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Methylglyoxal augments intracellular oxidative stress in human aortic endothelial cells.
In: Free Radical Research, Jg. 44 (2010), Heft 1, S. 101-108
Online
academicJournal
Zugriff:
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. [ABSTRACT FROM AUTHOR]
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Methylglyoxal augments intracellular oxidative stress in human aortic endothelial cells.
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Autor/in / Beteiligte Person: | Miyazawa, Noriko ; Abe, Michiaki ; Souma, Tomokazu ; Tanemoto, Masayuki ; Abe, Takaaki ; Nakayama, Masaaki ; Ito, Sadayoshi |
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Zeitschrift: | Free Radical Research, Jg. 44 (2010), Heft 1, S. 101-108 |
Veröffentlichung: | 2010 |
Medientyp: | academicJournal |
ISSN: | 1071-5762 (print) |
DOI: | 10.3109/10715760903321788 |
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