To investigate the effect of methylglyoxal (MG), intermediate metabolite of advanced glycation end products(AGE), on the induction of oxidative stress in human trabecular meshwork cells (HTMC).

Primarily cultured HTMC were exposed to at concentrations of 0, 30, 100, and 300 µM of MG for 18 hours, with or without co-exposure to N-acetyl-cysteine. Cellular survival and apoptosis were assessed by MTT assay and flow cytometry using annexin-PI double staining. Production of nitric oxide (NO), superoxide, and reactive oxygen species (ROS) was assessed by Griess assay, cytochrome c assay, and dichlorofluorescein diacetate assay, respectively.

MG did not affect cellular survival at concentrations under 100 µM, but induced apoptosis of HTMC at concentrations over 100 µM. MG decreased NO production, accompanied with increased superoxide production. In addition, MG increased ROS, which were abolished by N-acetylcysteine.

MG induced oxidative stress by decreasing NO production, accompanied by increasing superoxide and ROS productions in HTMC. AGE could induce trabecular meshwork dysfunction.