Radiation-induced formation of purine 5′,8-cyclonucleosides in isolated and cellular DNA: high stereospecificity and modulating effect of oxygen

2010 ◽  
Vol 8 (14) ◽  
pp. 3211 ◽  
Author(s):  
Nourreddine Belmadoui ◽  
Fabien Boussicault ◽  
Maurizio Guerra ◽  
Jean-Luc Ravanat ◽  
Chryssostomos Chatgilialoglu ◽  
...  
2005 ◽  
Vol 72 (2-3) ◽  
pp. 293-299 ◽  
Author(s):  
Jean Cadet ◽  
Thierry Douki ◽  
Didier Gasparutto ◽  
Jean-Luc Ravanat

1999 ◽  
Vol 152 (2) ◽  
pp. 144 ◽  
Author(s):  
Annamarie D. Horan ◽  
Albert R. Giandomenico ◽  
Cameron J. Koch

1956 ◽  
Vol 52 (0) ◽  
pp. 311-320 ◽  
Author(s):  
P. J. Berry ◽  
S. Lipsky ◽  
M. Burton

2014 ◽  
Vol 9 (9) ◽  
pp. 1934578X1400900
Author(s):  
Hyung-In Moon ◽  
Min Ho Jeong ◽  
Wol Soon Jo

Radiotherapy is an important form of treatment for a wide range of cancers, but it can damage DNA and cause adverse effects. We investigated if the diplacone analogs of P. tomentosa were radio-protective in a human lymphoblastoid cell line (AHH-1). Four geranylated flavonoids, diplacone, 3′- O-methyl-5′-hydroxydiplacone, 3′- O-methyl-5′- O-methyldiplacone and 3′- O-methyldiplacol, were tested for their antioxidant and radio-protective effects. Diplacone analogs effectively scavenged free radicals and inhibited radiation-induced DNA strand breaks in vitro. They significantly decreased levels of reactive oxygen species and cellular DNA damage in 2 Gy-irradiated AHH-1 cells. Glutathione levels and superoxide dismutase activity in irradiated AHH-1 cells increased significantly after treatment with these analogs. The enhanced biological anti-oxidant activity and radioprotective activity of diplacone analogs maintained the survival of irradiated AHH-1 cells in a clonogenic assay. These data suggest that diplacone analogs may protect healthy tissue surrounding tumor cells during radiotherapy to ensure better control of radiotherapy and allow higher doses of radiotherapy to be employed.


2019 ◽  
Vol 11 (4) ◽  
pp. 4514-4522 ◽  
Author(s):  
Ryan T. Frederick ◽  
J. Trey Diulus ◽  
Danielle C. Hutchison ◽  
May Nyman ◽  
Gregory S. Herman

1969 ◽  
Vol 13 (12) ◽  
pp. 2705-2719 ◽  
Author(s):  
Jitsuo Tsurugi ◽  
Tsugio Fukumoto ◽  
Masayuki Yamagami

1967 ◽  
Vol 5 (11) ◽  
pp. 2731-2743 ◽  
Author(s):  
Hiroshi Mitsui ◽  
Sueo Machi ◽  
Miyuki Hagiwara ◽  
Fumio Hosoi ◽  
Tsutomu Kagiya

1959 ◽  
Vol 37 (6) ◽  
pp. 1061-1066 ◽  
Author(s):  
W. F. Baldwin ◽  
T. N. Salthouse

The latent effects of X irradiation in delaying mitosis are readily observable in the epidermis of the insect Rhodnius owing to the degree of synchrony of division in these cells following a blood meal. At the dose employed in these studies, mitosis did not proceed beyond metaphase when the insects were exposed in air; after irradiation at the same dose in nitrogen, a prolonged division was completed with the greater part of the inhibition occurring during metaphase.


2011 ◽  
Vol 39 (01) ◽  
pp. 161-170 ◽  
Author(s):  
Ki Cheon Kim ◽  
In Kyung Lee ◽  
Kyoung Ah Kang ◽  
Bum Joon Kim ◽  
Daeshin Kim ◽  
...  

The ethylacetate fraction of Empetrum nigrum var. japonicum (ENE) was shown to reduce intracellular reactive oxygen species (ROS) generated by γ-radiation and activate antioxidant enzymes, such as superoxide dismutase (SOD), catalase (CAT), and gluthathion peroxidase (GPx). ENE protected cells against radiation-induced cellular DNA damage, membrane lipid peroxidation, and protein modification, which are the main points of radiation-induced damage. In addition, ENE recovered cell viability by inhibiting apoptosis after cells were treated with radiation. ENE treatment also reduced γ-radiation induced Bax, and caspase 9 and 3 expression in irradiated cells. However, irradiated cells with ENE recovered Bcl-2 expression, which was reduced by radiation. This anti-apoptotic effect of ENE was due to the inhibition of mitogen-activated protein kinase kinase-4 (MKK4/SEK1)-c-Jun NH2-terminal kinase (JNK) cascades induced by γ-radiation. In summary, these results suggest that ENE protects cells against γ-radiation-induced oxidative stress via the reduction of ROS and attenuation of apoptosis.


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