It is generally thought that younger people are more susceptible to cancer development after exposure to ionizing radiation in reference to epidemiological studies and animal experiments. However, little is known about the age-dependent alteration in DNA repair ability. In the present study, we examined the expression levels of proteins involved in the repair of DNA double-strand breaks through non-homologous end joining (NHEJ), i.e., DNA-dependent protein kinase catalytic subunit (DNA-PKcs), X-ray repair cross-complementing 4 (XRCC4) and XRCC4-like factor (XLF). We found that the expression of DNA-PKcs in brain tissues was higher in neonatal mice (1 week after birth) than in young adult mice (7 weeks after birth). In association with this, DNA double-strand breaks were repaired more rapidly in the brain tissues of neonatal mice than in those of young adult mice. The current results suggested a possible role for DNA-PKcs protecting developing brain tissues from DNA double-strand breaks.

中文翻译：

---

DNA依赖性蛋白激酶催化亚基在新生小鼠和年轻成年小鼠大脑中的差异表达。


流行病学研究和动物实验普遍认为，年轻人在接触电离辐射后更容易患癌症。然而，人们对 DNA 修复能力随年龄变化的变化知之甚少。在本研究中，我们检测了通过非同源末端连接（NHEJ）修复DNA双链断裂所涉及的蛋白质的表达水平，即DNA依赖性蛋白激酶催化亚基（DNA-PKcs），X射线修复交叉互补 4 (XRCC4) 和 XRCC4 样因子 (XLF)。我们发现新生小鼠（出生后1周）脑组织中DNA-PKcs的表达高于年轻成年小鼠（出生后7周）。与此相关的是，新生小鼠脑组织中 DNA 双链断裂的修复速度比年轻成年小鼠的脑组织更快。目前的结果表明 DNA-PKcs 可能发挥保护发育中的脑组织免受 DNA 双链断裂的作用。