Thermal stress and the disruption of redox-sensitive signalling and transcription factor activation: possible role in radiosensitization
Thermal stress and the disruption of redox-sensitive signalling and transcription factor activation: possible role in radiosensitization
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DOI：
10.1080/02656730310001619505
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发表时间：
2004-03-01
影响因子：
3.1
通讯作者：
Spitz, DR
中科院分区：
文献类型：
--
作者：
Gius, D;Mattson, D;Spitz, DR
尽管正在进行的研究工作，在电离辐射（IR）的细胞反应的热诱导的变化的具体机制（S）仍然是模糊的，部分原因是它们可能涉及多种机制和潜在的目标。其中一组潜在靶点包括一类被称为立即早期反应基因的细胞质信号传导和/或核转录因子，它们被认为在癌症治疗期间发挥细胞毒性和细胞保护作用。一种已建立的调节这些早期反应元件的活性的机制涉及细胞氧化/还原（氧化还原）状态的变化。在建立氧化应激和热暴露的早期反应基因的共同改变后，可以推断热休克可能与其他形式的诱导氧化应激的环境拮抗剂具有相似性。在这篇综述中，最近的证据支持热休克和氧化应激之间的机械联系将进行总结。此外，热休克改变细胞对抗癌药物（包括热辐射增敏）的反应的一种机制是通过热诱导的氧化还原敏感的信号传导因子的破坏的假设将被讨论。
In spite of ongoing research efforts, the specific mechanism(s) of heat-induced alterations in the cellular response to ionizing radiation (IR) remain ambiguous, in part because they likely involve multiple mechanisms and potential targets. One such group of potential targets includes a class of cytoplasmic signalling and/or nuclear transcription factors known as immediate early response genes, which have been suggested to perform cytotoxic as well as cytoprotective roles during cancer therapy. One established mechanism regulating the activity of these early response elements involves changes in cellular oxidation/reduction (redox) status. After establishing common alterations in early response genes by oxidative stress and heat exposure, one could infer that heat shock may have similarities to other forms of environmental antagonists that induce oxidative stress. In this review, recent evidence supporting a mechanistic link between heat shock and oxidative stress will be summarized. In addition, the hypothesis that one mechanism whereby heat shock alters cellular responses to anticancer agents (including hyperthermic radiosensitization) is through heat-induced disruption of redox-sensitive signalling factors will be discussed.