Potential inhibitory effects of low-dose thoron inhalation and ascorbic acid administration on alcohol-induced hepatopathy in mice.

Although thoron inhalation exerts antioxidative effects in several organs, there are no reports on whether it inhibits oxidative stress-induced damage. In this study, we examined the combined effects of thoron inhalation and ascorbic acid (AA) administration on alcohol-induced liver damage. Mice were subjected to thoron inhalation at 500 or 2000 Bq/m3 and were administered 50% ethanol (alcohol) and 300 mg/kg AA. Results showed that although alcohol administration increased the levels of glutamic oxaloacetic transaminase (GOT) and glutamic pyruvic transaminase (GPT) in the serum, the combination of thoron inhalation (500 Bq/m3) and AA administration 24 h after alcohol administration effectively inhibited alcohol-induced liver damage. The combination of thoron inhalation (500 Bq/m3) and AA administration 24 h after alcohol administration increased catalase (CAT) activity. Alcohol administration significantly decreased glutathione (GSH) levels in the liver. The GSH content in the liver after 2000 Bq/m3 thoron inhalation was lower than that after 500 Bq/m3 thoron inhalation. These findings suggest that the combination of thoron inhalation at 500 Bq/m3 and AA administration has positive effects on the recovery from alcohol-induced liver damage. The results also suggested that thoron inhalation at 500 Bq/m3 was more effective than that at 2000 Bq/m3, possibly because of the decrease in GSH content in the liver. In conclusion, the combination of thoron inhalation at 500 Bq/m3 and AA administration promoted an early recovery from alcohol-induced liver damage.

Radon inhalation decreases DNA damage induced by oxidative stress in mouse organs via the activation of antioxidative functions.

Radon inhalation decreases the level of lipid peroxide (LPO); this is attributed to the activation of antioxidative functions. This activation contributes to the beneficial effects of radon therapy, but there are no studies on the risks of radon therapy, such as DNA damage. We evaluated the effect of radon inhalation on DNA damage caused by oxidative stress and explored the underlying mechanisms. Mice were exposed to radon inhalation at concentrations of 2 or 20 kBq/m3 (for one, three, or 10 days). The 8-hydroxy-2'-deoxyguanosine (8-OHdG) levels decreased in the brains of mice that inhaled 20 kBq/m3 radon for three days and in the kidneys of mice that inhaled 2 or 20 kBq/m3 radon for one, three or 10 days. The 8-OHdG levels in the small intestine decreased by approximately 20-40% (2 kBq/m3 for three days or 20 kBq/m3 for one, three or 10 days), but there were no significant differences in the 8-OHdG levels between mice that inhaled a sham treatment and those that inhaled radon. There was no significant change in the levels of 8-oxoguanine DNA glycosylase, which plays an important role in DNA repair. However, the level of Mn-superoxide dismutase (SOD) increased by 15-60% and 15-45% in the small intestine and kidney, respectively, following radon inhalation. These results suggest that Mn-SOD probably plays an important role in the inhibition of oxidative DNA damage.

Evaluation of the redox state in mouse organs following radon inhalation.

Radon inhalation activates antioxidative functions in mouse organs, thereby contributing to inhibition of oxidative stress-induced damage. However, the specific redox state of each organ after radon inhalation has not been reported. Therefore, in this study, we evaluated the redox state of various organs in mice following radon inhalation at concentrations of 2 or 20 kBq/m3 for 1, 3 or 10 days. Scatter plots were used to evaluate the relationship between antioxidative function and oxidative stress by principal component analysis (PCA) of data from control mice subjected to sham inhalation. The results of principal component (PC) 1 showed that the liver and kidney had high antioxidant capacity; the results of PC2 showed that the brain, pancreas and stomach had low antioxidant capacities and low lipid peroxide (LPO) content, whereas the lungs, heart, small intestine and large intestine had high LPO content but low antioxidant capacities. Furthermore, using the PCA of each obtained cluster, we observed altered correlation coefficients related to glutathione, hydrogen peroxide and LPO for all groups following radon inhalation. Correlation coefficients related to superoxide dismutase in organs with a low antioxidant capacity were also changed. These findings suggested that radon inhalation could alter the redox state in organs; however, its characteristics were dependent on the total antioxidant capacity of the organs as well as the radon concentration and inhalation time. The insights obtained from this study could be useful for developing therapeutic strategies targeting individual organs.

Dosimetry of inhaled 219Rn progeny.

