دورية أكاديمية

p53-mediated metabolic response to low doses of ionizing radiation.

التفاصيل البيبلوغرافية
العنوان: p53-mediated metabolic response to low doses of ionizing radiation.
المؤلفون: Nagpal, Isha, Zhi-Min Yuan
المصدر: International Journal of Radiation Biology; 2023, Vol. 99 Issue 6, p934-940, 7p
مصطلحات موضوعية: IONIZING radiation, RADIATION doses, METABOLIC regulation, DNA damage, OXIDATIVE phosphorylation
مستخلص: Purpose: Unlike treatment with high doses of radiation that causes considerable DNA damage resulting in injury and p53 activation, exposure of cells or whole animals to low doses of radiation (LDR, -10cGy) can induce a protective radio adaptive response. Despite ample information about the contribution of the p53 pathway to high doses of radiation-induced effects, our understanding of the role of p53 in LDR-induced response remains incomplete. This review provides a brief summary of the p53 response to LDR exposure focusing on metabolic regulation. Conclusion: Consistent with growing evidence indicating a critical role of metabolic pathways in the modulation of stress responses, the radio adaptive response was mediated by the LDRinduced metabolic switch from oxidative phosphorylation to glycolysis. Remarkably, this metabolic reprogramming depends on p53 downregulation, suggesting a previously unrecognized p53-mediated metabolic response. Of note is that the LDR-induced p53 response is temporary but may become persistent if LDR exposure is recurrent and protracted. While further investigation is necessary, the model where LDR induces p53 downregulation concurrent with anabolic reprogramming may offer novel mechanistic insight into the radio adaptive response. It suggests a model in which LDR exposure is protective when transient or intermittent but may become detrimental when chronic because prolonged p53 downregulation would lead to inactivation of this critical tumor suppressor, causing a loss of p53-dependent DNA damage checkpoint, genomic instability, dysregulated metabolism, and thus increased cancer risk. [ABSTRACT FROM AUTHOR]
Copyright of International Journal of Radiation Biology is the property of Taylor & Francis Ltd and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)
قاعدة البيانات: Complementary Index
الوصف
تدمد:09553002
DOI:10.1080/09553002.2022.2142983