Abstract
The radiation-induced damage to the human body is primarily caused by excessive reactive oxygen species (ROS) production after irradiation. Therefore, the removal of the increase of ROS caused by ionizing radiation (IR) has been the focus of research on radiation damage protective agents. Hypoxia inducible factor (HIF) is a transcription factor in human and plays an important role in regulating the body metabolism. Factor inhibiting HIF (FIH) is an endogenous inhibitor factor of HIF protein under normoxia conditions. It has been shown that the high expression of HIF protein has a certain repair effect on radiation-induced intestinal injury and hematopoietic system damage in mice; however, it is not clear about the effect of HIF on the level of ROS after radiation. In this study, the role of N-oxalyl-d-phenylalanine (NOFD), an FIH inhibitor, for its effect on alleviating ROS level is investigated in the cells. Our results indicate that pretreatment with NOFD can mitigate ROS level and alleviate IR-induced DNA damage and apoptosis in vitro. Therefore, HIF can be used as a target on scavengers. Furthermore, in order to explore the relevant mechanism, we also test the expression of relevant HIF downstream genes in the cells, finding that Notch-2 gene is more sensitive to NOFD treatment. This experiment result is used to support the subsequent mechanism experiments.
Highlights
Radiation therapy is increasingly used in physical and medical fields, which is the important treatment of malignant tumors and severe diseases [1]
The cells will quickly produce excessive reactive oxygen species (ROS); in order to accurately evaluate the effect of NOFD, the cells after irradiation were immediately collected for treatment and subjected to DCFH-DA staining according to the instructions, and the results were presented with a fluorescence microscope
Radiation therapy has made good progress in many diseases, the damage caused by ionizing radiation cannot be overlooked
Summary
Radiation therapy is increasingly used in physical and medical fields, which is the important treatment of malignant tumors and severe diseases [1]. A lot of findings supported the role of HIF-1α in reducing the release of ROS in mitochondrion by inhibiting metabolic regulation under mitochondrial respiration, according to increasing the expression of glycolytic enzymes to facilitate anaerobic respiration [20,21,22,23,24]. Another experiment suggested that the increased mitochondrial ROS induced by hypoxia could be significantly inhibited in FIH-deficient cells [25].
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
