Subrahmanyam K, Rao K S
School of Life Sciences, University of Hyderabad, India.
Mech Ageing Dev. 1991 Mar;57(3):283-91. doi: 10.1016/0047-6374(91)90053-3.
DNA-repair capacity, by incorporation in vitro of [3H]thymidine into DNA of isolated neuronal cells and splenic lymphocytes of rat was studied as a function of age. The incubations were carried out both in the presence and absence of hydroxyurea (HU), a known inhibitor of replicative DNA synthesis. The results indicate that neurons, unlike lymphocytes, obtained from adult and old animals offer a good model system to measure the DNA-repair process without any possible interference of DNA replicative synthesis. Further, the 'spontaneous' DNA repair by unscheduled DNA synthesis (UDS) in old neurons remained unchanged as compared to the adult level. However, the response of aging neurons, in contrast to that of young and adult neurons or of lymphocytes of any age, to a mutagenic challenge like UV light is limited. It is suggested that this lack of responsive DNA-repair against a given damage may lead to a general metabolic deterioration and senescence.
通过体外将[3H]胸腺嘧啶核苷掺入大鼠离体神经元细胞和脾淋巴细胞的DNA中,研究了DNA修复能力与年龄的关系。在存在和不存在羟基脲(HU,一种已知的复制性DNA合成抑制剂)的情况下进行孵育。结果表明,与淋巴细胞不同,从成年和老年动物获得的神经元提供了一个良好的模型系统,可用于测量DNA修复过程,而不会受到DNA复制合成的任何可能干扰。此外,与成年水平相比,老年神经元中通过非预定DNA合成(UDS)进行的“自发”DNA修复保持不变。然而,与年轻和成年神经元或任何年龄的淋巴细胞不同,衰老神经元对紫外线等诱变挑战的反应是有限的。有人认为,针对特定损伤缺乏反应性DNA修复可能会导致整体代谢恶化和衰老。