During prostate cancer treatment with 223Ra. 219Rn (actinon) occurs and may be exhaled by the patient. Nurses and other hospital employees may inhale this radionuclide and its decay products. The alpha-emitting decay products of actinon deposited within a body will irradiate tissues and organs. Therefore. it is necessary to evaluate organ doses of actinon progeny. The purpose of this study is to set up a dosimetric method to assess dose coefficients for actinon progeny. The effective dose coefficients were calculated separately for three modes. The unattached mode which concerned the activity median thermodynamic diameter (AMTD) of 1 nm. and the nucleation and accumulation modes which are represented by activity median aerodynamic diameters (AMAD) of 60 and 500 nm respectively. The recent biokinetic models of actinon progeny developed in the Occupational Intakes of Radionuclides (OIR) publications series of the International Commission of Radiological Protection (ICRP) were implemented on BIOKMOD (Biokinetic Modeling) to calculate the number of nuclear transformations per activity intake of actinon progeny. The organ equivalent and effective dose coefficients were determined using the dosimetric approach of the ICRP. The inhalation dose coefficients of actinon progeny are dominated by the contribution of lung dose. The calculated dose coefficients of 211Pb and 211Bi are 5.78 × 10-8 and 4.84 × 10-9 Sv.Bq-1 for unattached particles (AMTD = 1 nm). and 1.4 × 10-8 and 3.55 × 10-9 Sv.Bq-1 for attached particles (AMAD = 60 nm). and 7.37 × 10-9 and 1.91 × 10-9 Sv.Bq-1 for attached particles (AMAD = 500 nm). These values are much closer to those of the recently published ICRP 137.

Evaluation of radiation dose from radon ingestion and inhalation in groundwater of a small tropical river basin, Kerala, India.

A comprehensive study was conducted to understand the radon (222Rn) distribution and associated radiation doses to the public in a small tropical river basin partly set in the western slope of the Southern Western Ghats of Kerala, India. Radon, though detected in all the 71 monitored wells (0.17-68.3 Bq L-1), exceeded the maximum contamination level (MCL) of 11.1 Bq L-1 for drinking water recommended by United States Environmental Protection Agency (USEPA) in eight samples from isolated pockets of highland, midland and lowland of the Karamana River Basin (KRB) and found to be well within 100 Bq L-1, the parametric value suggested by the World Health Organization (WHO) and the European Union (EU). The age-wise total annual effective doses (AEDs) of groundwater radon activity ranged from 0.5-208.4 µSv a-1 for infants, 0.4-172.2 for children and 0.5-189.7 µSv a-1 for adults. The results reveal that effective doses due to groundwater radon pose no potential public health risk in the study region. Since there is no previous background information on radon-induced radiation dose in the KRB, this work is a newfangled attempt from a public health point of view.

Comparison of antioxidative effects between radon and thoron inhalation in mouse organs.

Radon therapy has been traditionally performed globally for oxidative stress-related diseases. Many researchers have studied the beneficial effects of radon exposure in living organisms. However, the effects of thoron, a radioisotope of radon, have not been fully examined. In this study, we aimed to compare the biological effects of radon and thoron inhalation on mouse organs with a focus on oxidative stress. Male BALB/c mice were randomly divided into 15 groups: sham inhalation, radon inhalation at a dose of 500 Bq/m3 or 2000 Bq/m3, and thoron inhalation at a dose of 500 Bq/m3 or 2000 Bq/m3 were carried out. Immediately after inhalation, mouse tissues were excised for biochemical assays. The results showed a significant increase in superoxide dismutase and total glutathione, and a significant decrease in lipid peroxide following thoron inhalation under several conditions. Additionally, similar effects were observed for different doses and inhalation times between radon and thoron. Our results suggest that thoron inhalation also exerts antioxidative effects against oxidative stress in organs. However, the inhalation conditions should be carefully analyzed because of the differences in physical characteristics between radon and thoron.

Residential Radon and Histological Types of Lung Cancer: A Meta-Analysis of Case‒Control Studies.

