Comparison of repair of DNA double-strand breaks caused by neutron or gamma radiation in cultured human cells

Peak, Meyrick J.; Wang, L; Hill, Colin K.; Peak, Jennifer G.

doi:10.3109/09553009109169316

Cited by 31 publications

(9 citation statements)

References 29 publications

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“…The rejoining of double-strand breaks as a function of time shows a slow and fast component [112]. A higher proportion of double-strand breaks remain unrejoined after exposure to high-as opposed to low-LET radiation [46,61], and the lethality of double-strand breaks increases profoundly with the LET up to a maximum and then decreases [113].…”

Section: Dna Base Damage Repairmentioning

confidence: 99%

General aspects of the cellular response to low- and high-LET radiation

2001

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Radiobiological studies have shown for some time that the effects of ionising radiation on cells are mainly explained by modification of the DNA. Numerous studies over the past 50 years have accumulated clear evidence of the cause-effect relationship between damage to DNA and the cytotoxic and mutagenic effects of ionising radiation. However, the path from irradiation of the cells to the induction of biological effects comprises several complex steps. The first step involves interactions between the radiation and the cellular environment. These consist of physical and chemical reactions which produce ions, excited molecules and radical species. Excitations and ionisations are complete in about 10(-15) s, and are followed by a chemical thermal equilibrium of the species produced within 10(-12) s. These species then diffuse from their site of production and provoke alterations to a variety of cellular components. This damage is detected by cellular surveillance systems, which in turn activate signalling cascades, gene transcription and enzyme recruitment, which participate in the cellular response. In most cases, cell cycle arrest occurs, allowing, according to the biological relevance of the DNA damage, either a process of DNA repair or programmed cell death (apoptosis). The accuracy of the DNA repair which is performed depends on the complexity of the DNA lesion and on the DNA repair machinery fidelity itself. Improper DNA repair can lead to mutation, chromosome aberration, genetic instability, oncogenic transformation and, ultimately, cell death.

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Section: Dna Base Damage Repairmentioning

confidence: 99%

General aspects of the cellular response to low- and high-LET radiation

2001

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“…As the search for more sensitive and reliable predictive assays continues in the clinic and for radiation protection, an important determinant of cellular radiosensitivity is DNA repair proficiency (Weichselbaum 1986, Fox and McNally 1988, Peak et al 1991, Hu and Hill 1996, Britten and Murray 1997, Dolling et al 1998. As in the case of MN and apoptosis data, the conclusions of numerous DNA damage induction and repair studies are diverse and appear to be cell type dependent (Whitaker et al 1991, Smeets et al 1993, Olive et al 1994, Ruiz de Almodovar et al 1994, Dikomey et al 1998, Roos et al 2000, Theron et al 2000, Serafin et al 2003.…”

Section: Introductionmentioning

confidence: 99%

Influence of DNA double‐strand break rejoining on clonogenic survival and micronucleus yield in human cell lines

Akudugu

Theron

Serafin

et al. 2004

International Journal of Radiation Biology

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Fast DSB rejoining, possibly through interaction with slow DSB rejoining, appears to play an important role in the formation of micronuclei. However, total DSB rejoining reflects intrinsic radiosensitivity. Consideration of differences in DSB rejoining kinetics might contribute to a better understanding of the significance of cell survival and micronucleus data in the clinical and radiation protection setting.

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“…Repair of DSBs in mammalian cells seems to occur with a fast and a slow component (25)(26)(27). It has generally been found that DSBs induced by higher-LET radiation are repaired more slowly, with a larger fraction of nonrejoined breaks remaining several hours after irradiation (11,13,26,(28)(29)(30)(31)(32).…”

Section: Introductionmentioning

confidence: 99%

“…It has generally been found that DSBs induced by higher-LET radiation are repaired more slowly, with a larger fraction of nonrejoined breaks remaining several hours after irradiation (11,13,26,(28)(29)(30)(31)(32). This has been interpreted to mean that DSBs induced by high-LET radiation are more complex and difficult to repair.…”

Section: Introductionmentioning

confidence: 99%

DNA Double-Strand Breaks Induced by High-Energy Neon and Iron Ions in Human Fibroblasts. I. Pulsed-Field Gel Electrophoresis Method

Cooper¹,

Rydberg²,

Löbrich³

1994

Radiation Research

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The relative effectiveness of high-energy neon and iron ions for the production of DNA double-strand breaks was measured in one transformed and one nontransformed human fibroblast cell line using pulsed-field gel electrophoresis. The DNA released from the gel plug (fraction of activity released: FAR) as well as the size distribution of the DNA entering the gel were used to compare the effects of the heavy-ion exposure with X-ray exposure. Both methods gave similar results, indicating similar distributions of breaks over megabase-pair distances for the heavy ions and the X rays. The relative biological effectiveness (RBE) compared to 225 kVp X rays of initially induced DNA double-strand breaks was found to be 0.85 for 425 MeV/u neon ions (LET 32 keV/microns) and 0.42-0.55 for 250-600 MeV/u iron ions (LET 190-350 keV/microns). Postirradiation incubation showed less efficient repair of breaks induced by the neon ions and the 600 MeV/u iron ions compared to X rays. Survival experiments demonstrated RBE values larger than one for cell killing by the heavy ions in parallel experiments (neon: RBE = 1.2, iron: RBE = 2.3-3.0, based on D10 values). It is concluded that either the initial yield of DNA double-strand breaks induced by the high-energy particles is lower than the yield for X rays, or the breaks induced by heavy ions are present in clusters that cannot be resolved with the technique used. These results are confirmed in the accompanying paper (M. Löbrich, B. Rydberg and P. Cooper, Radiat. Res. 139, 142-151, 1994).

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Comparison of repair of DNA double-strand breaks caused by neutron or gamma radiation in cultured human cells

Cited by 31 publications

References 29 publications

General aspects of the cellular response to low- and high-LET radiation

General aspects of the cellular response to low- and high-LET radiation

Influence of DNA double‐strand break rejoining on clonogenic survival and micronucleus yield in human cell lines

DNA Double-Strand Breaks Induced by High-Energy Neon and Iron Ions in Human Fibroblasts. I. Pulsed-Field Gel Electrophoresis Method

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