Abstract
Purpose: 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). Methods: Primarily cultured HTMC were exposed to at concentrations of 0, 30, 100, and 300 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. Results: MG did not affect cellular survival at concentrations under 100 , but induced apoptosis of HTMC at concentrations over 100 . MG decreased NO production, accompanied with increased superoxide production. In addition, MG increased ROS, which were abolished by N-acetylcysteine. Conclusions: MG induced oxidative stress by decreasing NO production, accompanied by increasing superoxide and ROS productions in HTMC. AGE could induce trabecular meshwork dysfunction.
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