Epidemiological studies on residential radon exposure and the risk of histological types of lung cancer have yielded inconsistent results. We conducted a meta-analysis on this topic and updated previous related meta-analyses. We searched the databases of Cochrane Library, Embase, PubMed, Web of Science and Chinese National Knowledge Infrastructure for papers published up to 13 November 2018. The pooled odds ratio (OR) and 95% confidence interval (CI) were calculated using fixed and random effects models. Subgroup and dose‒response analyses were also conducted. This study was registered with PROSPERO (No. CRD42019127761). A total of 28 studies, which included 13,748 lung cancer cases and 23,112 controls, were used for this meta-analysis. The pooled OR indicated that the highest residential radon exposure was significantly associated with an increased risk of lung cancer (OR = 1.48, 95% CI = 1.26-1.73). All histological types of lung cancer were associated with residential radon. Strongest association with small-cell lung carcinoma (OR = 2.03, 95% CI = 1.52-2.71) was found, followed by adenocarcinoma (OR = 1.58, 95% CI = 1.31-1.91), other histological types (OR = 1.54, 95% CI = 1.11-2.15) and squamous cell carcinoma (OR = 1.43, 95% CI = 1.18-1.74). With increasing residential radon levels per 100 Bq/m3, the risk of lung cancer, small-cell lung carcinoma and adenocarcinoma increased by 11%, 19% and 13%, respectively. This meta-analysis provides new evidence for a potential relationship between residential radon and all histological types of lung cancer.

VARIATION SIMULATION OF RADON CONCENTRATION IN THE TISSUES AND ORGANS OF THE BODY BY AN ELECTRICAL CIRCUIT.

In this study, a new model based on electric circuit theory has been introduced to simulate the dynamics of radioactive chemically inert gases in the human body. For this manner, it is assumed that inert gas is transported through the body to various organs via the blood stream. In this simulation, a voltage source is equivalent to gas generation in the atmosphere, the conductivity is equivalent to the cardiac output of the organ, the capacitor capacitance is equivalent to the volume of blood or tissue and voltage across a capacitor is equivalent to the gas concentration in air or blood or a tissue. This simulation can be used to study the dynamics of any inert gas whose partition coefficients are known. We use this simulation to study the dynamics of radon in human body. The physiologically based pharmacokinetic (PBPK) model that describes the fate of radon in systemic tissue has been used for this simulation. Using this simulation, the effective dose equivalent resulting from inhalation of radon has been estimated. The calculated values agree with the previously reported value. Also, using the model, it has been shown that after inhalation of radon gas, absorbed dose has been decreased in different tissues by increasing the inhalation rate without radon. So that, by doubling the inhalation rate and the rate of cardiac output, the value of the absorbed dose has been decreased 11.88% in the adipose tissue, 25.49% in the red marrow tissue and 20.3% in the liver organ.

Impact of radon and combinatory radon/carbon dioxide spa on pain and hypertension: Results from the explorative RAD-ON01 study.

OBJECTIVES: Therapies with low doses of radon have beneficial effects on patients suffering from chronic painful degenerative and inflammatory diseases. We already showed that this is accompanied by systemic immune modulations. We here focus on pain-reducing effects of very low doses of radon by adding carbon dioxide water and its impact on heart rate variability (HRV), blood pressure and free radicals. METHODS: 97 of 103 patients receiving radon spa (1.200 Bq/l at 34 °C or 600 Bq/l, 1 g/l CO2 at 34 °C) were monitored before and at three different time points after therapy. Individual pain perception was analyzed and the capability to process radicals. At each time point, the hypertensive patients (n = 46) were examined over 24 h for blood pressure and HRV. RESULTS: Long-term pain reduction was observed in the majority of patients. A modulation of superoxide dismutase was identified, presumably representing a priming effect for lowering radiation stress. Further, lowering of blood pressure, especially in those patients who additionally received carbon dioxide, was seen. Radon did in particular impact on HRV implying lasting relaxation effects. CONCLUSION: Radon/carbon dioxide spa efficiently reduces pain. In particular, patients simultaneously suffering from painful and cardiovascular diseases should be treated by combination of radon and CO2.

Indoor Radon and Lung Cancer: Estimation of Attributable Risk, Disease Burden, and Effects of Mitigation.

PURPOSE: Exposure to indoor radon is associated with lung cancer. This study aimed to estimate the number of lung cancer deaths attributable to indoor radon exposure, its burden of disease, and the effects of radon mitigation in Korea in 2010. MATERIALS AND METHODS: Lung cancer deaths due to indoor radon exposure were estimated using exposure-response relations reported in previous studies. Years of life lost (YLLs) were calculated to quantify disease burden in relation to premature deaths. Mitigation effects were examined under scenarios in which all homes with indoor radon concentrations above a specified level were remediated below the level. RESULTS: The estimated number of lung cancer deaths attributable to indoor radon exposure ranged from 1946 to 3863, accounting for 12.5-24.7% of 15623 total lung cancer deaths in 2010. YLLs due to premature deaths were estimated at 43140-101855 years (90-212 years per 100000 population). If all homes with radon levels above 148 Bq/m³ are effectively remediated, 502-732 lung cancer deaths and 10972-18479 YLLs could be prevented. CONCLUSION: These findings suggest that indoor radon exposure contributes considerably to lung cancer, and that reducing indoor radon concentration would be helpful for decreasing the disease burden from lung cancer deaths.

