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Research Paper|Volume 2, Issue 9|pp 555—566

Adult-onset, short-term dietary restriction reduces cell senescence in mice

Chunfang Wang1, Mandy Maddick1, Satomi Miwa1, Diana Jurk1, Rafal Czapiewski2, Gabriele Saretzki2, Sabine A.S. Langie3, Roger W.L. Godschalk4, Kerry Cameron1, Thomas von Zglinicki1
  • 1Centre for Integrated Systems Biology of Ageing and Nutrition, Institute for Ageing and Health, Newcastle University, Newcastle Upon Tyne, UK
  • 2Crucible Laboratory, Institute for Ageing and Health, Newcastle University, Newcastle Upon Tyne, UK
  • 3Human Nutrition Research Centre and Centre for Brain Ageing and Vitality, Institute for Ageing and Health, Newcastle University, Newcastle Upon Tyne, UK
  • 4Nutrition and Toxicology Research Institute Maastricht (NUTRIM), Department of Health Risk Analysis and Toxicology, Maastricht University, Netherlands
Received: August 18, 2010Accepted: September 9, 2010Published: September 11, 2010

Copyright: © 2010 Wang et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Abstract

Dietary restriction (DR) extends the lifespan of a wide variety of species and reduces the incidence of major age-related diseases. Cell senescence has been proposed as one causal mechanism for tissue and organism ageing. We show for the first time that adult-onset, short-term DR reduced frequencies of senescent cells in the small intestinal epithelium and liver of mice, which are tissues known to accumulate increased numbers of senescent cells with advancing age. This reduction was associated with improved telomere maintenance without increased telomerase activity. We also found a decrease in cumulative oxidative stress markers in the same compartments despite absence of significant changes in steady-state oxidative stress markers at the whole tissue level. The data suggest the possibility that reduction of cell senescence may be a primary consequence of DR which in turn may explain known effects of DR such as improved mitochondrial function and reduced production of reactive oxygen species.