• Current Research on Agriculture and Life Sciences
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• 제4권
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• pp.65-69
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• 1986

혼합(混合) 조미료(調味料)의 효과적(效果的)인 살균(殺菌)을 목적(目的)으로 시료에 3~9kGy의 감마선을 조사한 뒤 $30^{\circ}C$에서 3개월 동안 저장하면서 미생물(微生物)의 생육도(生有度)와 살균처리(殺菌處理)에 따른 제품의 성분 및 관능적 품질을 평가해 본 결과는 다음과 같다. 1. 시료(試料)의 미생물(微生物) 혼입도(混入度)는 일반세균(一般細菌)이 g당(當) $7.5{\times}10^5$, 대장균군(大腸菌群)이 $1.2{\times}10^2$이었으나 대장균군(大腸菌群)은 3kGy, 일반세균(一般細菌)은 9kGy 미만(未滿) 조사(照射)로서 완전사멸(完全死滅)되었고, 세균(細菌)의 $D_{10}$값은 1.94kGy로 나타났다. 2. 시료(試料)의 이화학적(理化學的) 특성(特性)은 살균처리(殺菌處理)에 따라서 거의 변화되지 않았으며, 저장기간이 경과될수록 3~6kGy 조사구는 대조구나 9kGy 조사구보다 성분의 변화가 적었다. 3. 시료(試料)의 관능적(官能的) 품질검사(品質檢査)에서 고선량(高線量) 조사(照射)는 제품(製品)의 풍미(風味)에 변화를 초래하는 것으로 나타나 이에 대한 구체적인 검토(檢討)가 요망(要望)된다.

• 한국항공우주학회지
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• 제34권11호
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• pp.84-91
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• 2006

최근에 인공위성용 전자소자는 우주방사선에 좀 더 강한 소자를 요구되어진다. 왜냐하면, 인공위성의 수명과 기능은 우주방사선으로부터 영향을 받기 때문이다. 또한, 과거에는 부품단위의 우주방사선 시험을 수행하지 않고 유닛 또는 서브시스템 단위의 우주방사선 시험을 수행하였다. 게다가, 발사된 인공위성이 작동오류 상태에 있을 때 그 이유를 분석하기에는 그다지 쉬운 일은 아니다. 따라서, 발사 전 부품 단위 우주방사선 시험을 수행하여 주요 소자에 대한 우주방사선에 의한 영향을 분석 할 필요가 있으며, 지상에서 데이터를 확보할 필요가 있다. 그러므로, 본 논문에서는 모든 전자소자의 기본이라 할 수 있는 금속-산화막 반도체 전계효과 트랜지스터의 총이온화선량에 대한 영향 시험을 수행하기 위한 테스트 베드를 제안한다.

• Journal of Microbiology and Biotechnology
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• 제23권11호
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• pp.1493-1499
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• 2013

A novel radiation-resistant Filobasidium sp. yeast strain was isolated from seawater. Along with this strain, a total of 656 yeast isolates were purified from seawater samples collected from three locations in the West Sea of Korea and assessed for their radiation tolerance. Among these isolates, five were found to survive a 5 kGy radiation dose. The most radiation-resistant strain was classified as Filobasidium sp. based on 18S rDNA sequence analysis and hence was named Filobasidium RRY1 (Radiation-Resistant Yeast 1). RRY1 differed from F. elegans, which is closely related to RRY1, in terms of the optimal growth temperature and radiation resistance, and was resistant to high doses of ${\gamma}$-ionizing radiation ($D_{10}$: 6-7 kGy). When exposed to a high dose of 3 kGy irradiation, the RRY1 cells remained intact and undistorted, with negligible cell death. When these irradiated cells were allowed to recover, the cells fully repaired their genomic DNA within 3 h of growth recovery. This is the first report in which a radiation-resistant response has been investigated at the physiological, morphological, and molecular levels in a strain of Filobasidium sp.

• 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.

