Radiation-Induced Oxidative DNA Base Damage and Its Repair in Nuclear Matrix-Associated DNA and in Bulk DNA in Hepatic Chromatin of Rat Upon Whole-Body γ-Irradiation

1997 ◽  
Vol 22 (1-2) ◽  
pp. 101-107 ◽  
Author(s):  
Tomasz H Zastawny ◽  
Beata Czerwińska ◽  
Barbara Drzewiecka ◽  
Ryszard Oliński
1996 ◽  
Vol 43 (3) ◽  
pp. 579-582 ◽  
Author(s):  
T H Zastawny ◽  
B Czerwińska ◽  
B Drzewiecka ◽  
R Oliński

The amount of all bases, except for 5,6-dihydroxyuracil were significantly increased in rat DNA upon cobalt-60 gamma-irradiation. Control values were recovered 12 h after irradiation. The extent of DNA damage and repair was different for particular bases.


1999 ◽  
Vol 151 (5) ◽  
pp. 550 ◽  
Author(s):  
Judit P. Banáth ◽  
Susan S. Wallace ◽  
Jennifer Thompson ◽  
Peggy L. Olive ◽  
Judit P. Banath

Dose-Response ◽  
2017 ◽  
Vol 15 (2) ◽  
pp. 155932581770569 ◽  
Author(s):  
Farideh Koohian ◽  
Ahmad Shanei ◽  
Daryoush Shahbazi-Gahrouei ◽  
Seyed Hossein Hejazi ◽  
Mohammad-Taghi Moradi

In this study, we evaluated whether the protective potential of resveratrol (RSV; 3,5,4′-trihydroxy-trans-stilbene) against γ-radiation caused damages in peripheral blood lymphocyte of mice. Resveratrol as a polyphenolic compound scavenges free radicals. Various doses of RSV were administered intraperitoneally 2 hours to adult male mice before a single dose of whole-body γ-irradiation (2 Gy). To assess the protective ability of RSV, the alkaline comet assay in blood lymphocyte of mice was performed and the total comet score was evaluated. The results of the alkaline comet assay showed that RSV significantly inhibited radiation-induced DNA damage. We observed that RSV protects blood lymphocyte against radiation-induced damage in mice.


2002 ◽  
Vol 167 (suppl_1) ◽  
pp. 2-4
Author(s):  
James Z. Xing ◽  
Jane Lee ◽  
Steven A. Leadon ◽  
X. Chris Le ◽  
Michael Weinfeld

2008 ◽  
pp. 753-760
Author(s):  
D Driák ◽  
J Österreicher ◽  
Z Řeháková ◽  
Z Vilasová ◽  
J Vávrová

Gastrointestinal form is the second stage of acute radiation syndrome (ARS) with a threshold dose of 8 Gy in man. It represents an absolutely lethal clinical-pathological unit, necrohemorrhagic enteritis and proctocolitis, with unknown causal therapy. Elk-1 is a protein acting as a transcription factor activating specified genes. The purpose of our study was to examine the expression of phospho-Elk-1 in irradiated jejunum and transversal colon of rats with radiation-induced enterocolitis and to assess the importance of this transcriptional factor as a biodosimetric marker of radiation-induced enteropathy. The laboratory rats were randomly divided into 21 groups, 10 animals per group, and irradiated with whole body γ-irradiation of 1, 5, 10, 15, and 20 Gy. Samples of jejunum and transversal colon were taken 24, 48, 72, and 96 hours later, immunohistochemically stained, and the phospho-Elk-1 expression was examined using computer image analysis. A group of 10 shamirradiated animals was used as control. Significantly increased expression of phospho-Elk-1 in rat jejunum has been found in all time intervals after irradiation by sublethal doses of 1 and 5 Gy, whereas after the irradiation by lethal doses, the expression of phospho-Elk-1 in rat jejunum varied considerably. Significantly increased expression of phospho-Elk-1 in transversal colon has also been found in the first days after irradiation by sublethal doses of 1 and 5 Gy. After irradiation by lethal doses, tere was no uniform pattern of the changes in the expression of phospho-Elk1 in rat transversal colon. The detection of phospho-Elk-1 might be considered as a suitable and very sensitive biodosimetric marker of radiation-induced injury of small and large intestine. According to our knowledge, this is the first study on the phospho-Elk-1 expression in irradiated jejunum and transversal colon in the rat.


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