Accelerated formation of N epsilon-(carboxymethyl) lysine, an advanced glycation end product, by glyoxal and 3-deoxyglucosone in cultured rat sensory neurons.

The formation of advanced glycation end products (AGEs) is associated with pathophysiological changes with aging and disease processes. In the neurodegeneration in Alzheimer's disease and other neurodegenerative diseases. AGEs are speculated to play a role in their pathogenesis. We provide the first evidence for the induction of AGEs in cultured neuronal cells. Glyoxal and 3-deoxyglucosone (3-DG), AGE precursors, induced N epsilon-(carboxymethyl) lysine (CML), a well characterized and major AGE structure, in cultured rat sensory neurons in a time- and dose-dependent manner. CML formation was prevented by addition of aminoguanidine, an inhibitor of AGE formation. This culture system provides a useful model to analyze the role of the glycoxidation reaction in neuronal aging and neurodegenerative disorder.