High glucose and advanced glycation end products (AGEs) are believed to play a role as principal factors that cause injury to the endothelium as an early event in vascular inflammation. The toxic effects of AGEs on bovine retinal capillary endothelial cells (BREC) were studied. We examined the expression of E-selectin on BREC and the adherence to BREC of 51Cr-labeled neutrophils under the conditions of D-glucose (5.5, 15, and 30mmol/L) and bovine serum albumin-derived glycation end products (AGE-BSA, 50, 100, and 500 g/mL) after 24h incubation. We also measured neutrophil-mediated endothelial cell cytotoxicity using a 51Cr-release assay and release of activating markers (lactoferrin and myeloperoxidase) from neutrophils under same conditions. The expression of E-selectin was increased incubated with high glucose (30 mmol/L) or AGE-BSA (500 g/mL) compared to each control preparation(5.5 mmol/L glucose or untreated bovine serum albumin). Similarly, adherence of neutrophils to endothelium was significantly increased by high glucose or AGE-BSA. 51Cr-release from endothelial cells by neutrophils stimulated with high glucose or AGE-BSA was greater than control. Release of activating markers from neutrophils incubated with high glucose or AGE-BSA was greater than control. These results suggest that high glucose and AGE-BSA cause endothelial cell injury through neutrophil activation and these interactions may play an important role in the pathogenesis of inflammation of vascular endothelial cells.