Abstract
Ionizing radiation exposure may not only cause acute radiation syndrome, but also an increased risk of late effects. It has been hypothesized that induction of chronic oxidative stress mediates the late effects of ionizing radiation. However, only a few reports have analyzed changes in long-term antioxidant capacity after irradiation in vivo. Our previous study demonstrated changes in whole-blood antioxidant capacity and red blood cell (RBC) glutathione levels within 50 days after total body irradiation (TBI). In this study, seven-week-old, male, C57BL/6J mice exposed to total body irradiation by X-ray and changes in whole-blood antioxidant capacity and RBC glutathione levels at ≥ 100 days after TBI were investigated. Whole-blood antioxidant capacity was chronically decreased in the 5-Gy group. The RBC reduced glutathione (GSH) level and the GSH/oxidative glutathione (GSSG) ratio were chronically decreased after ≥ 1 Gy of TBI. Interestingly, the complete blood counts (CBC) changed less with 1-Gy exposure, suggesting that GSH and the GSH/GSSG ratio were more sensitive radiation exposure markers than whole-blood antioxidant capacity and CBC counts. It has been reported that GSH depletion is one of the triggers leading to cataracts, hypertension, and atherosclerosis, and these diseases are also known as radiation-induced late effects. The present findings further suggest that chronic antioxidant reduction may contribute to the pathogenesis of late radiation effects.
Highlights
Ionizing radiation exposure may cause acute radiation syndrome, and an increased risk of late effects
It has been reported that the mortality or morbidity of c ancer1, cataracts2, hypertension[3], heart diseases4, atherosclerosis[5], and strokes[4] was increased in atomic bomb survivors a few decades after exposure
Plasma reactive oxygen species (ROS), C-reactive protein (CRP), and interleukin-6 (IL-6) levels were increased in a dosedependent manner in atomic bomb s urvivors[6]
Summary
Ionizing radiation exposure may cause acute radiation syndrome, and an increased risk of late effects. Our previous study demonstrated changes in wholeblood antioxidant capacity and red blood cell (RBC) glutathione levels within 50 days after total body irradiation (TBI). It has been reported that the mortality or morbidity of c ancer1, cataracts2, hypertension[3], heart diseases4, atherosclerosis[5], and strokes[4] was increased in atomic bomb survivors a few decades after exposure Most of these diseases are correlated with oxidative stress and persistent inflammation. We analyzed changes in red blood cell (RBC) glutathione levels from 2 to 24 days after TBI in mice, finding that radiation decreased the GSH/GSSG ratio through an increase of GSSG levels and a decrease of GSH levels[7]. Mice were exposed to TBI, and Scientific Reports | (2021) 11:6716
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
