Page 277 - 2014 Printable Abstract Book
P. 277
treatment, indicating that the combination treatment induced the positive crosstalk between Nrf2 and
EGFR. TGF-β and hypoxia increased ROS accumulation and N-acetyl-L-cysteine (NAC) treatment abolished
Nrf2-EGFR activation. Our findings suggest that TGF-β and hypoxia/reoxygenation promote tumor
progression and radioresistance of lung cancer cells through ROS-mediated Nrf2-EGFR activation.
(PS4-72) Protective effects of radon inhalation on transient global cerebral ischemic injury in gerbils.
Takahiro Kataoka; Reo Etani; Yuji Takata; Atsushi Kawabe; Katsumi Hanamoto; Takehito Taguchi; and
Kiyonori Yamaoka, Okayama University, Okayama, Japan
3
Radon therapy (radon concentration; 2000 Bq/m ) is performed at Misasa Medical Center,
Okayama University Hospital. Most conditions treated with radon therapy are pain- or respiratory-related
diseases, such as osteoarthritis and bronchial asthma. 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 2000
3
Bq/m for 24 hours. After radon inhalation, transient global cerebral ischemia was induced by bilateral
occlusion of the common carotid artery. Gerbils were injected intraperitoneally with 50 mg/kg
pentobarbital. A midline incision was made, and the both CCAs were exposed and occluded with clips for
10 min, after which the clips were removed. Results showed that transient global cerebral ischemia
induced neuronal damage in the CA1, and the number of damaged neurons was significantly increased
compared with control. However, the number of damaged neurons of radon-treated gerbils was
significantly lower than ischemic gerbils. In contrast, radon inhalation did not affect neurons in the CA1.
Transient global cerebral ischemia with or without radon inhalation significantly decreased superoxide
dismutase (SOD) activity in serum. However, brain SOD activity in radon-treated gerbils was significantly
higher than in ischemic gerbils. These findings suggested that radon inhalation activates antioxidative
functions and inhibits transient global cerebral ischemic injury in gerbils. The results of this study provide
evidence that radon offers neuroprotective effects against neuronal damage due to cerebral ischemia.
(PS4-73) Propagation of stressful effects from irradiated tumors to bystander normal stem cells. Neha
Sharma, MSc; Sonia de Toledo, Ph.D; and Edouard Azzam, Ph.D, Rutgers University, Newark, NJ
Biological changes induced in normal human cells by therapeutic or accidental exposures to
ionizing radiation can cause degenerative effects and lead to the emergence of primary or secondary
cancers. Though changes in irradiated cells contribute to these outcomes, there is evidence that
irradiation has profound and similar deleterious effects on nearby non-irradiated (”bystander”) cells,
including stem cells, which could also play a major role in post-exposure pathologies.We have investigated
the induction of stress markers in bystander normal neural stem cells (NSCs; H9 cells) that were incubated
in growth medium harvested from irradiated or sham-treated glioma cells (T98G or U87 cells).
Immunoblot analyses showed that NSCs incubated for 24h in medium harvested from T98G cells exposed
to 0 or 12 Gy of cesium-137 γ rays (3 Gy/min), 72h earlier, upregulate the level of stress-sensitive FOXO3a
and p27Kip1. These changes were associated with an increase in the level of P-p53Ser15, a marker of DNA
damage, and with DNA fragmentation. Similar results were observed in NSCs intimately cocultured with
glioma cells in Transwell inserts. Notably, preliminary results indicated that regulation of stress-responsive
275 | P a g e
EGFR. TGF-β and hypoxia increased ROS accumulation and N-acetyl-L-cysteine (NAC) treatment abolished
Nrf2-EGFR activation. Our findings suggest that TGF-β and hypoxia/reoxygenation promote tumor
progression and radioresistance of lung cancer cells through ROS-mediated Nrf2-EGFR activation.
(PS4-72) Protective effects of radon inhalation on transient global cerebral ischemic injury in gerbils.
Takahiro Kataoka; Reo Etani; Yuji Takata; Atsushi Kawabe; Katsumi Hanamoto; Takehito Taguchi; and
Kiyonori Yamaoka, Okayama University, Okayama, Japan
3
Radon therapy (radon concentration; 2000 Bq/m ) is performed at Misasa Medical Center,
Okayama University Hospital. Most conditions treated with radon therapy are pain- or respiratory-related
diseases, such as osteoarthritis and bronchial asthma. 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 2000
3
Bq/m for 24 hours. After radon inhalation, transient global cerebral ischemia was induced by bilateral
occlusion of the common carotid artery. Gerbils were injected intraperitoneally with 50 mg/kg
pentobarbital. A midline incision was made, and the both CCAs were exposed and occluded with clips for
10 min, after which the clips were removed. Results showed that transient global cerebral ischemia
induced neuronal damage in the CA1, and the number of damaged neurons was significantly increased
compared with control. However, the number of damaged neurons of radon-treated gerbils was
significantly lower than ischemic gerbils. In contrast, radon inhalation did not affect neurons in the CA1.
Transient global cerebral ischemia with or without radon inhalation significantly decreased superoxide
dismutase (SOD) activity in serum. However, brain SOD activity in radon-treated gerbils was significantly
higher than in ischemic gerbils. These findings suggested that radon inhalation activates antioxidative
functions and inhibits transient global cerebral ischemic injury in gerbils. The results of this study provide
evidence that radon offers neuroprotective effects against neuronal damage due to cerebral ischemia.
(PS4-73) Propagation of stressful effects from irradiated tumors to bystander normal stem cells. Neha
Sharma, MSc; Sonia de Toledo, Ph.D; and Edouard Azzam, Ph.D, Rutgers University, Newark, NJ
Biological changes induced in normal human cells by therapeutic or accidental exposures to
ionizing radiation can cause degenerative effects and lead to the emergence of primary or secondary
cancers. Though changes in irradiated cells contribute to these outcomes, there is evidence that
irradiation has profound and similar deleterious effects on nearby non-irradiated (”bystander”) cells,
including stem cells, which could also play a major role in post-exposure pathologies.We have investigated
the induction of stress markers in bystander normal neural stem cells (NSCs; H9 cells) that were incubated
in growth medium harvested from irradiated or sham-treated glioma cells (T98G or U87 cells).
Immunoblot analyses showed that NSCs incubated for 24h in medium harvested from T98G cells exposed
to 0 or 12 Gy of cesium-137 γ rays (3 Gy/min), 72h earlier, upregulate the level of stress-sensitive FOXO3a
and p27Kip1. These changes were associated with an increase in the level of P-p53Ser15, a marker of DNA
damage, and with DNA fragmentation. Similar results were observed in NSCs intimately cocultured with
glioma cells in Transwell inserts. Notably, preliminary results indicated that regulation of stress-responsive
275 | P a g e
