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Redox Mechanisms in Radiotherapy and Hypoxic Preconditioning

Zhou, Tingyang
http://rave.ohiolink.edu/etdc/view?acc_num=osu1469019913

Abstract Details

2016, Master of Science, Ohio State University, Biophysics.
Reactive oxygen species (ROS) are chemically reactive molecules that are naturally produced within the biological system. The accumulation of ROS is controlled by antioxidant defense. Low levels of ROS act as important signaling messengers mediating cell apoptosis, inflammation and immune responses. However, this redox balance can be disturbed by pathological assaults, in which excessive ROS are generated, leading to oxidative damage and dysregulated cellular activities. The positive aspects of ROS as signaling molecules have been exploited in ischemic and hypoxic preconditioning; while the negative roles of ROS in mediating cell apoptosis and inducing oxidative damage have been extensively studied in cancer treatment. Particularly, as shown in my first project, ROS play a role in radiation-induced bystander effects, the phenomenon where irradiated cells can emit signals to affect neighboring cells. Due to such effects, a gradient dosage design demonstrates the potential to achieve a similar tumor killing efficiency as the uniform-dose profile but with less radiotoxicity on neighboring normal tissues. To examine the effectiveness of gradient irradiation in tumor curbing, we monitored the cell viability, intra- and extra-cellular ROS production patterns within 48h following gradient (8-2 Gy) and uniform (5 Gy) irradiation in breast cancer cells (MCF-7). Similar levels of ROS and lower cell viability were observed in the gradient irradiation group as compared to uniform irradiation group at 48h after irradiation. Our results suggest superior therapeutic effects of gradient irradiation, which promises great potential to be used in current radiotherapy for the benefits of cancer patients. My second project is to explore the molecular mechanism of hypoxic preconditioning (HPC), as HPC can exert strong protection on skeletal muscles that are exposed to hypoxia and the following reoxygenation; yet the underlying mechanisms remain elusive. HPC treatment is likely to induce changes in muscle redox status, which may improve muscle resistance to hypoxia through ROS-initiated pathways and Ca2+ handling. NADH is a critical mitochondrial redox indicator; potentially it is linked with ROS formation and Ca2+ release. Therefore, we used a photometer system to characterize the NADH fluctuations in HPC-treated mouse diaphragms. The results may provide useful insights into the protective mechanisms of HPC.
Li Zuo, PhD (Advisor)
Hua Zhu, PhD (Committee Member)
88 p.
Biology; Biophysics; Medicine; Physiology
Redox mechanisms, radiotherapy, hypoxic preconditioning

Recommended Citations

Citations

  • Zhou, T. (2016). Redox Mechanisms in Radiotherapy and Hypoxic Preconditioning [Master's thesis, Ohio State University]. OhioLINK Electronic Theses and Dissertations Center. http://rave.ohiolink.edu/etdc/view?acc_num=osu1469019913

    APA Style (7th edition)

  • Zhou, Tingyang. Redox Mechanisms in Radiotherapy and Hypoxic Preconditioning. 2016. Ohio State University, Master's thesis. OhioLINK Electronic Theses and Dissertations Center, http://rave.ohiolink.edu/etdc/view?acc_num=osu1469019913.

    MLA Style (8th edition)

  • Zhou, Tingyang. "Redox Mechanisms in Radiotherapy and Hypoxic Preconditioning." Master's thesis, Ohio State University, 2016. http://rave.ohiolink.edu/etdc/view?acc_num=osu1469019913

    Chicago Manual of Style (17th edition)

osu1469019913
556
© 2016, some rights reserved.Creative Commons License Redox Mechanisms in Radiotherapy and Hypoxic Preconditioning by Tingyang Zhou is licensed under a Creative Commons Attribution-NonCommercial-ShareAlike 3.0 Unported License. Based on a work at etd.ohiolink.edu.
This open access ETD is published by The Ohio State University and OhioLINK.