Modifying Radiation Damage
Kwanghee Kim and William H. McBride
Affiliation: Department of Radiation Oncology, Roy E. Coats Research Laboratories, Room B3-109, David Geffen School of Medicine, University of California at Los Angeles, Los Angeles, California 90095, USA.
Keywords: TBI, cytokines, RDS, inflammation, NF-κB, Radiation, immune, ROS, RT, IL-1, TNF-α, G-CSF, GM-CSF, FDA, DNA, anti-EGFR, chromatin, (HAT), (MRN), DSB, ATM, RH-3, (RNS), EGFR, PDGR, AP-1, (GI), (IKKß), (CAPE), MnSOD, (DRF), (ARE), (MTs), CELL DEATH, (GPCR), (TLR), (VEGF), (PDGF), (FGFs), (ACE)
Radiation leaves a fairly characteristic footprint in biological materials, but this is rapidly all but obliterated by the canonical biological responses to the radiation damage. The innate immune recognition systems that sense “danger” through direct radiation damage and through associated collateral damage set in motion a chain of events that, in a tissue compromised by radiation, often unwittingly result in oscillating waves of molecular and cellular responses as tissues attempt to heal. Understanding “natures whispers” that inform on these processes will lead to novel forms of intervention targeted more precisely towards modifying them in an appropriate and timely fashion so as to improve the healing process and prevent or mitigate the development of acute and late effects of normal tissue radiation damage, whether it be accidental, as a result of a terrorist incident, or of therapeutic treatment of cancer. Here we attempt to discuss some of the non-free radical scavenging mechanisms that modify radiation responses and comment on where we see them within a conceptual framework of an evolving radiation-induced lesion.
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