Abstract
A large-scale nuclear event has the ability to inflict mass casualties requiring point-of-care and laboratory-based diagnostic and prognostic biomarkers to inform victim triage and appropriate medical intervention. Extensive progress has been made to develop post-exposure point-of-care biodosimetry assays and to identify biomarkers that may be used in early phase testing to predict the course of the disease. Screening for biomarkers has recently extended to identify specific metabolomic and lipidomic responses to radiation using animal models. The objective of this review was to determine which metabolites or lipids most frequently experienced perturbations post-ionizing irradiation (IR) in preclinical studies using animal models of acute radiation sickness (ARS) and delayed effects of acute radiation exposure (DEARE). Upon review of approximately 65 manuscripts published in the peer-reviewed literature, the most frequently referenced metabolites showing clear changes in IR induced injury were found to be citrulline, citric acid, creatine, taurine, carnitine, xanthine, creatinine, hypoxanthine, uric acid, and threonine. Each metabolite was evaluated by specific study parameters to determine whether trends were in agreement across several studies. A select few show agreement across variable animal models, IR doses and timepoints, indicating that they may be ubiquitous and appropriate for use in diagnostic or prognostic biomarker panels.
Highlights
A nuclear accident or attack has the potential to produce large-scale mass casualties by exposing individuals to potentially life-threatening doses of ionizing irradiation (IR)
The primary objective of this review is to identify the most abundant metabolomic and lipidomic perturbations that are observed in studies with radiation exposure, including animal models of Acute radiation sickness (ARS)
Other metabolites that were moderately abundant among several publications include 20 deoxyuridine (C9 H12 N2 O5 ), arginine (C6 H14 N4 O2 ), palmitic acid (C16 H32 O2 ), glycine (C2 H5 NO2 ), uridine (C9 H12 N2 O6 ), inositol (C6 H12 O6 ), lactic acid (C3 H6 O3 ), leucine (C6 H13 NO2 ), linoleic acid (C18 H32 O2 ), methionine (C5 H11 NO2 S), glutamine (C5 H10 N2 O3 ), hippuric acid (C9 H9 NO3 ), tyrosine (C9 H11 NO3 ), and sebacic acid (C10 H18 O4 ) [4,13,14,15,16,17,18,19,20,21,22,23,24,25,26,27,28,29,30,31,32,33,34,35,36,37,38,39,40,41,42]
Summary
A nuclear accident or attack has the potential to produce large-scale mass casualties by exposing individuals to potentially life-threatening doses of ionizing irradiation (IR). Acute radiation sickness (ARS) occurs in humans at doses of total body irradiation (TBI) in excess of 0.5 Gy, with life- threatening bone marrow suppression occurring after exposure to 2 Gy or higher. The severity of ARS increases with radiation dose and quality (e.g., low or high linear energy transfer radiation) and is characterized by bone marrow suppression and/or failure, infection, hemorrhage, and severe acute anemia. Both evacuation and evaluation of the affected population surrounding the epicenter will require medical triage. First assessment will include the location of the incident, radiation exposure associated symptoms, and physical examination to identify the at-risk population
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