General Description
Clear yellow slightly viscous liquid with a pungent odor. Yellowish-green vapors. Faintly acidic to litmus.
Reactivity Profile
METHYLGLYOXAL(78-98-8) polymerizes readily. METHYLGLYOXAL(78-98-8) is hygroscopic. This chemical is incompatible with strong oxidizing agents and bases. METHYLGLYOXAL(78-98-8) is an aldehyde. Aldehydes are frequently involved in self-condensation or polymerization reactions. These reactions are exothermic; they are often catalyzed by acid. Aldehydes are readily oxidized to give carboxylic acids. Flammable and/or toxic gases are generated by the combination of aldehydes with azo, diazo compounds, dithiocarbamates, nitrides, and strong reducing agents. Aldehydes can react with air to give first peroxo acids, and ultimately carboxylic acids. These autoxidation reactions are activated by light, catalyzed by salts of transition metals, and are autocatalytic (catalyzed by the products of the reaction). The addition of stabilizers (antioxidants) to shipments of aldehydes retards autoxidation.
Air & Water Reactions
Water soluble.
Fire Hazard
Literature sources indicate that this chemical is nonflammable.
Occurrence
Reported found in the dry distillate of Manilla copal. Also reported found in apple juice, orange juice, celery root, rutabaga, tomato, wheaten bread, white bread, roasted and raw turkey, cognac, roasted barley, beer, cocoa, coffee and roasted pecans.
Definition
ChEBI: A 2-oxo aldehyde derived from propanal.
Preparation
By distilling a dilute solution of dihydroxyacetone from calcium carbonate; by oxidation of acetone with selenium dioxide; by heating dihydroxy acetone with phosphorus pentoxide; by warming isonitroso acetone with diluted H2SO4.
Taste threshold values
Taste characteristics at 0.1%: sweet, caramellic with a dairy creamy nuance
Flammability and Explosibility
Nonflammable
Environmental Fate
Methylglyoxal production and use as a chemical intermediate
and flavoring agent may result in its release to the environment
through various waste streams. If released into water, MG is not
expected to adsorb to suspended solids and sediment based on
the estimated Koc. Volatilization from water surfaces is not
expected to be an important fate process based upon the estimated
Henry’s Law constant. If released to soil, MG is expected
to have very high mobility based upon an estimated Koc of 1
determined from the structure estimation method. Hydrolysis
is not expected to be an important environmental fate process
since this compound lacks functional groups that hydrolyze
under environmental conditions.
Methylglyoxal serves as a substrate for the isozymes E1, E2,
and E3 of human aldehyde dehydrogenase. Oxidation of MG
by these isozymes generated pyruvate. Methylglyoxal is
a partially oxidized compound obtained from the tropospheric
oxidation of numerous hydrocarbons, of both biogenic and
anthropogenic origin. If released to the air, an estimated vapor
pressure of 27 mm Hg at 25 ℃ indicates MG will exist solely as
a vapor in the atmosphere. Vapor-phase MG will be degraded
in the atmosphere by reaction with photochemically produced
hydroxyl radicals; the half-life for this reaction in air is estimated
to be 30 h. Methylglyoxal absorbs light at wavelengths
>290 nm and, therefore, is susceptible to direct photolysis by
sunlight; half-lives of 2–4 h have been reported.
Purification Methods
Commercial 30% (w/v) aqueous solution is diluted to about 10% and distilled twice, taking the fraction boiling below 50o/20mm Hg. (This treatment does not remove lactic acid). [Beilstein 1 IV 3631.]
Toxicity evaluation
Endogenously formed MG modifies arginine and lysine residues
in proteins that form AGEs, which have been associated
with diabetic complications and some neurodegenerative
diseases. In different cell lines, MG treatment has been shown to induce apoptosis as measured by nuclear fragmentation and
apoptotic body formation, indicating an increase in apoptosis.
At the mitochondrial level, exogenous MG is highly toxic as it
promotes proliferation, swelling, and membrane derangement.
In both in vitro and in vivo studies, MG treatment has been
shown to significantly reduce antioxidant enzymes and elevate
reactive oxygen species that lead to oxidative stress-mediated
cell death. Genotoxicity has been observed in both in vivo
and in vitro studies, as MG is capable of binding to cellular
macromolecules and forming DNA adducts.
