• 제목/요약/키워드: Ionizing radiation effect

검색결과 152건 처리시간 0.032초

혈관내피세포에서 Vascular Endothelial Growth Factor가 방사선에 의해 유도된 apoptosis에 미치는 영향 (Vascular Endothelial Growth Factor Inhibits irradiation-induced Apoptosis in Human Umbilical Vein Endothelial Cells)

  • 이송재;김동윤
    • 대한방사선치료학회지
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    • 제14권1호
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    • pp.165-174
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    • 2002
  • 혈관내피세포 성장 인자(Vascular endothelial growth factor, VEGF)는 혈관내피세포 특이하게 성장요인으로 작용하는 물질로 알려져 있다. 전리방사선에 대한 혈관내피세포의 효과는 정상조직에 대한 반응에 있어 아주 중요한 요소일 것으로 생각된다. 본 연구는 방사선 조사에 의해 배양시킨 혈관내피세포에서 apoptosis가 유도되는지, 유도가 된다면 VEGF에 의해 apoptosis가 억제되는지 그리고 apoptosis의 억제가 어떤 경로를 경유하는지를 실험하였다. 혈관내피세포에 방사선를 조사한 결과, 대조군에 비하여 선량이 증가함에 따라 apoptosis가 증가하였다. 같은 조건하에서 VEGF는 농도 의존적으로 apoptosis를 억제하였다. Antiapoptotic factor로서 VEGF가 어떤 신호 과정을 경유하는지를 밝히고자, 혈관내피세포에 방사선을 조사하여 apoptosis를 유도하면서 Flt-1과 Flk-1/KDR receptor를 처리하였다. 그결과 VEGF에 유도된 apoptosis 억제효과가 차단되었다. Phosphatidylinositol 3'-kinase(PI3-kinase) 특정 억제 물질인 Wortmanin과 LY294002를 방사선 조사한 혈관내피에 VEGF와 함께 처리했을 때 VEGF에 의해 유도된 apoptosis를 억제하였다. 이같은 결과는 VEGF가 방사선 조사로 일어나는 세포 치사를 억제하는 중요한 역할을 담당하며, In Vivo의 실험이 더 이루어져야 할 것으로 생각된다.

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Pretreatment of Low Dose Radiation Reduces Radiation-Induced Apoptosis in Mouse Lymphoma (EL4) cells

  • Kim, Jeong-Hee;Hyun, Soo-Jin;Yoon, Moon-Young;Jioon, Young-Hoon;Cho, Chul-Koo;Yoo, Seong-Yul
    • Archives of Pharmacal Research
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    • 제20권3호
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    • pp.212-217
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    • 1997
  • Induction of an adaptive response to ionizing radiation in mouse lymphoma (EL4) cells was studied by using cell survival fraction and apoptotic nucleosomal DNA fragmentation as biological end points. Cells in early log phase were pre-exposed to low dose of ${\gamma}$-rays (0.01 Gy) 4 or 20 hrs prior to high dose ${\gamma}$-ray (4, 8 and 12 Gy for cell survival fraction analysis; 8 Gy for DNA fragmentation analysis) irradiation. Then cell survival fractions and the extent of DNA fragmentation were measured. Significant adaptive response, increase in cell survival fraction and decrease in the extent of DNA fragmentation were induced when low and high dose .gamma.-ray irradiation time interval was 4 hr. Addition of protein or RNA synthesis inhibitor, cycloheximide or 5,6-dichloro-1-.betha.-d-ribofuranosylbenzimidazole (DRFB), respectively during adaptation period, the period from low dose ${\gamma}$-ray irradiation to high dose ${\gamma}$-ray irradiation, was able to inhibit the induction of adaptive response, which is the reduction of the extent DNA fragmentation in irradiated EL4 cells. These data suggest that the induction of adaptive response to ionizing radiation in EL4 cells required both protein and RNA synthesis.

