Pannkuk Evan L, Laiakis Evagelia C, Garty Guy Y, Shuryak Igor, Kumar Kamendra, Suman Shubhankar, Ghandhi Shanaz A, Tan Yuewen, Ponnaiya Brian, Wu Xuefeng, Amundson Sally A, Brenner David J, Fornace Albert J
Department of Oncology, Lombardi Comprehensive Cancer Center, Georgetown University Medical Center, Washington, DC.
Department of Biochemistry and Molecular & Cellular Biology, Georgetown University Medical Center, Washington, DC.
Radiat Res. 2025 Jul 1;204(1):1-14. doi: 10.1667/RADE-25-00066.1.
Novel biodosimetry assays are needed to categorize both acute ionizing radiation injury and delayed effects of radiation exposure, such as radiation-induced lung injury (RILI) -associated mortality. In this study, we utilized the C57L/J mouse model, a well-established system for replicating the clinical pathology of RILI. Lung injury was induced using a combination of neutron total-body irradiation (TBI) (30% of total dose +7% of total dose concomitant gamma rays) and whole-thoracic X-irradiation (WTI) boost for the balance of the required dose at total doses of 9, 9.5, 10 and 10.5 Gy. The animals were monitored for a period of 180 days postirradiation to evaluate the progression of injury. Both male and female mice were included in the study, with cohorts exposed to either sham dose (0 Gy) or 100% X-ray WTI at 11.35 Gy (LD50/180 dose) to serve as controls. Tissue injury was characterized using whole-body plethysmography, histopathology, and targeted lipidomics. Urinary metabolites were detected using untargeted metabolomic profiling to determine if they could serve as early predictors of RILI survival. A survival rate of 40-45% was observed at 180 days postirradiation consistent with the established LD50/180 value for WTI (11.35 Gy), except at 10.5 Gy, where survival dropped to 20%. Irradiated mice exhibited increased pulmonary immune infiltration and collagen deposition, reduced alveolar spaces, thickened bronchiolar walls, and dose-independent alterations in lipid profiles that were not sex-specific. We developed a multiplex urinary metabolite panel that was associated with RILI and radiation exposure. Some compounds were statistically different between sham-irradiated male and female mice, with sex specific differences at 120 days were observed for homocitrulline, xanthosine, acetyl-arginine, methylhistidine, niacinamide, xanthurenic acid, cyclic adenosine monophosphate, taurine, and prolyl-proline urinary metabolite levels. Baseline differences in sham-irradiated C57L/J mice show sex needs to be considered as a variable when developing biomarker panels for long-term RILI effects. However, urinary metabolite panels can provide excellent to very good sensitivity and specificity at predicting survival from RILI.
需要新的生物剂量测定法来对急性电离辐射损伤和辐射暴露的延迟效应进行分类,例如与放射性肺损伤(RILI)相关的死亡率。在本研究中,我们使用了C57L/J小鼠模型,这是一个用于复制RILI临床病理学的成熟系统。通过中子全身照射(TBI)(总剂量的30% + 总剂量7%的伴随γ射线)和全胸X线照射(WTI)增强相结合的方式,在总剂量为9、9.5、10和10.5 Gy时诱导肺损伤,以达到所需剂量的其余部分。在照射后对动物进行180天的监测,以评估损伤的进展。研究中纳入了雄性和雌性小鼠,将接受假照射剂量(0 Gy)或11.35 Gy的100% X线WTI(LD50/180剂量)的队列作为对照。使用全身体积描记法、组织病理学和靶向脂质组学对组织损伤进行表征。使用非靶向代谢组学分析检测尿液代谢物,以确定它们是否可以作为RILI存活的早期预测指标。照射后180天观察到的存活率为40 - 45%,与已确定的WTI的LD50/180值(11.35 Gy)一致,但在10.5 Gy时,存活率降至20%。受照射的小鼠表现出肺部免疫浸润增加和胶原蛋白沉积,肺泡空间减小,细支气管壁增厚,以及脂质谱的剂量非依赖性改变,且无性别特异性。我们开发了一个与RILI和辐射暴露相关的多重尿液代谢物面板。一些化合物在假照射的雄性和雌性小鼠之间存在统计学差异,在120天时观察到高瓜氨酸、黄苷、乙酰精氨酸、甲基组氨酸、烟酰胺、黄尿酸、环磷酸腺苷、牛磺酸和脯氨酰 - 脯氨酸尿液代谢物水平存在性别特异性差异。假照射的C57L/J小鼠的基线差异表明,在开发用于长期RILI效应的生物标志物面板时,需要将性别作为一个变量考虑。然而,尿液代谢物面板在预测RILI的存活率方面可以提供优异到非常好的敏感性和特异性。