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.

In: Current Gerontology and Geriatrics Research, Vol. 2011, 01.01.2011, p. 859415.

Research output: Contribution to journal › Journal article › Research › peer-review

Harvard

Lebel, M, de Souza-Pinto, NC & Bohr, VA 2011, 'Metabolism, genomics, and DNA repair in the mouse aging liver', Current Gerontology and Geriatrics Research, vol. 2011, pp. 859415. https://doi.org/10.1155/2011/859415

APA

Lebel, M., de Souza-Pinto, N. C., & Bohr, V. A. (2011). Metabolism, genomics, and DNA repair in the mouse aging liver. Current Gerontology and Geriatrics Research, 2011, 859415. https://doi.org/10.1155/2011/859415

Vancouver

Lebel M, de Souza-Pinto NC, Bohr VA. Metabolism, genomics, and DNA repair in the mouse aging liver. Current Gerontology and Geriatrics Research. 2011 Jan 1;2011:859415. https://doi.org/10.1155/2011/859415

Author

Lebel, Michel ; de Souza-Pinto, Nadja C ; Bohr, Vilhelm A. / Metabolism, genomics, and DNA repair in the mouse aging liver. In: Current Gerontology and Geriatrics Research. 2011 ; Vol. 2011. pp. 859415.

Bibtex

@article{30d807125d784f918bee5728b7468048,
title = "Metabolism, genomics, and DNA repair in the mouse aging liver",
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.",
author = "Michel Lebel and {de Souza-Pinto}, {Nadja C} and Bohr, {Vilhelm A}",
year = "2011",
month = jan,
day = "1",
doi = "10.1155/2011/859415",
language = "English",
volume = "2011",
pages = "859415",
journal = "Current Gerontology and Geriatrics Research",
issn = "1687-7063",
publisher = "Hindawi Publishing Corporation",

}

RIS

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