MINORITY PREDOCTORAL FELLOWSHIP PROGRAM

描述（由申请人提供）：目前，缺乏对抗氧化剂如何影响辐射防护的理解。细胞的氧化还原平衡是通过一些抗氧化酶，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以及PI-3 K、PKC和MAPK信号级联，导致细胞抗氧化剂的诱导。探索电离辐射在细胞水平上对抗氧化剂表达的影响是至关重要的，然后才能使用这些途径来增强辐射防护。我们假设，有一个层次的反应，氧化应激，炎症和细胞死亡的辐射剂量。除了表征抗氧化剂的表达，我们将探讨修改这些氧化还原反应的辐射防护作用方面的潜力。该项目旨在提高抗氧化剂对电离辐射的反应的理解，并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.