Cellular and Subcellular Effects of Very Heavy Ions

Kiefer, Jürgen

doi:10.1080/09553008514552041

Cited by 58 publications

(14 citation statements)

References 65 publications

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“…This is a phenomenon known as "overkill". Track structure and mechanistic models have been developed to try and explain this effect [20] and to correlate cell kill with radiation track structure [14,21]. Overkill can be explained by the presence of a limited number of vital targets within the cells.…”

Section: Cell Survivalmentioning

confidence: 99%

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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: Cell Survivalmentioning

confidence: 99%

“…It is based on the evaluation of energy deposition at a nanometre scale by Monte Carlo codes reviewed in [11]. Such codes simulate electron and ion transport in biological or solid material [6,7,12,13,14,15] (Fig. 4).…”

Section: Radiation Tracksmentioning

confidence: 99%

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

2001

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“…To clarify this understanding, various studies on cell inactivation and genetic changes induced by ion beams as well as the relationship between LET and relative biological effectiveness (RBE) have been performed (e.g . [1][2][3]), although only a limited number of such studies have focussed on plants [4][5][6][7][8][9][10].…”

Section: Introductionmentioning

confidence: 99%

Biological effects of ion beams in Nicotiana tabacum L.

Hase

Shimono

Inoue

et al. 1999

Radiation and Environmental Biophysics

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The biological effects of ion beams on Nicotiana tabacum L., particularly the induction of chromosome aberrations, were investigated. Dry seeds were exposed to 12C5+, 4He2+ and 1H+ beams with linear energy transfer (LET) ranging from 1 to 111 keV/microm and irradiated with gamma-rays. Ion beams were more effective in reducing germination and survival of the seeds than gamma-rays. The LD50 for 12C5+ beams, 4He2+ beams and gamma-rays were 35, 60 and 500 Gy, respectively. The frequencies of mitotic cells with chromosome aberrations, such as chromosome bridges, acentric fragments and lagging chromosomes in the root tip cells of the exposed seeds, increased linearly with increasing doses. Relative biological effectiveness (RBE) values, based on the doses that induced a survival inhibition of 50% and a 10% frequency of aberrant cells, were 14.3-17.5 for the 12C5+ beams, 7.0-8.3 for the 4He2+ beams and 7.8 for the 1H+ beams. Furthermore, the relative ratios of the chromosome aberration types were significantly different between the ion beam and the gamma-ray regimes: chromosome fragments were more frequent in the former, and chromosome bridges in the latter. Based on these results, we concluded that the repair process of initial le

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“…Since it is not possible to obtain data with humans, in vitro experiments are necessary. While many investigations on cell inactivation after heavy ion treatment can be found in the literature (for reviews see [1,8,11]), this is not the case for heavy particle-induced mutations, where only a few experimental data are available so far [4,12,13,18,19].…”

Section: Introductionmentioning

confidence: 99%

Induction of HPRT- mutants in Chinese hamster V79 cells after heavy ion exposure

Stoll

Schneider

Kranert

et al. 1995

Radiat Environ Biophys

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The induction of resistance to 6-thioguanine by heavy ion exposure was investigated with various accelerated ions (oxygen-uranium) up to linear energy transfer (LET) values of about 15,000 keV/microns. Survival curves are exponential with fluence; mutation induction shows a linear dependence. Cross-sections (sigma i: inactivation, sigma m: mutation) were derived from the respective slopes. Generally, sigma i rises over the whole LET range, but separates into different declining curves for single ions with LET values above 200 keV/microns. Similar behaviour is seen for sigma m. The new SIS facility at GSI, Darmstadt, makes it possible to study the effects of ions with the same LET but very different energies and track structures. Experiments using nickel and oxygen ions (up to 400 MeV/u) showed that inactivation cross-sections do not depend very much on track structure, i.e. similar values are found with different ions at the same LET. This is not the case for mutation induction, where very energetic ions display considerably smaller induction cross-sections, compared with low-energy ions of identical LET. Preliminary analyses using the polymerase chain reaction (PCR) demonstrate that even heavy ions cause "small alterations" (small deletions or base changes). The proportion of the total deletions seems to increase with LET.

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Cellular and Subcellular Effects of Very Heavy Ions

Cited by 58 publications

References 65 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

Biological effects of ion beams in Nicotiana tabacum L.

Induction of HPRT- mutants in Chinese hamster V79 cells after heavy ion exposure

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