J Korean Ophthalmol Soc > Volume 50(10); 2009 > Article
Journal of the Korean Ophthalmological Society 2009;50(10):1569-1575.
DOI: https://doi.org/10.3341/jkos.2009.50.10.1569    Published online October 15, 2009.
Effect of Methylglyoxal on the Oxidative Stress in Trabecular Meshwork Cells.
Seung Hee Lee, Sin Hoo Kim, Jae Woo Kim
Department of Ophthalmology, Catholic University of Daegu College of Medicine, Daegu, Korea. jwkim@cu.ac.kr
메칠글라이옥살이 섬유주세포의 산화스트레스에 미치는 영향
이승희ㆍ김신후ㆍ김재우
Department of Ophthalmology, Catholic University of Daegu College of Medicine, Daegu, Korea
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 micrometer 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 micrometer, but induced apoptosis of HTMC at concentrations over 100 micrometer. 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.
Key Words: Advanced glycation end products;Methylglyoxal;Oxidative stress;Trabecular meshwork cells


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