Advanced glycation end products (AGEs), also known as glycotoxins, are a diverse group of highly oxidant compounds with pathogenic significance in diabetes and in several other chronic diseases (1–6). AGEs are created through a nonenzymatic reaction between reducing sugars and free amino groups of proteins, lipids, or nucleic acids. This reaction is also known as the Maillard or browning reaction (7). The formation of AGEs is a part of normal metabolism, but if excessively high levels of AGEs are reached in tissues and the circulation they can become pathogenic (2). The pathologic effects of AGEs are related to their ability to promote oxidative stress and inflammation by binding with cell surface receptors or cross-linking with body proteins, altering their structure and function (8–10). Among the better-studied AGEs are the stable and relatively inert Nε-carboxymethyllysine (CML) and the highly reactive derivatives of methyl-glyoxal (MG). Both these AGEs can be derived from protein and lipid glycoxidation (11,12).