• 환경생물
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• 제23권4호
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• pp.390-397
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• 2005

The inhibition of cell recovery might be proceeded via either the damage of the mechanism of the recovery itself or via the formation of irreversible damage which could not be repaired at all. Both these processes may take place at the same time. Any of these possibilities would result in a decrease in both the rate and extent of cell recovery. To distinguish them, a quantitative approach describing the process of recovery as a decrease in the effective radiation dose was applied to experimental data on the recovery from potentially lethal damage in Chinese hamster cells exposed to X-rays alone or combined with various chemicals (pyruvate, novobiocin, lactate, nalidixic acid, 3-aminobenzamide). For these particular cases, it is concluded that the recovery process itself is not damaged and the inhibition of the recovery is entirely due to the enhanced yield of the irreversibly damaged cells.

• 방사선산업학회지
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• 제10권4호
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• pp.199-204
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• 2016

The dependence of cell survival on exposure dose and the duration of the liquid-holding recovery (LHR) was obtained for diploid yeast cells irradiated with ionizing radiation of different linear energy transfer (LET) and recovering from radiation damage without and with various concentrations of cisplatin - the most widely used anticancer drug. The ability of yeast cells to recover from radiation damage was less effective after cell exposure to high-LET radiation, when cells were irradiated without drug. The increase in cisplatin concentration resulted in the disappearance of this difference whereas the fraction of irreversible damage was permanently enlarged independently of radiation quality. The probability of cell recovery was shown to be constant for various conditions of irradiation and recovery. A new mechanism of cisplatin action was suggested according with which the inhibition of cell recovery after exposure to ionizing radiations was completely explained by the production of irreversible damage.

• 한국환경성돌연변이발암원학회지
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• 제25권4호
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• pp.129-133
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• 2005

We investigated the cytoprotective effect of phloroglucinol, which was isolated from Ecklonia cava (brown seaweed), against oxidative stress induced cell damage in Chinese hamster lung fibroblast(V79-4) cells. Phloroglucinol was found to scavenge intracellular reactive oxygen species (ROS) generated by $\gamma-ray$ radiation. In addition, Phloroglucinol inhibited cell damage induced by radiation through scavenging ROS. Phloroglucinol increased the superoxide dismutase and glutathione peroxidase activity, Taken together, the results suggest that phloroglucinol protectes V79-4 cells against oxidative damage by enhancing the cellular antioxidant enzymes activity.

• BMB Reports
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• 제47권10호
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• pp.575-580
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• 2014

In this study, we investigate whether arsenite-induced DNA damage leads to p53-dependent premature senescence using human glioblastoma cells with p53-wild type (U87MG-neo) and p53 deficient (U87MG-E6). A dose dependent relationship between arsenite and reduced cell growth is demonstrated, as well as induced ${\gamma}H2AX$ foci formation in both U87MG-neo and U87MG-E6 cells at low concentrations of arsenite. Senescence was induced by arsenite with senescence-associated ${\beta}$-galactosidase staining. Dimethyl- and trimethyl-lysine 9 of histone H3 (H3DMK9 and H3TMK9) foci formation was accompanied by p21 accumulation only in U87MG-neo but not in U87MG-E6 cells. This suggests that arsenite induces premature senescence as a result of DNA damage with heterochromatin forming through a p53/p21 dependent pathway. p21 and p53 siRNA consistently decreased H3TMK9 foci formation in U87M G-neo but not in U87MG-E6 cells after arsenite treatment. Taken together, arsenite reduces cell growth independently of p53 and induces premature senescence via p53/p21-dependent pathway following DNA damage.

• 대한방사선기술학회지:방사선기술과학
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• 제43권1호
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• pp.29-34
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• 2020

Mitochondria was observed much around the nuclear membrane of liver tissue where the energy metabolism process is active. Testis tissue had a large number of undifferentiated cells, and cristae in Inner membrane of Mitochondria was not observed clearly. Morphological damage occurred first in Inner membrane rather than the outer membrane. The kidney tissue was clearly observed in the form of cristae. Radiation-induced damage occurred at the edges of both ends, and the membrane was observed bursting with the thickness of the outer membrane. Small intestine cells were observed in many mitochondria in the tissues around the villus, where bowel movements were active. Morphological damage occurred with the outer and inner membranes getting tangled. Mitochondria sensitivity to radiation was sensitized in testis and small intestine tissues, and kidney, ovary and liver tissues were found to be resistant.

• 대한방사선협회지
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• 제30권1호
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• pp.70-76
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• 2004

To evaluate the process of radiation-induced cell damage in human promyelocytic leukemia cell HL-60 cell and chinese hamster cell CHO cell lines. I irradiated HL-60 cells, CHO cell line, using the V - radiation from Cs-137 cell irradiation(Gamma cell 3000

• 한국원자력학회:학술대회논문집
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• 한국원자력학회 2005년도 추계학술발표회
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• pp.862-863
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• 2005

• Journal of Radiation Protection and Research
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• 제42권3호
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• pp.146-153
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• 2017

Background: Acute radiation syndrome (ARS) primarily refers to damage to the hematopoietic system, myeloid system, and gastrointestinal (GI) system caused by radiation exposure. Such damage progresses to become life-threatening. In particular, as the syndrome develops very rapidly-within several hours from radiation exposure-prompt and accurate diagnosis and treatment are needed, as is further research into appropriate diagnostic and treatment modalities. Materials and Methods: Minipigs, which display human-like properties, underwent whole-body irradiation at 2 or 4 Gy (doses causing hematopoietic ARS) or at higher doses of 7 or 12 Gy. Changes in the blood cells and clinical symptoms were analyzed and we performed a necropsy when the animals succumbed to ARS. Results and Discussion: The minipig irradiated with 2 Gy showed a decrease in white blood cells, including neutrophils, lymphocytes, and platelets in the early stages. However, the blood cell counts gradually increased and returned to normal values. The minipig irradiated with 4 Gy succumbed due to hematopoietic ARS. In contrast, the minipigs irradiated with 7 or 12 Gy exhibited clinical symptoms of combined GI damage and hematopoietic syndrome. Moreover, a characteristic pattern of platelet changes was observed in the 7 and 12 Gy irradiated minipigs. Conclusion: The changes in the platelet count caused by radiation exposure observed in minipigs, which are hematologically and pathohistologically similar to humans, suggest that they can be used as a novel diagnostic criterion.

• 한국원자력학회:학술대회논문집
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• 한국원자력학회 2005년도 추계학술발표회
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• pp.838-839
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• 2005

• 대한방사선기술학회지:방사선기술과학
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• 제41권5호
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• pp.471-478
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• 2018

Oogenesis process of ovary produces a lot of undifferentiated cells. Especially, the radiation exposure of early immature cells in the process of growth to oocyte causes serious disabilities. This study examined the radiation damage mechanism of undifferentiated cells and organelles in oogenesis process, and the radioprotection after injection of alliin. The ultrastructure after 7Gy X-ray irradiation on the white rat was observed in the experiment. The results is as follows. It was observed that the nucleus membrane of an oogonium was damaged and vacuolated in the several parts after 15 days of irradiation. The damage of mitochondria membrane and flow in cytoplasm after 20 and 30 days was found in the oogonium. After 40 days observation, peroxidation of fat droplets was found and organelles were tangled each other in ovary tissue. The partial damage of nuclear membrane in oogonium past 15 days after injection of alliin was found, but decreased remarkably. Mitochondria, Golgi body, and rough endoplasmic reticulum were also clearly observed, therefore, radioprotection effects in alliin was confirmed partially.