ePrints

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

Lookup NU author(s): Dr Joao Passos, Dr Sharon Olijslagers, Professor Thomas von Zglinicki

Downloads

Full text for this publication is not currently held within this repository. Alternative links are provided below where available.

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. © 2007 Elsevier Inc. All rights reserved.

Publication metadata

Author(s): Ksiazek K, Passos JF, Olijslagers S, von Zglinicki T

Publication type: Article

Publication status: Published

Journal: Biochemical and Biophysical Research Communications

Year: 2008

Volume: 366

Issue: 3

Pages: 793-799

ISSN (print): 0006-291X

ISSN (electronic): 1090-2104

Publisher: Academic Press

URL: http://dx.doi.org/10.1016/j.bbrc.2007.12.021

DOI: 10.1016/j.bbrc.2007.12.021

PubMed id: 18082137

Altmetrics

Share