Optimization and characterization of acute radiation-induced esophagitis in mice.

Abstract

Purpose: To optimize an animal model of acute radiation-induced esophagitis (RIE) in C57BL/6 mice and characterize the histopathological features of RIE at different stages.

Materials and methods: C57BL/6 mice were subjected to single thoracic X-ray irradiation at doses ranging from 5 to 30 Gy. Changes in body weight, daily food and water intake, and survival were monitored and compared within 2 weeks after radiation exposure. Epithelial damage to the esophagus, apoptosis, and inflammation at different times after irradiation were examined to characterize the pathological process of RIE.

Results: The incidence of acute RIE was strongly correlated with increasing radiation dose across all the experimental groups. No deaths were observed in mice that received 5 or 10 Gy of irradiation, whereas complete mortality was observed within 15 days after exposure to 30 Gy of irradiation. The mice in 20 Gy irradiation group had a low mortality rate. The peak of esophageal tissue damage occurred at Day 7 and was healed by Day 14 after exposure to 20 Gy of thoracic irradiation. The pathology of RIE was induced by radiation-induced DNA damage, apoptosis, reactive oxygen species (ROS), and mitochondrial impairment.

Conclusions: In this study, we found that a single 20 Gy thoracic irradiation was the optimal dose to establish acute RIE in C57BL/6 mice. Acute esophageal injury peaked on Day 7 after radiation, and the process of regeneration and repair was complete within 14 days. This work may be a useful reference for experimental research concerning RIE.