Browse by author
Lookup NU author(s): Dr Joao Passos,
Dr Sharon Olijslagers,
Professor Thomas von Zglinicki
Full text for this publication is not currently held within this repository. Alternative links are provided below where available.
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. © 2007 Elsevier Inc. All rights reserved.
Author(s): Ksiazek K, Passos JF, Olijslagers S, von Zglinicki T
Publication type: Article
Publication status: Published
Journal: Biochemical and Biophysical Research Communications
ISSN (print): 0006-291X
ISSN (electronic): 1090-2104
Publisher: Academic Press
PubMed id: 18082137
Altmetrics provided by Altmetric