MINORITY PREDOCTORAL FELLOWSHIP PROGRAM

描述(申请人提供)：目前，对抗氧化剂如何影响辐射防护缺乏了解。细胞的氧化还原平衡是通过许多抗氧化酶来维持的，如血红素加氧酶1、超氧化物歧化酶、过氧化氢酶和谷胱甘肽。氧化应激和电离辐射激活转录因子，如AP-1、NF-kB和NRF-2，PI-3K、PKC和MAPK信号转导通路导致细胞抗氧化剂的诱导。在这些途径被用于增强辐射防护之前，在细胞水平上探索电离辐射对抗氧化剂表达的影响是必不可少的。我们假设存在对氧化应激、炎症和细胞死亡的分级反应，以响应辐射剂量。除了表征抗氧化剂的表达外，我们还将探索根据它们的辐射防护作用来修饰这些氧化还原反应的可能性。该项目旨在提高对抗氧化剂对电离辐射的响应的理解，并将阐明这些机制对辐射防护的重要性。

DESCRIPTION (provided by applicant): At present, there is a lack in the understanding of how antioxidants impact radioprotection. The cellular redox balance is maintained through a number of antioxidant enzymes such as heme oxygenase 1, superoxide dimutase, catalase, and glutathione. Oxidative stress and ionizing radiation activate transcriptional factors such as AP-1, NF-kB, and NRF-2 and PI-3K, PKC, and MAPK signaling cascades resulting in the induction of cellular antioxidants. Exploring the effects of ionizing radiation on antioxidant expression at the cellular level is essential before these pathways can be used to enhance radioprotection. We hypothesize that there is a hierarchal response to oxidative stress, inflammation, and cellular death in response to radiation dose. In addition to characterizing the antioxidant expression, we will explore the potential of modifying these redox responses in terms of their radioprotective effects. This project aims to improve the understanding of antioxidants in response to ionizing radiation and will clarify the importance of these mechanisms for radioprotection.