Methylglyoxal induces cellular damage by increasing argpyrimidine accumulation and oxidative DNA damage in human lens epithelial cells

作者：Kim Junghyun; Kim Nan Hee; Sohn Eunjin; Kim Chan Sik; Kim Jin Sook

来源：Biochemical and Biophysical Research Communications, 2010, 391(1): 346-351.

DOI：10.1016/j.bbrc.2009.11.061

• Apoptosis
• Argpyrimidine
• Lens epithelial cell
• Methylglyoxal
• Oxidative stress

Methylglyoxal (MGO) is a cytotoxic metabolite and modifies tissue proteins through the Maillard reaction, resulting in advanced glycation end products (AGEs), which can alter protein structure and functions. Several MGO-derived AGEs have been described, including argpyrimidine, a fluorescent product of the MGO reaction with arginine residues. Herein, we evaluated the cytotoxic: role of MGO in human lens epithelial cell line (HLE-B3). HLE-B3 cells were exposed to 400 mu M MGO in the present or absence of pyridoxamine for 24 h. We then examined the formation of argpyrimidine, apoptosis and oxidative stress in HLE-B3 cells. In MGO-treated HLE-B3 cells, the accumulation of argpyrimidine was markedly increased, and caspase-3 and 8-hydroxydeoxyguanosine (8-OHdG) were highly expressed, which paralleled apoptotic cell death However, pyridoxamine (AGEs inhibitor) prevented the argpyrimidine formation and apoptosis of MGO-treated HLE-B3 cells.

• 出版日期2010-1-1