Effect of Methylglyoxal on the Oxidative Stress in Trabecular Meshwork Cells.
10.3341/jkos.2009.50.10.1569
- Author:
Seung Hee LEE
1
;
Sin Hoo KIM
;
Jae Woo KIM
Author Information
1. Department of Ophthalmology, Catholic University of Daegu College of Medicine, Daegu, Korea. jwkim@cu.ac.kr
- Publication Type:Original Article
- Keywords:
Advanced glycation end products;
Methylglyoxal;
Oxidative stress;
Trabecular meshwork cells
- MeSH:
Acetylcysteine;
Apoptosis;
Cytochromes c;
Flow Cytometry;
Glycosylation End Products, Advanced;
Humans;
Nitric Oxide;
Oxidative Stress;
Pyruvaldehyde;
Reactive Oxygen Species;
Superoxides;
Trabecular Meshwork
- From:Journal of the Korean Ophthalmological Society
2009;50(10):1569-1575
- CountryRepublic of Korea
- Language:Korean
-
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.
