Induction and Repair of DNA DSB as Revealed by H2AX Phosphorylation Foci in Human Fibroblasts Exposed to Low- and High-LET Radiation: Relationship with Early and Delayed Reproductive Cell Death

2015 ◽  
Vol 183 (4) ◽  
pp. 417-431 ◽  
Author(s):  
F. Antonelli ◽  
A. Campa ◽  
G. Esposito ◽  
P. Giardullo ◽  
M. Belli ◽  
...  
Keyword(s):  
Cell Death ◽  
Human Fibroblasts ◽  
H2ax Phosphorylation ◽  
Reproductive Cell ◽  
High Let Radiation ◽  
High Let ◽  
Reproductive Cell Death

High yields of isochromatid breaks and successive formation of chromosome exchanges may lead to reproductive cell death following high-LET irradiation

2008 ◽  
Vol 3 (2) ◽  
pp. 121-133
Author(s):  
Eisuke Gotoh ◽  
Aya Funada ◽  
Mayumi Mohri ◽  
Ryonfa Lee ◽  
Kaoru Takakura
Keyword(s):  
Cell Death ◽  
Charged Particle ◽  
Chromosomal Aberrations ◽  
High Energy ◽  
Carbon Ions ◽  
Particle Radiation ◽  
Subsequent Formation ◽  
Reproductive Cell ◽  
High Let ◽  
Reproductive Cell Death

AbstractTo clarify the relationship between cell death and chromosomal aberrations following exposure to heavy-charged ion particles beams, exponentially growing Human Salivary Gland Tumor cells (HSG cells) were irradiated with various kinds of high energy heavy ions; 13 keV/μm carbon ions as a low-LET charged particle radiation source, 120 keV/μm carbon ions and 440 keV/μm iron ions as high-LET charged particle radiation sources. X-rays (200 kVp) were used as a reference. Reproductive cell death was evaluated by clonogenic assays, and the chromatid aberrations in G2/M phase and their repairing kinetics were analyzed by the calyculin A induced premature chromosome condensation (PCC) method. High-LET heavy-ion beams introduced much more severe and un-repairable chromatid breaks and isochromatid breaks in HSG cells than low-LET irradiation. In addition, the continuous increase of exchange aberrations after irradiation occurred in the high-LET irradiated cells. The cell death, initial production of isochromatid breaks and subsequent formation of chromosome exchange seemed to be depend similarly on LET with a maximum RBE peak around 100–200 keV/μm of LET value. Conversely, un-rejoined isochromatid breaks or chromatid breaks/gaps seemed to be less effective in reproductive cell death. These results suggest that the continuous yield of chromosome exchange aberrations induced by high-LET ionizing particles is a possible reason for the high RBE for cell death following high-LET irradiation, alongside other chromosomal aberrations additively or synergistically.

scholarly journals The complexity of clustered DNA DSBs in human fibroblasts under the action of low and high-LET radiation

2021 ◽  
Author(s):  
Daria D. Shamina ◽  
Alla V. Boreyko ◽  
Mariia G. Zadneprianetc ◽  
Tatiana S. Hramco ◽  
Marina E. Krupnova ◽  
...  
Keyword(s):  
Human Fibroblasts ◽  
Dna Dsbs ◽  
High Let Radiation ◽  
High Let

scholarly journals Protective Effects of p53 Regulatory Agents Against High-LET Radiation-Induced Injury in Mice

2020 ◽  
Vol 8 ◽  
Author(s):  
Akinori Morita ◽  
Bing Wang ◽  
Kaoru Tanaka ◽  
Takanori Katsube ◽  
Masahiro Murakami ◽  
...  
Keyword(s):  
Cell Death ◽  
Radiation Injury ◽  
Ion Irradiation ◽  
Heavy Ion ◽  
Protective Effects ◽  
Iron Ion ◽  
Normal Tissues ◽  
High Let Radiation ◽  
High Let ◽  
Radiation Induced

