Mitochondrial dysfunction is a possible cause of accelerated senescence of mesothelial cells exposed to high glucose

Krzysztof Ksiazek, João F. Passos, Sharon Olijslagers, Thomas von Zglinicki

Research output: Contribution to journalArticle

31 Scopus citations

Abstract

High glucose has been found to accelerate cell senescence in vitro. The exact mechanism of this effect is, however, still poorly understood. In this paper we show that human peritoneal mesothelial cells (HPMCs) propagated under high (30 mM) glucose were characterized by higher density of DNA double-strand breaks than cells exposed to standard (5 mM) glucose concentration. Under both low and high glucose conditions, the vast majority of DNA damage localized to non-telomeric regions of the genome. Moreover, exposure to high glucose resulted in increased accumulation of lipofuscin, increased production of superoxides and peroxides as well as reduced mitochondrial membrane potential and increased mitochondrial mass. Treatment of cells with the free radical scavenger PBN partially rescued the premature senescence caused by high glucose. Together, these results indicate that high glucose may accelerate senescence of HPMCs by impairing mitochondrial function, resulting in overproduction of reactive oxygen species and extensive DNA damage.

Original languageEnglish (US)
Pages (from-to)793-799
Number of pages7
JournalBiochemical and Biophysical Research Communications
Volume366
Issue number3
DOIs
StatePublished - Feb 15 2008

Keywords

  • Accelerated senescence
  • DNA damage
  • High glucose
  • Mesothelial cells
  • Mitochondria
  • Oxidative stress

ASJC Scopus subject areas

  • Biophysics
  • Biochemistry
  • Molecular Biology
  • Cell Biology

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