Methylglyoxal augments intracellular oxidative stress in human aortic endothelial cells.

Journal Article (Journal Article)

Methylglyoxal (MGO) is a non-enzymatic metabolite in the glycolytic pathway and its concentration in blood and tissues is elevated in diabetes and renal failure. MGO induces tissue injuries via ROS; however, the mechanism remains to be clarified. The present study examined the harmful actions of MGO. Human aortic endothelial cells were assessed under real-time fluorescent microscopy with continuous superfusion. Increases in intracellular ROS were measured with fluorescent indicator, 5-(and-6)-chloromethyl-2',7'-dichlorodihydrofluorescein diacetate acetyl ester (DCFH-DA). The addition of MGO rapidly increased the ROS in a dose-dependent manner. The increment of DCF was entirely abolished by pre-treatment with superoxide anion scavenger and membrane-permeable catalase, indicating that MGO induces superoxide production. The increment was completely inhibited by 2-thenoyltrifluoroacetone or carbonyl cyanide 3-chlorophenylhydrazone and partially inhibited by N-methyl-L-arginine. These data suggest that MGO stimulates superoxide production from mitochondria and partially stimulates nitric oxide synthase in human endothelial cells.

Full Text

Duke Authors

Cited Authors

  • Miyazawa, N; Abe, M; Souma, T; Tanemoto, M; Abe, T; Nakayama, M; Ito, S

Published Date

  • January 2010

Published In

Volume / Issue

  • 44 / 1

Start / End Page

  • 101 - 107

PubMed ID

  • 19886746

Electronic International Standard Serial Number (EISSN)

  • 1029-2470

Digital Object Identifier (DOI)

  • 10.3109/10715760903321788


  • eng

Conference Location

  • England