• BMB Reports
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• 제34권2호
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• pp.123-129
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• 2001

Cellular response to ionizing radiation is affected by cell types, radiation doses, and post-irradiation time. Based on the trypan blue dye exclusion assay in normal oral mucosal cells (OM cells), a 48 h post-irradiation was sufffcient and an adequate time point for the evaluation of radiation sensitivity Its $LD_{50}$ was approximately 1.83 Gy To investigate possible biomarkers useful for the biological radiodosimetry of normal epithelial cells (p53, c-fos, cyclin D1, cdc-2, pRb) EGF receptor phosphorylation and Erk activation were evaluated at different radiation doses and different post-irradiation times. From 0.5 Gy, p53 was accumulated in the nucleus of basal cells of the OM raft culture at 4 h post-irradiation and sustained up to 24 h post-irradiation, which suggests that radiation-induced apoptosis or damage repair was not yet completed. The number of p53 positive cells and biosynthesis of p53 were correlated with radiation doses. Both cyclin D1 and c-fos were only transiently induced within 1 h post-irradiation. Cyclin D1 was induced at all radiation doses. However, cfos induction was highest at 0.1 Gy, approximately 7.3 fold more induction than the control, whose induction was reduced in a reverse correlation with radiation dose. The phosphorylation pattern of cdc-2 and pRb were unaffected by radiation. In contrast to A431 tails overexpressing the EGF receptor approximately 8.5 fold higher than normal epithelial, the OM cells reduced the basal level of the EGF receptor phosphorylation in a radiation dose dependent fashion. In conclusion, among radiation-induced biomolecules, the p53 nuclear accumulation may be considered for the future development of a useful marker far biological radiodosimetry in normal epithelial tissue since it was sustained for a longer period and showed a dose response relationship. Specific c-fos induction at a low dose may also be an important finding in this study It needs to be studied further for the elucidation of its possible connection with the low dose radio-adaptive response.

• Imaging Science in Dentistry
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• 제30권4호
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• pp.275-279
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• 2000

Purpose: Radiation damage is produced and viable cell number is reduced. We need to know the type of cell death by the ionizing radiation and the amount and duration of cell cycle arrest. In this study, we want to identified the main cause of the cellular damage in the oral cancer cells and normal keratinocytes with clinically useful radiation dosage. Materials and Methods: Human gingival tissue specimens obtained from healthy volunteers were used for primary culture of the normal human oral keratinocytes (NHOK). Primary NHOK were prepared from separated epithelial tissue and maintained in keratinocyte growth medium containing 0.15 mM calcium and a supplementary growth factor bullet kit. Fadu and Hep-2 cell lines were obtained from KCLB. Cells were irradiated in a /sup 137/Cs γ-irradiator at the dose of 10 Gy. The dose rate was 5.38 Gy/min. The necrotic cell death was examined with Lactate Dehydrogenase (LDH) activity in the culture medium. Every 4 day after irradiation, LDH activities were read and compared control group. Cell cycle phase distribution and preG1-incidence after radiation were analyzed by flow cytometry using Propidium Iodine staining. Cell cycle analysis were carried out with a FAC Star plus flowcytometry (FACS, Becton Dickinson, USA) and DNA histograms were processed with CELLFIT software (Becton Dickinson, USA). Results: LDH activity increased in all of the experimental cells by the times. This pattern could be seen in the non-irradiated cells, and there was no difference between the non-irradiated cells and irradiated cells. We detected an induction of apoptosis after irradiation with a single dose of 10 Gy. The maximal rate of apoptosis ranged from 4.0% to 8.0% 4 days after irradiation. In all experimental cells, we detected G2/M arrest after irradiation with a single dose of 10 Gy. Yet there were differences in the number of G2/M arrested cells. The maximal rate of the G2/M ranges from 60.0% to 80.0% 24h after irradiation. There is no significant changes on the rate of the G0/G1 phase. Conclusion: Radiation sensitivity was not related with necrosis but cell cycle arrest and apoptosis. These data suggested that more arrested cell is correlated with more apoptosis.

• Archives of Pharmacal Research
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• 제18권6호
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• pp.410-414
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• 1995

Adaptive response induced by low dese .gamma.-ray irradiation in human cervical carcinoma cells was examined. Cells were exposured to low dose of .gamma.-ray irradiation in human cervical carcinoma cells was examined. Cells were exposured to low dose of .gamma.-ray (1-cGy) followed by high doses of r-ray irradiation (0,1,2,3,5,7 and 9Gy for chlnogenic assay or 1.5Gy for micronucleus assay) with various time intervals. Survival fractions of cells in both low dose-irradiated and unirrated groups were analyzed by clonogenic assay. Surviva fractions of low dose-irradiated in cell survival was maximum when low and high dose irradiation time interval was 4 hr. Frequencies of micronuclei which is an indicative of chromosome aberration were also enutained from survival fractions analyzed by clonogenic assay, maximum when low and high dose irradiation time interval was 4hr. Frequencies of micronuclei which is an indicative of chromosome aberration were also enumerated in both low dose-irradiated and unirradiated groups. In consiststent with the result obtained from survival fractions analyzed by clonogenic assay, maximum reduction in frquencies of micronuclei was observed when low dose radiation was given 4 hr prior to high response to subsequent high dose .gamma.-ray irradiation in human cervical carcinomal cells. Our data suggest that one of the possible mechanisms of adaptive response induced by low dose rediation is the increase in repair of DNA double strand breaks in low dose radiation-adapted cells.

