Contributions of the Direct and Indirect Effects of Ionizing Radiation to Reproductive Cell Death

1992 ◽  
Vol 129 (2) ◽  
pp. 228 ◽  
Author(s):  
Yu. N. Korystov
Keyword(s):  
Cell Death ◽  
Ionizing Radiation ◽  
Indirect Effects ◽  
Direct And Indirect Effects ◽  
Reproductive Cell ◽  
Reproductive Cell Death

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

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.

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