Radiation damage to normal tissues is one of the most serious concerns in radiation therapy, and the tolerance dose of the normal tissues limits the therapeutic dose to the patients. p53 is well known as a transcription factor closely associated with radiation-induced cell death. We recently demonstrated the protective effects of several p53 regulatory agents against low-LET X- or γ-ray-induced damage. Although it was reported that high-LET heavy ion radiation (>85 keV/μm) could cause p53-independent cell death in some cancer cell lines, whether there is any radioprotective effect of the p53 regulatory agents against the high-LET radiation injury in vivo is still unclear. In the present study, we verified the efficacy of these agents on bone marrow and intestinal damages induced by high-LET heavy-ion irradiation in mice. We used a carbon-beam (14 keV/μm) that was shown to induce a p53-dependent effect and an iron-beam (189 keV/μm) that was shown to induce a p53-independent effect in a previous study. Vanadate significantly improved 60-day survival rate in mice treated with total-body carbon-ion (p < 0.0001) or iron-ion (p < 0.05) irradiation, indicating its effective protection of the hematopoietic system from radiation injury after high-LET irradiation over 85 keV/μm. 5CHQ also significantly increased the survival rate after abdominal carbon-ion (p < 0.02), but not iron-ion irradiation, suggesting the moderate relief of the intestinal damage. These results demonstrated the effectiveness of p53 regulators on acute radiation syndrome induced by high-LET radiation.

scholarly journals Ionizing Radiation Induces Delayed Hyperrecombination in Mammalian Cells

2004 ◽  
Vol 24 (11) ◽  
pp. 5060-5068 ◽  
Author(s):  
Lei Huang ◽  
Suzanne Grim ◽  
Leslie E. Smith ◽  
Perry M. Kim ◽  
Jac A. Nickoloff ◽  
...  
Keyword(s):  
Cell Death ◽  
Ionizing Radiation ◽  
Genomic Instability ◽  
Mammalian Cells ◽  
Chromosomal Instability ◽  
Radiation Risk ◽  
Green Fluorescence Protein ◽  
Initial Exposure ◽  
Reproductive Cell ◽  
Reproductive Cell Death

ABSTRACT Exposure to ionizing radiation can result in delayed effects that can be detected in the progeny of an irradiated cell multiple generations after the initial exposure. These effects are described under the rubric of radiation-induced genomic instability and encompass multiple genotoxic endpoints. We have developed a green fluorescence protein (GFP)-based assay and demonstrated that ionizing radiation induces genomic instability in human RKO-derived cells and in human hamster hybrid GM10115 cells, manifested as increased homologous recombination (HR). Up to 10% of cells cultured after irradiation produce mixed GFP+/− colonies indicative of delayed HR or, in the case of RKO-derived cells, mutation and deletion. Consistent with prior studies, delayed chromosomal instability correlated with delayed reproductive cell death. In contrast, cells displaying delayed HR showed no evidence of delayed reproductive cell death, and there was no correlation between delayed chromosomal instability and delayed HR, indicating that these forms of genome instability arise by distinct mechanisms. Because delayed hyperrecombination can be induced at doses of ionizing radiation that are not associated with significantly reduced cell viability, these data may have important implications for assessment of radiation risk and understanding the mechanisms of radiation carcinogenesis.

scholarly journals A Caenorhabditis elegans tissue model of radiation-induced reproductive cell death

2006 ◽  
Vol 103 (26) ◽  
pp. 9946-9951 ◽  
Author(s):  
J. B. Weidhaas ◽  
D. M. Eisenmann ◽  
J. M. Holub ◽  
S. V. Nallur
Keyword(s):  
Cell Death ◽  
Caenorhabditis Elegans ◽  
Tissue Model ◽  
Reproductive Cell ◽  
Radiation Induced ◽  
Reproductive Cell Death

scholarly journals High LET Radiation Enhances Nocodazole Induced Cell Death in HeLa Cells through Mitotic Catastrophe and Apoptosis

2011 ◽  
Vol 52 (4) ◽  
pp. 481-489 ◽  
Author(s):  
Ping LI ◽  
Libin ZHOU ◽  
Zhongying DAI ◽  
Xiaodong JIN ◽  
Xinguo LIU ◽  
...  
Keyword(s):  
Cell Death ◽  
Hela Cells ◽  
Mitotic Catastrophe ◽  
High Let Radiation ◽  
High Let
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