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

The effect of pCO2 on size-fractionated phytoplankton community in the Southern Ocean

第3回極域科学シンポジウム　横断セッション「南極海季節的海氷域における生物地球化学」11月26日（月） 統計数理研究所 セミナー

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

Insulin-like growth factor binding protein-3 has dual effects on gastrointestinal stromal tumor cell viability and sensitivity to the anti-tumor effects of imatinib mesylate in vitro

<p>Abstract</p> <p>Background</p> <p>Imatinib mesylate has significantly improved survival and quality of life of patients with gastrointestinal stromal tumors (GISTs). However, the molecular mechanism through which imatinib exerts its anti-tumor effects is not clear. Previously, we found up-regulation of insulin-like growth factor binding protein-3 (IGFBP3) expression in imatinib-responsive GIST cells and tumor samples. Because IGFBP3 regulates cell proliferation and survival and mediates the anti-tumor effects of a number of anti-cancer agents through both IGF-dependent and IGF-independent mechanisms, we hypothesized that IGFBP3 mediates GIST cell response to imatinib. To test this hypothesis, we manipulated IGFBP3 levels in two imatinib-responsive GIST cell lines and observed cell viability after drug treatment.</p> <p>Results</p> <p>In the GIST882 cell line, imatinib treatment induced endogenous IGFBP3 expression, and IGFBP3 down-modulation by neutralization or RNA interference resulted in partial resistance to imatinib. In contrast, IGFBP3 overexpression in GIST-T1, which had no detectable endogenous IGFBP3 expression after imatinib, had no effect on imatinib-induced loss of viability. Furthermore, both the loss of IGFBP3 in GIST882 cells and the overexpression of IGFBP3 in GIST-T1 cells was cytotoxic, demonstrating that IGFBP3 has opposing effects on GIST cell viability.</p> <p>Conclusion</p> <p>This data demonstrates that IGFBP3 has dual, opposing roles in modulating GIST cell viability and response to imatinib <it>in vitro</it>. These preliminary findings suggest that there may be some clinical benefits to IGFBP3 therapy in GIST patients, but further studies are needed to better characterize the functions of IGFBP3 in GIST.</p

No Different Sensitivity in Terms of Whole-Body Irradiation between Normal and Acatalasemic Mice

To elucidate the radiosensitivity of an acatalasemic mouse, we examined the time and dose-dependency in the survival rates, the lymphocytes and the intestinal epithelial cells, and the antioxidant function after 3.0 to 12.0 Gy whole body irradiation. Results showed that no significant differences between acatalasemic mice and normal mice were observed in the survival rates and the histological changes in spleens and small intestine after each irradiation. The catalase activities in livers and spleens of acatalasemic mice were significantly lower than those of normal mice and the glutathione peroxidase activity in livers of acatalasemic mice was significantly higher than that of normal mice. At 10 days after 6.0 Gy irradiation, the catalase activities in livers of acatalasemic and normal mice and that in spleens of normal mice significantly decreased compared with no-irradiation control, and there were no differences between those catalase activities. The total glutathione content in acatalasemic mice was significantly higher than that in normal mice at 10 days after 6.0 Gy irradiation. These findings suggested that the radiosensitivity of acatalasemic mice in terms of whole body irradiation doesn’t significantly differ from that of normal mice, probably due to compensated sufficient contents of glutathione peroxidase and total glutathione in acatalasemic mice