Methylglyoxal augments intracellular oxidative stress in human aortic endothelial cells

Noriko Miyazawa, Michiaki Abe*, Tomokazu Souma, Masayuki Tanemoto, Takaaki Abe, Masaaki Nakayama, Sadayoshi Ito

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

52 Scopus citations


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.

Original languageEnglish (US)
Pages (from-to)101-107
Number of pages7
JournalFree Radical Research
Issue number1
StatePublished - 2010


  • Carbonyl stress
  • Endothelial cell
  • Methylglyoxal
  • Oxidative stress

ASJC Scopus subject areas

  • Biochemistry


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