Let dependence of cell death, mutation induction and chromatin damage in human cells irradiated with accelerated carbon ions

Suzuki, Masao; Watanabe, Masami; Kanai, Tatsuaki; Kase, Yoko; Yatagai, Fumio; Kato, Tadahiro; Matsubara, Sho

doi:10.1016/0273-1177(95)00799-k

Cited by 68 publications

(61 citation statements)

References 26 publications

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“…Accordingly, high-and low-LET irradiation sources may produce qualitatively and This result almost coincides with previous studies on the same HSG cells [51]. In the other studies using different cell lines and different irradiation sources, the LET dependence of cell death was reported to have a sharp increase or a peak in LET range of 100 -120 keV/ mm C-ion irradiation [21] or 120 -300 keV/mm Ne-ion irradiation [52], which also seemed in accordance with the present study. Compared to the LET-dependence of the cell death with that of the chromosomal aberrations, the LET-dependence of the exchange formation after 12 hours irradiation is fairly similar to that of cell death, but less similarity of LET-dependence of isochromatid breaks or breaks/gaps at after 12 hours irradiation was obtained (shown in Figure 7b).…”

Section: Discussionsupporting

confidence: 90%

“…Several studies have reported the relationship between cell death and chromatin breaks using high-LET irradiation [21,[52][53][54]. In these studies, un-rejoined chromatin breaks following irradiation showed a strong correlation to the cell death.…”

Section: Discussionmentioning

confidence: 99%

“…However, few studies have been published on the relationship between cell death and chromosomal aberrations [18][19][20][21]. In this study, we used a unique human salivary gland tumor cell line (HSG) and tried to analyze the relationship of cell death and chromosomal aberrations on the same cell line.…”

Section: Introductionmentioning

confidence: 99%

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

Gotoh¹,

Funada

Mohri

et al. 2008

Open Life Sciences

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To 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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Section: Discussionsupporting

confidence: 90%

Section: Discussionmentioning

confidence: 99%

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

Gotoh¹,

Funada

Mohri

et al. 2008

Open Life Sciences

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“…As reported in previous studies, cells exposed to various radiations resulted in chromosome breaks including chromatid discontinuity, misalignment of the distal, chromatid ring and so on. [2][3][4][5][6][7] These potential changes possibly cause the death of cells. 1,7 Since Gotoh et al have reported the chemically induced premature condensed chromosome technique in 1995, an easy and quick method on detecting chromosome breakage was widely applied in the radiobiological and oncology works.…”

Section: Introductionmentioning

confidence: 99%

“…8 Murakami et al used atom force microscope (AFM) to assess the accuracy of chemically induced PCC breakages in comparison with the results acquired through the light microscope vision; there was no significant difference between two methods, and thus it was validated that the PCC technique was suitable and reliable for radiation induced chromosome damage analysis. 9 Suzuki et al [4][5][6][7] , Kawata et al 2,3 have employed different heavy ions with various LET and X rays to investigate the radiation induced chromosome breaks both in human normal fibroblast cells and malignant cells. The number of chromatid breaks was found to be linearly correlated with the absorbed dose of radiation.…”

Section: Introductionmentioning

confidence: 99%

A method on theoretical simulation of chromosome breaks in cells exposed to heavy ions

Yang¹,

Li²,

Jing³

et al. 2008

Radiology and Oncology

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Heavy‐ion‐induced mutations in the gpt delta transgenic mouse: Effect of p53 gene knockout

Yatagai

Kurobe

Nohmi

et al. 2002

Environ and Mol Mutagen

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The influence of the loss of p53 gene on heavy-ion-induced mutations was examined by constructing a new line of transgenic mice, p53 knockout (p53(-/-)) gpt delta. In this mouse model, deletions in lambda DNA integrated into the mouse genome are preferentially selected as Spi(-) phages, which can then be subjected to molecular analysis. Mice were exposed to 10 Gy of whole-body carbon-ion irradiation. The carbon ions were accelerated to 135 MeV/u by the RIKEN Ring Cyclotron. The p53 defect markedly enhanced the Spi(-) mutant frequency (MF) in the kidneys of mice exposed to C-ion irradiation: the Spi(-) MF increased 4.4- and 2.8-fold over the background level after irradiation in p53(-/-) and p53(+/+) mice, respectively. There was no significant difference in the background Spi(-) MF between p53(-/-) and p53(+/+) mice. Sequence analysis of the Spi(-) mutants indicated that the enhancement of kidney Spi(-) MF in p53(-/-) mice was primarily due to an increase in complex or rearranged-type deletions. In contrast to the kidney, the p53 defect had no effect on the Spi(-) MF in liver: Spi(-) MF increased 3.0- and 2.7-fold after the irradiation in p53(-/-) and p53(+/+) mice, respectively. Our results suggest that p53 suppresses deletion mutations induced by heavy-ion irradiation in an organ-specific manner.

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Let dependence of cell death, mutation induction and chromatin damage in human cells irradiated with accelerated carbon ions

Cited by 68 publications

References 26 publications

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

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

A method on theoretical simulation of chromosome breaks in cells exposed to heavy ions

Heavy‐ion‐induced mutations in the gpt delta transgenic mouse: Effect of p53 gene knockout

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