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Current Gerontology and Geriatrics Research
Volume 2011 (2011), Article ID 859415, 15 pages
http://dx.doi.org/10.1155/2011/859415
Review Article

Metabolism, Genomics, and DNA Repair in the Mouse Aging Liver

1Centre de Recherche en Cancérologie de l'Université Laval, Hôpital Hôtel-Dieu de Québec, 9 McMahon Street Quebec City, QC, Canada G1R 2J6
2Departmento de Bioquímica, Instituto de Química, Universiade de São Paulo, Avenue Prof. Lineu Prestes, 748, 05508-900 São Paulo, SP, Brazil
3Laboratory of Molecular Gerontology, National Institute on Aging, National Institutes of Health, 5600 Nathan Shock Drive, Baltimore, MD 21224, USA

Received 27 December 2010; Accepted 11 February 2011

Academic Editor: Victoria Cogger

Copyright © 2011 Michel Lebel et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

The liver plays a pivotal role in the metabolism of nutrients, drugs, hormones, and metabolic waste products, thereby maintaining body homeostasis. The liver undergoes substantial changes in structure and function within old age. Such changes are associated with significant impairment of many hepatic metabolic and detoxification activities, with implications for systemic aging and age-related disease. It has become clear, using rodent models as biological tools, that genetic instability in the form of gross DNA rearrangements or point mutations accumulate in the liver with age. DNA lesions, such as oxidized bases or persistent breaks, increase with age and correlate well with the presence of senescent hepatocytes. The level of DNA damage and/or mutation can be affected by changes in carcinogen activation, decreased ability to repair DNA, or a combination of these factors. This paper covers some of the DNA repair pathways affecting liver homeostasis with age using rodents as model systems.