• Horticultural Science & Technology
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• v.34 no.1
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• pp.122-133
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• 2016

While ion beams are widely used in plant breeding, little is known about the sensitivity of Lavandula angustifolia (lavender) to ionizing radiation. To compare the biological effects of different types of ionizing radiation on the germination and survival rates of lavender, we exposed lavender seeds to gamma rays, 3 MeV electron beams, and 1.89 MeV proton ion beams. We observed that the seed germination rate decreased with increasing dosages of all three types of ionizing radiation. The malformation rate of lavender seedlings exposed to electron beams and gamma rays increased with increasing radiation dosage. By contrast, the effect of the accelerated proton beams on the malformation rate was negatively correlated with the dosage used. The survival rate of lavender seedlings exposed to the three types of ionizing radiation decreased in a dose-dependent manner. In addition, the survival rate of seedlings irradiated with proton and electron beams decreased more slowly than did that of seedlings irradiated with gamma rays. The half-lethal dose of gamma rays, electron beams, and proton beams was determined to be 48.1 Gy, 134.3 Gy, and 277.8 Gy, respectively, and the most suitable proton-ion energy for lavender seeds in terms of penetration depth was determined to be 5 MeV. These findings provide valuable information for the breeding of lavender by radiation mutation.

• Tuberculosis and Respiratory Diseases
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• v.71 no.4
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• pp.259-265
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• 2011

Background: Epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors, gefitinib and erlotinib, are effective therapies for non-small cell lung cancer (NSCLC) patients whose tumors harbor somatic mutations in EGFR. The mutations are, however, only found in about 30% of Asian NSCLC patients and all patients ultimately develop resistance to these agents. Ionizing radiation has been shown to induce autophosphorylation of EGFR and activate its downstream signaling pathways. In the present study, we have tested whether the effect of gefitinib treatment can be enhanced after ionizing radiation. Methods: We compared the PC-9 and A549 cell line with its radiation-resistant derivatives after gefitinib treatment with cell proliferation and apoptosis assay. We also analyzed the effect of gefitinib after ionizing radiation in PC-9, A549, and NCI-H460 cells. Cell proliferation was determined by MTT assay and induction of apoptosis was evaluated by flow cytometry. Caspase 3 activation and PARP cleavage were evaluated by western blot analysis. Results: PC-9 cells having mutated EGFR and their radiation-resistant cells showed no significant difference in cell viability. However, radiation-resistant A549 cells were more sensitive to gefitinib than were their parental cells. This was attributable to an increased induction of apoptosis. Gefitinib-induced apoptosis increased significantly after radiation in cells with wild type EGFR including A549 and NCI-H460, but not in PC-9 cells with mutated EGFR. Caspase 3 activation and PARP cleavage accompanied these findings. Conclusion: The data suggest that gefitinib-induced apoptosis could increase after radiation in cells with wild type EGFR, but not in cells with mutated EGFR.

• 대한방사선방어학회:학술대회논문집
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• 2010.04a
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• pp.148-149
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• 2010

• The Korean Journal of Nuclear Medicine
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• v.26 no.1
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• pp.8-13
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• 1992

Low doses of ionizing radiation from external or internal sources cause heterogeneous distribution of energy deposition events in the exposed biological system. With the cell being the individual element of the tissue system, the fraction of cells hit, the dose received by the hit, and the biological response of the cell to the dose received eventually determine the effect in tissue. The hit cell may experience detriment, such as change in its DNA leading to a malignant transformation, or it may derive benefit in terms of an adaptive response such as a temporary improvement of DNA repair or temporary prevention of effects from intracellular radicals through enhanced radical detoxification. These responses are protective also to toxic substances that are generated during normal metabolism. Within a multicellular system, the probability of detriment must be weighed against the probability of benefit through adaptive responses with protection against various toxic agents including those produced by normal metabolism. Because irradiation can principally induce both, detriment and adaptive responses, one type of affected cells may not be simply summed up at the expense of cells with other types of effects, in assessing risk to tissue. An inventory of various types of effects in the blood forming system of mammals, even with large ranges of uncertainty, uncovers the possibility of benefit to the system from exposure to low doses of low LET radiation. This experimental approach may complement epidemiological data on individuals exposed to low doses of ionizing radiation and may lead to a more rational appraisal of risk.

• BMB Reports
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• v.36 no.1
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• pp.144-148
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• 2003

During the past 2 decades, radiation tumorigenesis researchers have focused on cellular and molecular mechanisms. We reviewed some of these research fields, since they may specifically relate to the induction of cancer by ionizing radiation. First, radiation-mediated mutation was discussed. Then the initiating event in radiation carcinogenesis, as well as other genetic events that may by involved, is discussed in terms of the possible role of the activation of genes and the loss of cell-cycle checkpoints.