Factors Modifying the Radon-Related Lung Cancer Risk at Low Exposures and Exposure Rates among German Uranium Miners.

It is still not fully understood whether and how factors such as time, age and smoking modify the relationship between lung cancer and radon at low exposures and exposure rates. Improved knowledge is necessary for the dose conversion of radon in working level month (WLM) into effective dose, as currently discussed by the International Commission on Radiological Protection (ICRP). An update of the German uranium miner cohort study (n = 58,974 men) with a 10-year extension of mortality follow-up (1946-2013) was used to further examine this issue. Internal Poisson regression was applied to estimate the excess relative risk (ERR) for lung cancer mortality per unit of cumulative radon exposure in WLM with exponential time-related effect modifiers. In the full cohort restricted to <100 WLM the estimated overall ERR/WLM was 0.006 [95% confidence interval (CI): 0.003; 0.010] based on 1,254 lung cancer deaths and 1,620,190 person-years at risk. Both age at and time since exposure turned out to be important modifiers of the ERR/WLM and were included in the final model. Here, the ERR/WLM centered on age at exposure of 30 years, and 20 years since exposure was 0.016 (95% CI: 0.008; 0.028). This value decreased statistically significantly by approximately 40% and 60% for each 10-year increase in age at exposure and time since exposure, respectively. The joint effect of smoking and radon exposure was investigated in the sub-cohort of miners hired in 1960 or later, which includes data on smoking status. The centered ERR/WLM was slightly higher for non/light smokers compared to moderate/heavy smokers (0.022 versus 0.013). The current findings provide evidence for an increased lung cancer risk at low radon exposures or exposure rates that is modified by age and time. The observed risk is lower, but statistically compatible to those of other miner studies at low exposures or exposure rates. These findings reject an additive- and support a sub- to (supra-) multiplicative interaction between smoking and radon.

Radon inhalation induces manganese-superoxide dismutase in mouse brain via nuclear factor-κB activation.

Although radon inhalation increases superoxide dismutase (SOD) activities in mouse organs, the mechanisms and pathways have not yet been fully clarified. The aim of this study was to determine the details of SOD activation in mouse brain tissue following the inhalation of radon at concentrations of 500 or 2000 Bq/m3 for 24 h. After inhalation, brains were removed quickly for analysis. Radon inhalation increased the manganese (Mn)-SOD level and mitochondrial SOD activity. However, the differences were not significant. There were no changes in the Cu/Zn-SOD level or cytosolic SOD activity. Radon inhalation increased the brain nuclear factor (NF)-κB content, which regulates the induction of Mn-SOD, in the nuclear and cytosolic compartments. The level of inhibitor of nuclear factor κB kinase subunit ß (IKK-ß), which activates NF-κB, was slightly increased by radon inhalation. The expression of cytoplasmic ataxia-telangiectasia mutated kinase in mice inhaling radon at 500 Bq/m3 was 50% higher than in control mice. In addition, NF-κB-inducing kinase was slightly increased after inhaling radon at 2000 Bq/m3. These findings suggest that radon inhalation might induce Mn-SOD protein via NF-κB activation that occurs in response to DNA damage and oxidative stress.

Protective effects of hot spring water drinking and radon inhalation on ethanol-induced gastric mucosal injury in mice.

Radon therapy using radon (222Rn) gas is classified into two types of treatment: inhalation of radon gas and drinking water containing radon. Although short- or long-term intake of spa water is effective in increasing gastric mucosal blood flow, and spa water therapy is useful for treating chronic gastritis and gastric ulcer, the underlying mechanisms for and precise effects of radon protection against mucosal injury are unclear. In the present study, we examined the protective effects of hot spring water drinking and radon inhalation on ethanol-induced gastric mucosal injury in mice. Mice inhaled radon at a concentration of 2000 Bq/m3 for 24 h or were provided with hot spring water for 2 weeks. The activity density of 222Rn ranged from 663 Bq/l (start point of supplying) to 100 Bq/l (end point of supplying). Mice were then orally administered ethanol at three concentrations. The ulcer index (UI), an indicator of mucosal injury, increased in response to the administration of ethanol; however, treatment with either radon inhalation or hot spring water inhibited the elevation in the UI due to ethanol. Although no significant differences in antioxidative enzymes were observed between the radon-treated groups and the non-treated control groups, lipid peroxide levels were significantly lower in the stomachs of mice pre-treated with radon or hot spring water. These results suggest that hot spring water drinking and radon inhalation inhibit ethanol-induced gastric mucosal injury.