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Evaluation of apoptosis after ionizing radiation in feeding and starving rats

  • Lee, Jae-Hyun;Cho, Kyung-Ja;Hong, Seok-Il;Park, Min-Kyung
    • 한국수의병리학회지
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    • 제2권1호
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    • pp.37-46
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    • 1998
  • It has been known that $\gamma$-irradiation usually induces cell death in regenerating stem cell in normal tissues like skin, intestine and hematopoietic organ. The experiment were carried out to evaluate the early response of radiation injury in radiosensitive and intermediate radiosensitive tissues in feeding and starving rats with the doses of 3.5 and 7.0 Gy. The results of the study showed that the histological phenomenon was apoptosis in the doses of the radiation as the early response of tissue injury. Apoptosis were showed organ-specific and cellular specific responses suggesting that the selection of apoptosis be exactly focused on highly renewal organs and cells. It was interesting that the rats starved for 72 hours prior to irradiation induced less apoptosis in liver than fed rats. As for cellular responses it appeared that apoptotic cells were mostly distributed in ductal or periportal cells in liver of feeding rats unlikely in liver of Starving rots which showed no difference in zonal distribution. In salivary gland apoptotic cells in fed rats were highly induced in intercalating and ductal cell population than in acinar cell population although unlikely in starved rats. This study showed the value of apoptosis using the detection system of TUNEL for evaluating cellular damage after radiation injury and the diminished effect of starvation on cell damage after ionizing irradiation.

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Non-linear Responses of Hordeum vulgare Germs to Low Doses of Ionizing Radiation

  • Kim, Jin-Kyu;Alla A. Oudalova;Vladimir G. Dikarev
    • 환경생물
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    • 제21권4호
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    • pp.384-391
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    • 2003
  • The induction of chromosome aberrations in Hordeum vulgare germs after irradiation is studied for the dose range of 10 to 1,000 mGy. The relationship between the frequency of aberrant cells and the absorbed dose is shown to be non -linear and has a dose-independent plateau within the range of 56-467 mGy where the level of cytogenetic damage is statistically significantly distinguished from the spontaneous level. The comparison of the goodness of the experimental data fitting with mathematical models of different complexities, using the most common quantitative criteria, demonstrates the benefit of the piecewise linear model over the linear and polynomial ones in approximating the cytogenetical disturbance frequency. The results of our study support the conclusion about indirect mechanism of chromosome aberrations induced by low doses or dose rates mutagenesis.

Saccharomyces cerevisiae에서 이온화 방사선과 N-acetyl-L-cysteine 처리에 따른 세포 생존과 Superoxide Dismutase와 Catalase 유전자 발현 (Cell Survival and Expression of Superoxide Dismutase and Catalase Genes in Saccharomyces cerevisiae Treated with N-acetyl-L-cysteine and Ionizing Radiation)

  • 박지영;백동원;모하마드닐리;김진규
    • 환경생물
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    • 제29권1호
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    • pp.61-67
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    • 2011
  • NAC는 GSH의 전구물질로, thiol기를 포함하는 항산화제 중 하나로 잘 알려져 있으며, 방사선 조사 시 발생하는 생체 내 영향을 감소시켜 생체 손상의 방호 및 회복에 도움을 주는 방사선 방어제로 이용된다. S. cerevisiae에서 항산화제 NAC를 전처리 함에 따라 이온화 방사선 조사에 따른 효모의 세포사멸 방어효과 및 superoxide dismutase (SOD), catalase, glutathione peroxidase (GPx)와 같은 항산화 효소들의 유전자 발현을 분석하여 NAC의 항산화적 효과를 확인하였다. 효모는 다양한 농도의 NAC 전처리 후 다양한 선량의 이온화 방사선에 조사되었으며, 세포생존율은 세포형성단위(CFU)를 계수해 측정되었고, 항산화 효소의 유전자 발현은 real-time PCR수행 후 분석하였다. 우선적으로 효모에 NAC 처리를 위한 적정농도를 확인하였는데, 35 mM 이상의 NAC 농도에서 효모세포의 성장이 억제 되었다. NAC 전처리는 감마선 조사에 의한 세포사멸을 방어하지 않았으며, 100 Gy 방사선 조사는 항산화 효소들의 유전자 발현을 유도하였다. NAC 전처리 후 항산화 효소들의 유전자 발현은NAC의 농도 증가에 따라 감소하였다. 이러한 결과로,NAC의 높은 농도(35 mM 이상)는 효모세포의 성장을 저해하며, NAC는 이온화 방사선 조사에 따른 세포사멸을 방어할 수 없으나, 생체 내에서 활성산소종을 제거 하여 세포를 보호하는 유용한 항산화제임을 알 수 있었다.

