• Journal of the Korean Society of Radiology
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• v.11 no.3
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• pp.147-151
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• 2017

Potentially lethal damage repair (PLDR) in HFL-I was investigated by delayed plating experiments. The surviving fraction data were fitted to the linear Quadratic equation ($LogSn=-n{\gamma}({\alpha}d+{\beta}d^2$) where ${\gamma}=1$ for immediate plating). And a repair factor ${\gamma}$ was developed to compare survival for immediate and delayed plating. When we only took into account the repair factor of PLDR ${\gamma}$ which was derived from the delay assay, the cell survival response th fractionated carbon ion irradiation was not fully matched. This gap suggested that consideration of another repair process is necessary. So this suggests that the various repair process plays an important role in the fractionated irradiations.

• Journal of the Korean Society of Radiology
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• v.9 no.6
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• pp.417-420
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• 2015

We obtained Surviving Fraction (SF) after irradiation carbon beam to compare the applicability of the Linear-Quadratic model, Incomplete Repair model, Marchese model. Mathematica software(ver 9.0) used to calcurate parameters and compared result. LQ model could not explain the entire response of fractionated carbon beam irradiation. It becomes necessary to construct models that extend the LQ model of conventional radiotherapy for the carbon beam therapy. By combining both Potentially Lethal Damage Repair (PLDR) and Sublethal Damage Repair (SLDR) a new LQ model can develop that aptly modeled the cellular response to fractionated irradiation.

• Korean Journal of Environmental Biology
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• v.20 no.1
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• pp.35-39
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• 2002

The significance of cell ploidy and repair ability for the radioprotective efficiency of cysteamine was studied in DNA repair - proficient and repair - deficient yeast cells irradiated $^{60}C0\;\gamma-rays.$ Results have been obtained for the cell survival of two groups of yeasts-diplont and haplont cells, both in haploid and diploid states. For diploid Saccharomyces cerevisiae yeast cells, the correlation between the radio-protective action of cysteamine and the cell repair capacity was demonstrated. Such a correlation was not clearly expressed for haploid yeast cells. In addition, evidence was obtained indicating that the degree of the radioprotective action was independent of the number of chromosome sets in haplont yeast Pichia guilliermondii cells and in some radiosensitive mutants defective in the diploid-specific recovery. It is concluded on this basis that the radioprotective action may involve the cellular recovery process, which may be mediated by a recombination-like mechanism, for which the diploid state is required. The results obtained clearly show that the radioprotective effect was dependent on DNA repair status and indicate that the mechanism of the radioprotective action may be realized on the level of primary radiation damage production as well as on the level of postradiation recovery from potentially lethal radiation damage.

• Korean Journal of Environmental Biology
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• v.20 no.4
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• pp.277-286
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• 2002

An increase in the overall biological effect under the combined action of ionizing radiation with another inactivating agent can be explained in two ways. One is the supposition that synergism may attribute to a reduced cellular capacity of damn-ge repair after the combined action. The other is the hypothesis that synergism may be related to an additional lethal or potentially lethal damage that arises from the interaction of sublesions induced by both agents. These sublesions ave considered to be in-effective when each agent is applied separately. Based on this hypothesis, a simple mathematical model was established. The model can predict the greatest value of the synergistic effect, and the dependence of synergy on the intensity of agents applied, as well. This paper deals with the model validation and the peculiarity of simultaneous action of various factors with radiation on biological systems such as bacteriophage, bacterial spores, yeast and mammalian cells. The common rules of the synergism aye as follows. (1) For any constant rate of exposure, the synergy can be observed only within a certain temperature range. The temperature range which synergistically increases the effects of radiation is shifted to the lower temperature fer thermosensitive objects. Inside this range, there is a specific temperature that maximizes the synergistic effect. (2) A decrease in the exposure rate results in a decrease of this specific temperature to achieve the greatest synergy and vice versa. For a constant temperature at which the irradiation occurs, synergy can be observed within a certain dose rate range. Inside this range an optimal intensity of the physical agent may be indicated, which maximizes the synergy. As the exposure temperature reduces, the optimal intensity decreases and vice versa. (3) The recovery rate after combined action is decelerated due to an increased number of irreversible damages. The probability of recovery is independent of the exposure temperature for yeast cells irradiated with ionizing or UV radiation. Chemical inhibitors of cell recovery act through the formation of irreversible damage but not via damaging the recovery process itself.

• Journal of the Korean Society of Radiology
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• v.11 no.4
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• pp.177-181
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• 2017

Dose response curves using absorbed dose to the biological effect are usually available in case of conventional X beam. However, absorbed dose is not consider in treatment planning for carbon beam such as heavy ions. Because the biological effects also depend on other quantities such as the local variation, which is often characterized by the linear energy transfer (LET). So LQ model cannot explain the entire response of fractionated carbon beam irradiation. The variation in LET with penetration depth leads to substantial differences in biological effect of carbon beam. And it is therefore essential in treatment planning to calculate not only the absorbed dose but also the LET to estimate the biological outcome of the radiation of interest. LET variation plays an important role in the fractionated irradiations. It is suggested that consideration of LET is necessary in biophysical model.

• Radiation Oncology Journal
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• v.6 no.1
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• pp.1-11
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• 1988

Recovery from potentially lethal damage (PLDR) after irradiation was studied in plateau-phase culture of Vero cells in vitro. Unfed plateau-phase cells were irradiated with dose of 1 to 9Gy using Cs-137 irradiator. Cells then were incubated again and left in situ for 0, 1, 2, 3, 4, 5, 6, and 24 hours and then were trypsinized explanted, and subcultured in fresh RPMI-1640 media containing $0.33\%$ agar. Cell survival was measured by colony forming ability. An adequate number of heavily irradiated Vero cells were added as feeder cells to make the total cell number constant in every culture dish. As the postirradiation in situ incubation time increased, surviving fraction increased by PLDR. The rate of PLDR was so rapid that increased surviving fraction reached saturation level at 2 to 4 hours after in situ incubation. As the radiation dose increased, the rate of PLDR fastened and the magnitude of increased surviving fraction at saturation level by PLOR also increased. In analysis of cell survival curve fitted to the linear-quadratic model, the linear inactivation coefficient $(\alpha)$ decreased largely and reached nearly to zero but the quadratic inactivation coefficient $(\beta)$ increased minimally by increment of postirradiation in situ incubation time. So PLDR mainly affected the damage expressed as $\alpha$, In the multitarget model, significant change was not obtained in $D_0\;but\;in D_q$. Therefore, shoulder region in cell survival curve was mainly affected by PLDR and terminal slope was not influenced at all. And dose-modifying factor by PLDR was relatively higher in shoulder region, that is, in low dose area below 3 Gy.