Effect of Hydration on the Induction of Strand Breaks and Base Lesions in Plasmid DNA Films by γ-Radiation

2002 ◽  
Vol 124 (30) ◽  
pp. 8859-8866 ◽  
Author(s):  
Akinari Yokoya ◽  
Siobhan M. T. Cunniffe ◽  
Peter O'Neill
2012 ◽  
Vol 177 (5) ◽  
pp. 614-627 ◽  
Author(s):  
Takeshi Ushigome ◽  
Naoya Shikazono ◽  
Kentaro Fujii ◽  
Ritsuko Watanabe ◽  
Masao Suzuki ◽  
...  

2008 ◽  
Vol 84 (1) ◽  
pp. 23-33 ◽  
Author(s):  
Ayumi Urushibara ◽  
Naoya Shikazono ◽  
Peter O'Neill ◽  
Kentaro Fujii ◽  
Seiichi Wada ◽  
...  

2009 ◽  
Vol 172 (3) ◽  
pp. 296-305 ◽  
Author(s):  
Akinari Yokoya ◽  
Siobhan M. T. Cunniffe ◽  
Ritsuko Watanabe ◽  
Katsumi Kobayashi ◽  
Peter O'Neill

2012 ◽  
Vol 2012 ◽  
pp. 1-6
Author(s):  
R. A. S. Silva ◽  
J. D. T. Arruda-Neto ◽  
L. Nieto

Breaks in DNA, resulting in fragmented parts, can be produced by ionizing radiation which, in turn, is the starting point in the search for novel physical aspects of DNA strands. Double-strand breaks in particular cause disruption of the DNA strand, splitting it into several fragments. In order to study effects produced by radiation in plasmid DNA, a new simple mechanical model for this molecule is proposed. In this model, a Morse-like potential and a high-LET component are used to describe the DNA-radiation interaction. Two power laws, used to fit results of the model, suggest that, firstly, distribution of fragment size is nonextensive and, secondly, that a transition phase is present in the DNA fragment distribution pattern.


2013 ◽  
Vol 98 (10) ◽  
pp. E1645-E1654 ◽  
Author(s):  
Soetkin Versteyhe ◽  
Natacha Driessens ◽  
Chiraz Ghaddhab ◽  
Maxime Tarabichi ◽  
Candice Hoste ◽  
...  

Abstract Context: Radiation is an established cause of thyroid cancer, and growing evidence supports a role for hydrogen peroxide (H2O2) in spontaneous thyroid carcinogenesis. Little is known about the molecular programs activated by these agents in thyrocytes. Objective: The purpose of this study was to compare the responses of thyrocytes and T cells to H2O2 and radiation. Methods: We profiled the DNA damage and cell death induced by γ-radiation (0.1–5 Gy) and H2O2 (0.0025–0.3 mM) in primary human thyrocytes and T cells. We next prepared thyroid and T-cell primary cultures from 8 donors operated for noncancerous thyroid pathological conditions and profiled their genome-wide transcriptional response 4 hours after (1) exposure to 1-Gy radiation, (2) treatment with H2O2 and (3) no treatment. Two H2O2 concentrations were investigated, calibrated in each cell type to elicit levels of single- and double-strand breaks equivalent to 1-Gy γ-radiation. Results: Although thyrocytes and T cells had comparable radiation responses, 3- to 10-fold more H2O2 was needed to induce detectable DNA damage in thyrocytes. At H2O2 and radiation doses inducing double-strand breaks, cell death occurred after 24 hours in T cells but not in thyrocytes. The transcriptional responses of thyrocytes and T cells to radiation were similar, involving DNA repair and cell death genes. In addition to this transcriptional program, H2O2 also up-regulated antioxidant genes in thyrocytes, including glutathione peroxidases and heme oxygenase at the double-strand breaks–inducing concentration. In contrast, a transcriptional storm involving thousands of genes was raised in T cells. Finally, we showed that inhibiting glutathione peroxidases activity increased the DNA damaging effect of H2O2 in thyrocytes. Conclusion: We propose that high H2O2 production in thyrocytes is matched with specific transcriptionally regulated antioxidant protection.


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