Ra-226 bioaccumulation and growth indices in fish.

PURPOSE: To determine the accumulated activity of Ra-226 in fathead minnows fed with environmentally relevant levels of Ra-226 for 5 months in water at 20 °C, and to evaluate the influence of this level of Ra-226 on the growth of fathead minnows. METHODS: Fathead minnows were fed with fish food containing 10-10,000 mBq/g Ra-226 for 5 months. At the end of the experiment, the fish were sacrificed, flash frozen in liquid nitrogen and kept at -20 °C. Longitudinal sections of 40 µm thickness were cut at the middle of the fish body using a cryostat. The activity of Ra-226 in each section was determined using autoradiography with a nuclear track detector CR-39. According to the weight and the width of the fish, the activity of Ra-226 in the whole fish body could be estimated. In addition, the length and the weight of the fish were measured and the condition factor was calculated to evaluate the growth and fitness of the fish. RESULTS: There is a positive but non-linear relationship between the accumulated activity of Ra-226 in fish body and the concentration of Ra-226 in fish food. The highest activity of Ra-226 accumulated in fish body was found from fish fed with 10,000 mBq/g Ra-226 food. This was calculated as 256.4 ± 49.1 mBq/g, p < 0.05, and the calculated dose rate was 6.2 ± 1.2 mGy/y. For fish fed with food containing lower concentration of Ra-226 (up to 1000 mBq/g), the bioaccumulation of Ra-226 in the body saturated. The Ra-226 concentration factor (CF) for fish was inversely proportional to the Ra-226 activity in food, and the highest CF value was 2.489, obtained from the lowest dietary Ra-226 activity (10 mBq/g). In addition, condition factors (K) of fish in all Ra-226-treated groups were significantly lower than those of the controls. CONCLUSION: The results show that the bioaccumulation of Ra-226 in fish is not simply related to the dietary Ra-226 activity, and has a saturation value when the dietary activity is low. In addition, the environmental level of Ra-226 in the fish food has a small adverse effect on the growth and fitness of fathead minnows.

Difference in the action mechanism of radon inhalation and radon hot spring water drinking in suppression of hyperuricemia in mice.

Although radon therapy is indicated for hyperuricemia, the underlying mechanisms of action have not yet been elucidated in detail. Therefore, we herein examined the inhibitory effects of radon inhalation and hot spring water drinking on potassium oxonate (PO)-induced hyperuricemia in mice. Mice inhaled radon at a concentration of 2000 Bq/m(3) for 24 h or were given hot spring water for 2 weeks. Mice were then administrated PO at a dose of 500 mg/kg. The results obtained showed that serum uric acid levels were significantly increased by the administration of PO. Radon inhalation or hot spring water drinking significantly inhibited elevations in serum uric acid levels through the suppression of xanthine oxidase activity in the liver. Radon inhalation activated anti-oxidative functions in the liver and kidney. These results suggest that radon inhalation inhibits PO-induced hyperuricemia by activating anti-oxidative functions, while hot spring water drinking may suppress PO-induced elevations in serum uric acid levels through the pharmacological effects of the chemical compositions dissolved in it.

Activation of Antioxidative Functions by Radon Inhalation Enhances the Mitigation Effects of Pregabalin on Chronic Constriction Injury-Induced Neuropathic Pain in Mice.

Radon inhalation brings pain relief for chronic constriction injury- (CCI-) induced neuropathic pain in mice due to the activation of antioxidative functions, which is different from the mechanism of the pregabalin effect. In this study, we assessed whether a combination of radon inhalation and pregabalin administration is more effective against neuropathic pain than radon or pregabalin only. Mice were treated with inhaled radon at a concentration of 1,000 Bq/m(3) for 24 hours and pregabalin administration after CCI surgery. In mice treated with pregabalin at a dose of 3 mg/kg weight, the 50% paw withdrawal threshold of mice treated with pregabalin or radon and pregabalin was significantly increased, suggesting pain relief. The therapeutic effects of radon inhalation or the combined effects of radon and pregabalin (3 mg/kg weight) were almost equivalent to treatment with pregabalin at a dose of 1.4 mg/kg weight or 4.1 mg/kg weight, respectively. Radon inhalation and the combination of radon and pregabalin increased antioxidant associated substances in the paw. The antioxidant substances increased much more in radon inhalation than in pregabalin administration. These findings suggested that the activation of antioxidative functions by radon inhalation enhances the pain relief of pregabalin and that this combined effect is probably an additive effect.

