Journal List > J Korean Ophthalmol Soc > v.50(10) > 1008399

Lee, Kim, and Kim: Effect of Methylglyoxal on the Oxidative Stress in Trabecular Meshwork Cells



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.


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Figure 1.
Effect of methylglyoxal (MG) on the survival of trabecular meshwork cells. MG and co-exposure of 50 μM N-acetyl-cysteine (NAC) did not affect on the cellular survival significantly except at 300 μM MG. (* p<0.05)
Figure 2.
Effect of methylglyoxal on the induction of apoptosis in cultured trabecular meshwork cells. Methylglyoxal induced apoptosis from 100 μM. (* p<0.05)
Figure 3.
Effect of methylglyoxal (MG) on the generation of nitric oxide in cultured trabecular meshwork cells. MG decreased nitric oxide production from 30 μM. (* p<0.05)
Figure 4.
Effect of methylglyoxal on the generation of superoxide. Methylglyoxal increased superoxide production from 30 μM. (* p<0.05)
Figure 5.
Effect of methylglyoxal (MG) on the generation of reactive oxygen species. MG increased reactive oxygen species, which were abolished by co-exposed N-acetyl cysteine (NAC). (*,** p<0.05)
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