Metabolism, genomics, and DNA repair in the mouse aging liver
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Metabolism, genomics, and DNA repair in the mouse aging liver. / Lebel, Michel; de Souza-Pinto, Nadja C; Bohr, Vilhelm A.
I: Current Gerontology and Geriatrics Research, Bind 2011, 01.01.2011, s. 859415.Publikation: Bidrag til tidsskrift › Tidsskriftartikel › Forskning › fagfællebedømt
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TY - JOUR
T1 - Metabolism, genomics, and DNA repair in the mouse aging liver
AU - Lebel, Michel
AU - de Souza-Pinto, Nadja C
AU - Bohr, Vilhelm A
PY - 2011/1/1
Y1 - 2011/1/1
N2 - 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.
AB - 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.
U2 - 10.1155/2011/859415
DO - 10.1155/2011/859415
M3 - Journal article
C2 - 21559242
VL - 2011
SP - 859415
JO - Current Gerontology and Geriatrics Research
JF - Current Gerontology and Geriatrics Research
SN - 1687-7063
ER -
ID: 33492534