] It may form from 3-aminoacetone, 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,[4] and then further metabolized into D-lactate by glyoxalase II.[5]

The proximate and ultimate causes for biological methylglyoxal production remain unknown, but it may be involved in the formation of advanced glycation endproducts (AGEs).[6] 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.[7]

Recently, one mechanism of activity in humans of methylglyoxal has been identified.[8][9] Methylglyoxal binds directly to the nerve endings and by that increases the chronic extremity soreness in diabetic neuropathy.

Other glycation agents include the reducing sugars:

Natural occurrence

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 through glycation causes a fourfold increase of atherogenesis in diabetics.[10]

Although methylglyoxal has been shown to increase carboxymethyllysine levels,[11] methylglyoxal has been suggested to be a better marker for investigating the association between AGEs with adverse health outcomes.

Methylglyoxal is an active component of manuka honey and is the dominant antibacterial constituent.[12] However, after neutralization of this compound, manuka honey retains bactericidal activity.[13] implying that there are other contributors to the antimicrobial and antibacterial activities.[14]

References

  1. ^ Loeffler Kirsten W.; Koehler Charles A.; Paul Nichole M.; De Haan David O. (2006). "Oligomer Formation in Evaporating Aqueous Glyoxal and Methyl Glyoxal Solutions". Environmental Science & Technology. 40: 6318–6323. doi:10.1021/es060810w.
  2. ^ Frieder W. Lichtenthaler "Carbohydrates as Organic Raw Materials" in Ullmann's Encyclopedia of Industrial Chemistry 2010, Wiley-VCH, Weinheim. doi:10.1002/14356007.n05_n07
  3. ^ Inoue Y, Kimura A (1995). "Methylglyoxal and regulation of its metabolism in microorganisms". Adv. Microb. Physiol. Advances in Microbial Physiology. 37: 177–227. doi:10.1016/S0065-2911(08)60146-0. ISBN 978-0-12-027737-7. PMID 8540421.
  4. ^ Thornalley PJ (2003). "Glyoxalase I—structure, function and a critical role in the enzymatic defence against glycation". Biochem. Soc. Trans. 31 (Pt 6): 1343–8. doi:10.1042/BST0311343. PMID 14641060.
  5. ^ Vander Jagt DL (1993). "Glyoxalase II: molecular characteristics, kinetics and mechanism". Biochem. Soc. Trans. 21 (2): 522–7. PMID 8359524.
  6. ^ Shinohara M; Thornalley, PJ; Giardino, I; Beisswenger, P; Thorpe, SR; Onorato, J; Brownlee, M (1998). "Overexpression of glyoxalase-I in bovine endothelial cells inhibits intracellular advanced glycation endproduct formation and prevents hyperglycemia-induced increases in macromolecular endocytosis". J Clin Invest. 101 (5): 1142–7. doi:10.1172/JCI119885. PMC 508666. PMID 9486985.
  7. ^ Bair WB 3rd, Cabello CM, Uchida K, Bause AS, Wondrak GT (April 2010). "GLO1 overexpression in human malignant melanoma". Melanoma Res. 20 (2): 85–96. doi:10.1097/CMR.0b013e3283364903. PMC 2891514. PMID 20093988.{{cite journal}}: CS1 maint: multiple names: authors list (link) CS1 maint: numeric names: authors list (link)
  8. ^ Spektrum: Diabetische Neuropathie: Methylglyoxal verstärkt den Schmerz DAZ.online. Deutsche-apotheker-zeitung.de (2012-05-21). Retrieved on 2012-06-11.
  9. ^ Bierhaus, Angelika; Fleming, Thomas; Stoyanov, Stoyan; Leffler, Andreas; Babes, Alexandru; Neacsu, Cristian; Sauer, Susanne K; Eberhardt, Mirjam; et al. (2012). "Methylglyoxal modification of Nav1.8 facilitates nociceptive neuron firing and causes hyperalgesia in diabetic neuropathy". Nature Medicine. 18 (6): 926–33. doi:10.1038/nm.2750. PMID 22581285.
  10. ^ Rabbani N; Godfrey, L; Xue, M; Shaheen, F; Geoffrion, M; Milne, R; Thornalley, PJ (May 26, 2011). "Glycation of LDL by methylglyoxal increases arterial atherogenicity. A possible contributor to increased risk of cardiovascular disease in diabetes". Diabetes. 60 (7): 1973–80. doi:10.2337/db11-0085. PMC 3121424. PMID 21617182.
  11. ^ Cai, W., Uribarri, J., Zhu, L., Chen, X., Swamy, S., Zhao, Z., Grosjean, F., Simonaro, C., Kuchel, G. A., Schnaider-Beeri, M., Woodward, M., Striker, G. E., and Vlassara, H. (2014) Oral glycotoxins are a modifiable cause of dementia and the metabolic syndrome in mice and humans. PNAS 111.
  12. ^ Mavric, E (April 2008). "Identification and quantification of methylglyoxal as the dominant antibacterial constituent of Manuka (Leptospermum scoparium) honeys from New Zealand". Molecular nutrition & food research. 52 (4): 483–9. doi:10.1002/mnfr.200700282. PMID 18210383.
  13. ^ Kwakman PHS; te Velde AA; de Boer L; Vandenbroucke-Grauls CMJE; Zaat SAJ (2011). "Two major medicinal honeys have different mechanisms of bactericidal activity". PLoS ONE. 6 (3): e17709. doi:10.1371/journal.pone.0017709. PMC 3048876. PMID 21394213.{{cite journal}}: CS1 maint: unflagged free DOI (link)
  14. ^ Molan, P. (2008). "An explanation of why the MGO level in manuka honey does not show the antibacterial activity". New Zealand BeeKeeper. 16 (4): 11–13.
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