作为一种泛素化分子，一氧化氮可诱导许多生物学效应，并且在肿瘤的演化和进展中也起到非常重要的作用。一氧化氮可参与多个导致蛋白发生变化的信号转导机制。并且这些蛋白的变化是浓度依赖性的。不断产生的持续剂量的一氧化氮通过激活Caspase诱导凋亡；而生理浓度或者低剂量的一氧化氮则抑制细胞凋亡。我们以往的研究也表明细胞放射损伤抑制的产生和染色体畸变的降低可以用p53和一氧化氮的相互作用这一信号通路模式来阐述。然而一氧化氮对肿瘤细胞放射敏感性诱导的具体机制尚不十分清楚。本课题的目的是阐明不同浓度的一氧化氮对肿瘤细胞放射敏感性的影响以及与p53、细胞周期、DNA双链断裂修复相关的可能性机制，为揭示一氧化氮参与肿瘤细胞放射敏感性诱导的详细机制增添新内容，也为其临床应用奠定理论和实验基础。

Nitric oxide is a ubiquitous molecule capable of inducing a multitude of biological effects, and also plays an extremely critical role in the regulation of tumor evolution and progression. Nitric oxide (NO) is concerned with multiplicative signaling mechanisms which lead to the modifications of proteins. These protein changes are concentration-dependent. Sustained production of NO modulate apoptosis by activating caspases, whereas low or physiological concentrations of NO prevent cells from entering apoptosis. Our previous research has led to a signaling pathway model which attempts to describe the induction of radioresistance and the depression of chromosome aberrations via the action of p53 and NO radicals. However, these initial observations are very recent, and the detailed mechanisms which are responsible for the induction of cellular sensitivity to NO radicals are still not fully understood. The aim of the study described here was to clarify the effect of different doses of NO radicals on the induction of cellular sensitivity in cancer cells, and their possible molecular mechanisms related to p53, cell cycle and repair of NO-induced DNA double-strand breaks (DSBs). This research not only adds new contents to reveal the detailed mechanism in the radiosensitivity of tumor cells induced by the involvement of nitric oxide, but also lays the basis of theory and experiment for its clinical appliacation.