Inhibitory Effects of Pretreatment with Radon on Acute Alcohol-Induced Hepatopathy in Mice

We previously reported that radon inhalation activates antioxidative functions in the liver and inhibits carbon tetrachloride-induced hepatopathy in mice. In addition, it has been reported that reactive oxygen species contribute to alcohol-induced hepatopathy. In this study, we examined the inhibitory effects of radon inhalation on acute alcohol- induced hepatopathy in mice. C57BL/6J mice were subjected to intraperitoneal injection of 50% alcohol (5 g/kg bodyweight) after inhaling approximately 4000 Bq/m(3) radon for 24 h. Alcohol administration significantly increased the activities of glutamic oxaloacetic transaminase (GOT), glutamic pyruvic transaminase (GPT) in serum, and the levels of triglyceride and lipid peroxide in the liver, suggesting acute alcohol- induced hepatopathy. Radon inhalation activated antioxidative functions in the liver. Furthermore, pretreatment with radon inhibited the depression of hepatic functions and antioxidative functions. These findings suggested that radon inhalation activated antioxidative functions in the liver and inhibited acute alcohol- induced hepatopathy in mice

Inhibitory Effects of Prior Low-dose X-irradiation on Cold-induced Brain Injury in Mouse

We examined the inhibitory effects of low-dose X-irradiation on mouse brain tissue with cold-induced injury by comparing tissue samples from three groups of mice: control, sham-irradiated cold-exposed, and X-ray-irradiated (0.5 Gy) cold-exposed mice. The water content in brain increased significantly in the sham-irradiated group following the cold-induced injury relative to the control group. However, water content in brain tissue from the X-ray-irradiated group was significantly lower than that from the sham-irradiated group. Levels of antioxidants, such as superoxide dismutase and glutathione, in brain tissue from the X-ray-irradiated group were higher than those from the sham-irradiated group. Moreover, the cold injury-induced cell death, particularly apoptosis, while low-dose irradiation inhibited cell death, especially among glial cells, but not numeral cells. These findings suggest that prior low-dose X-irradiation activated antioxidant function and inhibited cold-induced brain injury

Low-dose X-irradiation inhibits brain injury 1 Regular Paper Inhibitory effects of prior low-dose X-irradiation on cold-induced brain injury in mouse

Running title: Low-dose X-irradiation inhibits brain injury ABBREVIATIONS: BBB, blood-brain barrier; ROS, reactive oxygen species; SOD, superoxide dismtase; GPx, glutathione peroxidase; GR, glutathione reductase; total GSH, total glutathione; EDTA, ethylendiaminetetraacetic acid; NBT, nitroblue tetrazolium; H 2 O 2 , hydrogen peroxide; MDA, malondialdehyde; HE, hematoxylin-eosin; KB, Kluver-Barrera; TUNEL, Terminal dUTP in situ nick-end labeling; PBS, phosphate-buffered saline; DAB, 3,39-diaminobenzidine; SEM, standard error of the mean; MCA, middle cerebral artery Low-dose X-irradiation inhibits brain injury 2 Abstract We examined the inhibitory effects of low-dose X-irradiation on mouse brain tissue with cold-induced injury by comparing tissue samples from three groups of mice: control, sham-irradiated cold-exposed, and X-ray-irradiated (0.5 Gy) cold-exposed mice. The water content in brain increased significantly in the sham-irradiated group following the cold-induced injury relative to the control group. However, water content in brain tissue from the X-ray-irradiated group was significantly lower than that from the sham-irradiated group. Levels of antioxidants, such as superoxide dismutase and glutathione, in brain tissue from the X-ray-irradiated group were higher than those from the sham-irradiated group. Moreover, the cold injury induced cell death, particularly apoptosis, while low-dose irradiation inhibited cell death, especially among glial cells, but not numeral cells. These findings suggest that prior low-dose X-irradiation activated antioxidant function and inhibited cold-induced brain injury

Study of the Response of Superoxide Dismutase in Mouse Organs to Radon Using a New Large-scale Facility for Exposing Small Animals to Radon

We examined dose–dependent or dose rate–dependent changes of superoxide dismutase (SOD) activity using a new large-scale facility for exposing small animals to radon. Mice were exposed to radon at a concentration of 250, 500, 1000, 2000, or 4000 Bq/m3 for 0.5, 1, 2, 4, or 8 days. When mice were exposed to radon at 2000 day•Bq/m3, activation of SOD activities in plasma, liver, pancreas, heart, thymus, and kidney showed dose–rate effects. Our results also suggested that continuous exposure to radon increased SOD activity, but SOD activity transiently returned to normal levels at around 2 days. Moreover, we classified the organs into four groups (1. plasma, brain, lung; 2. heart, liver, pancreas, small intestine; 3. kidney, thymus; 4. stomach) based on changes in SOD activity. Thymus had the highest responsiveness and stomach had lowest. These data provide useful baseline measurements for future studies on radon effects