scholarly journals An experimental platform for studying the radiation effects of laser accelerated protons on mammalian cells

AIP Advances ◽  
2021 ◽  
Vol 11 (6) ◽  
pp. 065208
Author(s):  
J. Ehlert ◽  
M. Piel ◽  
F. Boege ◽  
M. Cerchez ◽  
R. Haas ◽  
...  
2014 ◽  
Vol 104 (1) ◽  
pp. 419-431 ◽  
Author(s):  
C. Arena ◽  
V. De Micco ◽  
E. Macaeva ◽  
R. Quintens

1968 ◽  
Vol 70 (2) ◽  
pp. 152-162
Author(s):  
R. H. Mole

As the three previous papers in this Symposium have shown (Ord and Stocken 1968; Evans 1968; Court-Brown 1968) the exploration of radiation effects within the cell has its own intrinsic fascination quite apart from its relevance to an understanding of the phenomena which may be observed after irradiation of the complex organism, vertebrate or invertebrate. Whitmore (cf. Whitmore Gulyas and Botond 1965) has been one of the pioneer workers on a previously unsuspected phenomenon, the quantitatively substantial recovery of the ability to divide which occurs within the first hour or two after exposure to low LET radiation. In cultures of mammalian cells in vitro this kind of recovery was shown to have nothing to do with cell division, to occur at all stages of the cell cycle, and to be little, if at all, affected by a reduction in temperature which would be expected a priori to modify profoundly the rate of chemical reactions. Whitmore's technique for synchronising asynchronously dividing cell cultures by the selective suicide of DNA synthesising cells following the incorporation of radioactively labelled DNA precursors with high specific activity has a wide application (Whitmore and Gulyas 1966). Workers from his laboratory have proposed an interesting approach to the real meaning of “ability to divide” and “recovery” based on the idea that there is a certain probability of failure at each cell division and that this probability may be permanently increased by exposure to radiation (Till, McCulloch and Siminovitch 1964). Thus radiation damage may be expressed by failure of cell division not only at the first or second divisions after exposure but also at any subsequent division in the distant future.


1957 ◽  
Vol 106 (4) ◽  
pp. 485-500 ◽  
Author(s):  
Theodore T. Puck ◽  
Dimitry Morkovin ◽  
Philip I. Marcus ◽  
Steven J. Cieciura

Survival curves of normal human cells from a variety of tissues exposed to varying doses of x-irradiation have been constructed, which permit definition of the intrinsic radiation sensitivity of the reproductive power of each cell type. The mean lethal dose of x-irradiation for all the cells employed, including those from normal and cancerous organs, those exhibiting diploid and polyploid chromosome number; those from embryonic and adult tissues, including recently isolated cells and cultures which had been maintained in vitro for many years, and cells exhibiting either epithelioid or fibroblastic morphology, was found to be contained between the limits of 50 to 150 r. Other similarities in the pattern of radiation effects, such as giant formation and abortive colonial growth, in these cells and that of the HeLa S3, previously studied, confirm the hypothesis that the pattern of reaction to x-irradiation previously elucidated, is representatative, at least in over-all outline, for a large variety of human cells. While the radiation survival curves of various human cells are similar in the gross, small but important characterizing differences have been found. All epithelioid cells so far studied are approximately 2-hit, and more radioresistant than the fibroblast-like cells whose survival data correspond to a mean lethal dose of around 60 r, and which so far can be fitted by either 1-hit or 2-hit curves. The earlier prediction that the major radiobiologic damage to mammalian cells is lodged in the genetic apparatus was confirmed by the demonstration of high frequency of mutants among the survivors of doses of 500 to 900 r. All the data on the x-radiosensitivity of these cells can be explained on the basis of a defect resulting from primary damage localized in one or more chromosomes. These considerations afford a convincing explanation of several aspects of the mammalian radiation syndrome.


1990 ◽  
Vol 68 (9) ◽  
pp. 872-886 ◽  
Author(s):  
Dudley T. Goodhead

Insult from ionizing radiation is in the form of microscopic tracks that are highly structured from the atomic level upwards. The internal composition of mammalian cells, too, is highly structured, from dimensions smaller than the DNA molecule (diameter ~2 nm) up to the entire cell [Formula: see text]. There is a wide spectrum of initial physical and chemical damage, subsequent biochemical modification, and final cellular response. The vast majority of the physical, chemical, and biochemical damage is apparently of little relevance to final observable cellular effects. This predominance of "irrelevant" damage masks the nature of that which is of prime relevance. Nevertheless, systematic studies of the effects of radiations on cells have revealed that there are unifying features in the observed responses of different cell types to induction of different effects, and by different radiations. This implies that there are dominant mechanisms that are open to kinetic analysis. Relevant processes may be dominated by the non-linear kinetics of clusters of ionizations and excitations that are within the macromolecule of interest (DNA) or shared with closely adjacent bound molecules. Quantitative models of radiobiological action have concentrated on the relative kinetics of single-track versus multitrack modes and describe the elementary damage either in terms of single ionizations or of clusters of energy depositions.


1984 ◽  
Vol 97 (1) ◽  
pp. 211 ◽  
Author(s):  
Kunio Shinohara ◽  
Takashi Ito ◽  
Atsushi Ito ◽  
Kotaro Hieda ◽  
Katsumi Kobayashi ◽  
...  

2019 ◽  
Vol 186 (2-3) ◽  
pp. 159-162
Author(s):  
A Sedlák

Abstract The topic of the article is to define the average value of linear energy transfer (LET) for carcinogenic effects of radon progeny. The microdosimetric model of boundary specific energy is used. It follows that the effect at high LET should decrease approximately with the third power of LET. This is verified by the analysis of the relationship between radiation effects ratio and LET in published experiments with oncogenic transformation of mammalian cells irradiated with the monoenergetic alpha particles. If these cells are exposed with the radon irradiator, our analysis leads us to conclude that the oncogenic effect of radon progeny is comparable to that of alpha particles with a LET of 75 keV/μm. It is about a quarter lower than the LET value, where the effect of the monoenergetic alpha particles reaches its maximum level. Some implications for lung cancer due to radon inhalation may also be carefully examined.


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