Background: The general increase in reactive oxygen species generated from glucose-derived advanced glycation endproducts (AGEs) is among the key mechanisms implicated in tissue injury due to diabetes. AGE-rich foods could exacerbate diabetic injury, at least by raising the endogenous AGE. Materials and Methods: Herein, we tested whether, prior to ingestion, diet-derived AGEs contain species with cell activating (TNF␣), chemical (cross-linking) or cell oxidative properties, similar to native AGEs. Glutathione (GSH) and GSH peroxidase (GPx) were assessed after exposure of human umbilical vein endothelial cell (HUVECs) to affinity-purified food-AGE extracts, each exposed to 250ЊC, for 10 min, along with synthetic AGEs. Results: Animal product-derived AGE, like synthetic methylglyoxal-bovine serum albumin (MG-BSA