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Metabolism and the chemical instability of triose phosphates are sources of cellular cytotoxic α-ketoaldehydes such as methylglyoxal (MG; pyruvaldehyde; 2-oxopropanal).1–4  Owing to its chemical structure, MG and other α-ketoaldehydes are predictably highly electrophilic and can covalently modify DNA, RNA, and proteins and result in the formation of advanced glycation end-products (AGE) in cells.5–7  In Escherichia coli, the enzyme MG synthase can convert dihydroxyacetone phosphate (DHAP) into MG.8–10  It has been proposed that this enzyme in concert with the glyoxalase enzymes, elaborated later in this chapter, produces d-lactate, which upon conversion into pyruvate by the bacterial enzyme d-lactate dehydrogenase, serves as a “glycolytic bypass” that is important under inorganic phosphate limiting growth conditions.10  Other sources of MG include threonine catabolism and biological oxidation of acetone.11,12 

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