Effective Dose Radon 222 of the Tap Water in Children and Adults People; Minab City, Iran.

(222)Rn is a radioactive, odorless, and colorless element which has a half-life of 3.83 days. One of (222)Rn main resources are Groundwater (wells, springs, etc.). Hence, the use of groundwater with high concentration of (222)Rn can increase the risk of lung and stomach cancers. Concentration of (222)Rn in tap water of Minab city in two temperatures 5 and 15 ºC was measured by radon meter model RTM1668-2. The effective dose was calculated by equations proposed by UNSCEAR. Geometric mean concentration of (222)Rn in drinking water was found to be 0.78±0.06 and 0.46±0.04 Bq/l at 5 and 15 ̊C (p value<0.05), respectively. The effective doses were 0.006 and 0.003 mSv/y for adults, and 0.011 and 0.007 mSv/y for the children, respectively (p value<0.05). Besides, the effective dose for adult through inhaling (222)Rn at 5 and 15 ̊C were estimated 0.0021 and 0.0012mSv/y, respectively. Geometric mean concentration in (222)Rn drinking water and effective dose received from drinking water and inhalation of (222)Rn is lower than WHO and EPA standard limits. Increasing temperature of drinking water will decrease the effective dose received. Annual Effective dose received from inhalation and consumption of (222)Rn in drinking water in children is more than adults.

Analyses of local dose distributions in the lungs for the determination of risk apportionment factors.

For radiation protection purposes, the relative contributions of bronchial (BB), bronchiolar (bb) and alveolar-interstitial (AI) doses to lung cancer risk are represented by their corresponding apportionment factors. The current assumption of equal apportionment factors can be tested by comparing different radon and thoron progeny exposures, which produce different regional dose distributions, with the pathologically observed regional cancer distributions: (1) radon progeny inhalation, (2) thoron progeny inhalation, (3) thoron and thoron progeny exhalation (Thorotrast patients) and (4) RP inhalation in rats, and cigarette smoke inhalation as smoking is the dominant cause of lung cancer. Comparison with the pathologically observed regional cancer distributions suggests (1) a smaller apportionment factor for the AI region as compared with BB and bb regions and (2) a higher value for the BB region relative to that for the bb region.

Measuring the activity of inhaled ²²²Rn using a lung counting system.

A new method of directly measuring (222)Rn progeny in a worker's lung using a lung counting system is introduced. To determine the efficiency of the lung counting system, a torso phantom manufactured by the China Institute for Radiation Protection was used, where activated carbon that had been loaded in a radon chamber with a defined quantity of radon represented the lungs, which were usually made of urethane foam. The minimum detectable activity (MDA) of (214)Bi, one of the (222)Rn progenies, was estimated to be 7.3 Bq for a measurement time of 4000 s. Based on the time (222)Rn progenies stay in the lung, it may be concluded that the lung counting system described can be well used for directly measuring the activity of (214)Bi in the lung short time after a worker inhaled (222)Rn at his/her workplace.

Radon inhalation protects against transient global cerebral ischemic injury in gerbils.

Although brain disorders are not the main indication for radon therapy, our previous study suggested that radon inhalation therapy might mitigate brain disorders. In this study, we assessed whether radon inhalation protects against transient global cerebral ischemic injury in gerbils. Gerbils were treated with inhaled radon at a concentration of 2,000 Bq/m(3) for 24 h. After radon inhalation, transient global cerebral ischemia was induced by bilateral occlusion of the common carotid artery. Results showed that transient global cerebral ischemia induced neuronal damage in hippocampal CA1, and the number of damaged neurons was significantly increased compared with control. However, radon treatment inhibited ischemic damage. Superoxide dismutase (SOD) activity in the radon-treated gerbil brain was significantly higher than that in sham-operated gerbils. These findings suggested that radon inhalation activates antioxidative function, especially SOD, thereby inhibiting transient global cerebral ischemic injury in gerbils.