Metabolism, genomics, and DNA repair in the mouse aging liver.
Metabolism, genomics, and DNA repair in the mouse aging liver.
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DOI：
10.1155/2011/859415
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发表时间：
2011
影响因子：
--
通讯作者：
Bohr VA
中科院分区：
文献类型：
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作者：
Lebel M;de Souza-Pinto NC;Bohr VA
肝脏在营养物质、药物、激素和代谢废物的代谢中起着关键作用，从而维持身体的稳态。肝脏在老年时在结构和功能上发生了重大变化。这些变化与许多肝脏代谢和解毒活动的显著受损有关，并对系统性衰老和年龄相关疾病产生影响。使用啮齿动物模型作为生物学工具，随着年龄的增长，以总DNA重排或点突变形式存在的遗传不稳定性在肝脏中积累，这一点已经变得很清楚。DNA损伤，如氧化碱基或持续断裂，随着年龄的增长而增加，并与衰老肝细胞的存在密切相关。DNA损伤和/或突变的水平可能受到致癌物活化变化、DNA修复能力下降或这些因素组合的影响。本文涵盖了一些DNA修复途径影响肝脏稳态与年龄使用啮齿动物作为模型系统。
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.