How Cellular Energy Systems Could Protect Against Radiation Damage

Authors
Journal
Life Sciences
Year
DOI
10.1016/j.lfs.2020.117570
Study Type
clinical
Peer Reviewed
Yes
Country
Iran
Health Condition
Radiation Exposure
Body System
Cellular

TL;DR

When people get exposed to radiation, it messes up how their cells handle dangerous molecules called free radicals, which causes damage—but scientists think they can fix this by targeting specific things that control how cells work. This discovery is important because it could lead to new treatments that help people recover from accidental radiation exposure.

Key Finding

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Summary

Scientists examined how radiation exposure damages cells by disrupting normal energy production and increasing harmful free radicals. The study found that radiation causes mitochondrial dysfunction, triggers inflammatory responses, and alters cellular metabolism through multiple pathways. Researchers identified that targeting specific molecular mechanisms like mTOR and PPAR could provide protection against radiation injury. The approach would be tissue-specific, meaning different organs would require different protective strategies. This research provides important insights for developing treatments to protect people from accidental radiation exposure, offering hope for better countermeasures in nuclear emergencies or medical radiation treatments.

Abstract

Accidental exposure to ionizing radiation is a serious concern to human life. Studies on the mitigation of side effects following exposure to accidental radiation events are ongoing. Recent studies have shown that radiation can activate several signaling pathways, leading to changes in the metabolism of free radicals including reactive oxygen species (ROS) and nitric oxide (NO). Cellular and molecular mechanisms show that radiation can cause disruption of normal reduction/oxidation (redox) system. Mitochondria malfunction following exposure to radiation and mutations in mitochondria DNA (mtDNA) have a key role in chronic oxidative stress. Furthermore, exposure to radiation leads to infiltration of inflammatory cells such as macrophages, lymphocytes and mast cells, which are important sources of ROS and NO. These cells generate free radicals via upregulation of some pro-oxidant enzymes such as NADPH oxidases, inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2). Epigenetic changes also have a key role in a similar way. Other mediators such as mammalian target of rapamycin (mTOR) and peroxisome proliferator-activated receptor (PPAR), which are involved in the normal metabolism of cells have also been shown to regulate cell death following exposure to radiation. These mechanisms are tissue specific. Inhibition or activation of each of these targets can be suggested for mitigation of radiation injury in a specific tissue. In the current paper, we review the cellular and molecular changes in the metabolism of cells and ROS/NO following exposure to radiation. Furthermore, the possible strategies for mitigation of radiation injury through modulation of cellular metabolism in irradiated organs will be discussed.