환경재해에 관한 생물정보로서의 이온화 방사선과 살충제의 인체 위해성 비교 연구 (Comparative Study on Human Risk by Ionizing Radiation and Pesticide as Biological Information about Environmental Disaster)

  • 김진규;현성희
    • Journal of Radiation Protection and Research
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    • 제26권4호
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    • pp.385-392
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    • 2001
  • 환경독성물질이나 생물 위해 요소의 환경내 준위가 일정 수준 이상일 경우 환경재해가 유발될 수 있다. 이온화 방사선의 산업적 의료적 이용이 점차 증가하고 있으며 병해충을 막기 위한 살충제 사용의 점진적 증가로 인해 이들에 의한 재해 가능성을 배제할 수 없다. 이들 재해 요인들에 의한 인체 위해도를 비교하기 위하여 단세포 겔 전기영동법 (SCGE)을 이용하여 사람 림프구 DNA 손상에 미치는 방사선과 살충제의 영향을 각각 평가하였다. 각기 다른 농도로 살충제를 10분간 처리한 림프구에 대한 SCGE 분석을 실시하였고 또한 $0{\sim}2.0Gy$의 방사선을 조사한 림프구에 대한 SCGE 분석을 실시하여 DNA 손상도를 평가하였다. DNA 손상도는 감마선에 대해서 뚜렷한 선량-반응 관계를 나타내었을 뿐 아니라 살충제에 대해서도 명확한 농도-반응 관계를 나타내었다. 파라치온은 농업권장 사용농도인 $1mg{\ell}^{-1}$에서도 림프구에 대해 강한 유전독성을 나타내는데 이러한 유전독성은 0.1 Gy의 감마선에 의해 유발되는 DNA 손상에 상응하며 $2mg{\ell}^{-1}$의 파라치온은 임상적 증상을 야기할 가능성이 있는 전신 외부피폭 방사선량인 0.25 Gy에 상응하는 세포손상을 유발하였다. 이와 같은 연구를 통해 방사선과 살충제의 인체 위해도를 비교할 수 있는 실험적 자료와 환경재해 예방에 필요한 생물정보를 제공할 수 있다.

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즉발감마선에 의한 상용전자소자의 피해현상분석 연구 (The Study of Transient Radiation Effects on Commercial Electronic Devices)

  • 오승찬;이남호;이흥호
    • 전기학회논문지
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    • 제61권10호
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    • pp.1448-1453
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    • 2012
  • In this study, we carried out transient radiation test for identify failure situation by a transient radiation effect on operational amplifier devices. This experiments were carried out using a 60 MeV electron beam pulse of the LINAC(Linear Accelerator) facility in the Pohang Accelerator Laboratory. In this test, we has found that a serious failure as a burn-out effect due to overcurrent on the partial electronic devices.

Theoretical Conception of Synergistic Interactions

  • Kim, Jin-Kyu;Vladislav G. Petin
    • 환경생물
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    • 제20권4호
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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.

Hormesis as a Confounding Factor in Epidemiological Studies of Radiation Carcinogenesis

  • Sanders Charles L.
    • Journal of Radiation Protection and Research
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    • 제31권2호
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    • pp.69-89
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    • 2006
  • Biological mechanisms for ionizing radiation effects are different at low doses than at high doses. Radiation hormesis involves low-dose-induced protection and high-dose-induced harm. The protective component is associated with a reduction in the incidence of cancer below the spontaneous frequency, brought about by activation of defensive and repair processes. The Linear No-Threshold (LNT) hypothesis advocated by the International Commission on Radiological Protection (ICRP) and the Biological Effects of ionizing Radiation (BEIR) Report VII for cancer risk estimations Ignores hormesis and the presence of a threshold. Cancer incidences significantly less than expected have been found in a large number of epidemiological studies including, airline flight personnel, inhabitants of high radiation backgrounds, shipyard workers, nuclear site workers in scores of locations throughout the world, nuclear power utility workers, plutonium workers, military nuclear test site Participants, Japanese A-bomb survivors, residents contaminated by major nuclear accidents, residents of Taiwan living in $^{60}Co$ contaminated buildings, fluoroscopy and mammography patients, radium dial painters, and those exposed to indoor radon. Significantly increased cancer was not found at doses <200 $mSv^*$. Evidence for radiation hormesis was seen in both sexes for acute or chronic exposures, low or high LET radiations, external whole- or partial body exposures, and for internal radionuclides. The ubiquitous nature of the Healthy Worker Effect (HWE)-like responses in cellular, animal and epidemiological studies negates the HWE as an explanation for radiation hormesis. The LNT hypothesis is wrong and does not represent the true nature of the dose-response relationship, since low doses or dose-rates commonly result in thresholds and reduce cancer incidences below the spontaneous rate. Radiation protection organizations should seriously consider the cost and health implications of radiation hormesis.