• Journal of Radiation Protection and Research
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• v.34 no.2
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• pp.49-54
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• 2009

Mitochondrial DNA (mtDNA) deletion is a well-known marker for oxidative stress and aging and also contributes to their unfavorable effects in cultured cells and animal tissues. This study was conducted to investigate the effect of ionizing radiation (IR) on mtDNA deletion and the involvement of reactive oxygen species (ROS) in this process in human lung fibroblast (IMR-90) cells. Young IMR-90 cells at population doubling (PD) 39 were irradiated with $^{137}Cs$ $\gamma$-rays and the intracellular ROS level was determined by 2',7'-dichlorofluorescein diacetate (DCFH-DA) and mtDNA common deletion (4977bp) was detected by nested PCR. Old cells at PD 55 and $H_2O_2$-treated young cells were compared as the positive control. IR increased the intracellular ROS level and mtDNA 4977 bp deletion in IMR-90 cells dose-dependently. The increases of ROS level and mtDNA deletion were also observed in old cells and $H_2O_2$-treated young cells. To confirm the increased ROS level is essential for mtDNA deletion in irradiated cells, the effects of N-acetylcysteine (NAC) on IRinduced ROS and mtDNA deletion were examined. 5 mM NAC significantly attenuated the IR-induced ROS increase and mtDNA deletion. These results suggest that IR induces the mtDNA deletion and this process is mediated by ROS in IMR-90 cells.

• BMB Reports
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• v.45 no.4
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• pp.242-246
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• 2012

The use of ionizing radiation (IR) is essential for treating many human cancers. However, radioresistance markedly impairs the efficacy of tumor radiotherapy. IR enhances the production of reactive oxygen species (ROS) in a variety of cells which are determinant components in the induction of apoptosis. Much interest has developed to augment the effect of radiation in tumors by combining it with radiosensitizers to improve the therapeutic ratio. In the current study, the radiosensitizing effects of resveratrol and piperine on cancer cells were evaluated. Cancer cell lines treated with these natural products exhibited significantly augmented IR-induced apoptosis and loss of mitochondrial membrane potential, presumably through enhanced ROS generation. Applying natural products as sensitizers for IR-induced apoptotic cell death offers a promising therapeutic approach to treat cancer.

• Journal of the Korean Society for Aeronautical & Space Sciences
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• v.34 no.11
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• pp.76-83
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• 2006

Space radiation environment for COMS is simulated by NASA AP8/AE8, JPL91 and NRL CREME models, respectively for trapped particle, solar proton and cosmic-ray. The radiation effects on electronic devices in communication payload are also estimated by using simulation results. Dose-depth curve and LET spectrum are calculated for estimating total ionizing dose(TID) effect and single event effect(SEE) respectively. Spherical sector method is applied to dose estimation at each position in the units of communication payload to consider shielding effect of platform and housing. Total ionizing dose at each position varies by 8 times through shielding effect under the same external space radiation environment.

• Biomedical Science Letters
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• v.26 no.4
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• pp.249-255
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• 2020

Radiation therapy is one of the primary options for the treatment of malignant tumors. Even though it is an effective anti-cancer treatment, it can cause serious complications owing to radiation-induced damage to the normal tissue around the tumor. It was recently reported that normal stem cell response to the genotoxic stress of ionizing radiation can boost the therapeutic effectiveness of radiation by repairing damaged cells. Therefore, we focused on annexin A-1 (ANXA1), one of the genes induced by low-dose irradiation, and assessed whether it can protect adipose-derived stem cells (ADSCs) against oxidative stress-induced damage caused by low-dose irradiation and improve effectively cell survival. After confirming ANXA1 expression in ADSCs transfected with an ANXA1 expression vector, exposure to hydrogen peroxide (H2O2) was used to mimic cellular damage induced by a chronic oxidative environment to assess cell survival under oxidative conditions. ANXA1-transfected ADSCs demonstrated that increased viability compared with un-transfected cells and exhibited enhanced anti-oxidative properties. Taken together, these results suggest that ANXA1 could be used as a potential therapeutic target to improve the survival of stem cells after low-dose radiation treatment.

• Korean Journal of Environmental Biology
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• v.28 no.2
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• pp.101-107
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• 2010

Metal ions are essential to life. However, some metals such as mercury are harmful, even when present at trace amounts. Toxicity of mercury arises mainly from its oxidizing properties. Ionizing radiation (IR) is an active tool for destruction of cancer cells and diagnosis of diseases, etc. IR induces DNA double strand breaks in the nucleus, In addition, it causes lipid peroxidation, ceramide generation, and protein oxidation in the membrane, cytoplasm and nucleus. Yeasts have been a commonly used material in biological research. In yeasts, the physiological response to changing environmental conditions is controlled by the cell types. Growth rate, mutation and environmental conditions affect cell size and shape distributions. In this work, the effect of IR and mercury chloride (II) on the morphology of yeast cells were investigated. Saccharomyces cerevisiae cells were treated with IR, mercury chloride (II) and IR combined with mercury chloride (II). Non-treated cells were used as a control group. Morphological changes were observed by a scanning electron microscope (SEM). The half-lethal condition from the previous experimental results was used to the IR combined with mercury. Yeast cells were exposed to 400 and 800 Gy at dose rates of 400Gy $hr^{-1}$ or 800 Gy $hr^{-1}$, respectively. Yeast cells were treated with 0.05 to 0.15 mM mercury chloride (II). Oxidative stress can damage cellular membranes through a lipidic peroxidation. This effect was detected in this work, after treatment of IR and mercury chloride (II). The cell morphology was modified more at high doses of IR and high concentrations of mercury chloride(II). IR and mercury chloride (II) were of the oxidative stress. Cell morphology was modified differently according to the way of oxidative stress treatment. Moreover, morphological changes in the cell membrane were more observable in the frequently stress treated cells than the temporarily stress treated cells.