• 한국식품과학회지
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• 제21권5호
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• pp.669-675
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• 1989

감마선 조사 (0, 1, 2, 3kGy)에 의한 생양송이 버섯의 저장성 연장에 관한 연구결과는 다음과 같다. $9{\pm}1^{\circ}C,\;80{\pm}7%$ RH 저장조건에서 비조사구는 저장 3일경부터 갓핌과 줄기가 크게 신장하고 노후현상을 보여 상품가치를 상실한데 반해 감마선 조사구는 자연적 숙성으로 지연으로 1kGy 조사구는 10일정도, 2-3kGy 조사구는 20일까지도 신선도를 유지하였다. 양송이의 조직은 저장기간 동안 모든 시험구에서 연화를 보였으나 감마선 조사구가 비조사구에 비해 양호하였다. 중량 변화는 골판지 상자에 양송이를 담고 polyethylene 필름으로 겉씌우기를 한 것이 골판지 단독 포장구보다 중량감소 억제효과가 매우 현저하였고, 저장 5일 이후부터는 2-3kGy 조사구가 비조사구에 비해 중량 감소율이 낮았다. 이러한 결과는 생양송이에 2-3kGy의 감마선 조사 후 $9{\pm}1^{\circ}C,\;80{\pm}7%$ RH 의 저장조건에서 숙도지연에 따른 고려할 만한 저장성 연장효과를 나타내었다.

• Radiation Oncology Journal
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• 제31권2호
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• pp.57-65
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• 2013

Beta-lapachone (${\beta}$-Lap; 3,4-dihydro-2, 2-dimethyl-2H-naphthol[1, 2-b]pyran-5,6-dione) is a novel anti-cancer drug under phase I/II clinical trials. ${\beta}$-Lap has been demonstrated to cause apoptotic and necrotic death in a variety of human cancer cells in vitro and in vivo. The mechanisms underlying the ${\beta}$-Lap toxicity against cancer cells has been controversial. The most recent view is that ${\beta}$-Lap, which is a quinone compound, undergoes two-electron reduction to hydroquinone form utilizing NAD(P)H or NADH as electron source. This two-electron reduction of ${\beta}$-Lap is mediated by NAD(P)H:quinone oxidoreductase (NQO1), which is known to mediate the reduction of many quinone compounds. The hydroquinone forms of ${\beta}$-Lap then spontaneously oxidizes back to the original oxidized ${\beta}$-Lap, creating futile cycling between the oxidized and reduced forms of ${\beta}$-Lap. It is proposed that the futile recycling between oxidized and reduced forms of ${\beta}$-Lap leads to two distinct cell death pathways. First one is that the two-electron reduced ${\beta}$-Lap is converted first to one-electron reduced ${\beta}$-Lap, i.e., semiquinone ${\beta}$-Lap $(SQ)^{{\cdot}-}$ causing production of reactive oxygen species (ROS), which then causes apoptotic cell death. The second mechanism is that severe depletion of NAD(P)H and NADH as a result of futile cycling between the quinone and hydroquinone forms of ${\beta}$-Lap causes severe disturbance in cellular metabolism leading to apoptosis and necrosis. The relative importance of the aforementioned two mechanisms, i.e., generation of ROS or depletion of NAD(P)H/NADH, may vary depending on cell type and environment. Importantly, the NQO1 level in cancer cells has been found to be higher than that in normal cells indicating that ${\beta}$-Lap may be preferentially toxic to cancer cells relative to non-cancer cells. The cellular level of NQO1 has been found to be significantly increased by divergent physical and chemical stresses including ionizing radiation. Recent reports clearly demonstrated that ${\beta}$-Lap and ionizing radiation kill cancer cells in a synergistic manner. Indications are that irradiation of cancer cells causes long-lasting elevation of NQO1, thereby sensitizing the cells to ${\beta}$-Lap. In addition, ${\beta}$-Lap has been shown to inhibit the repair of sublethal radiation damage. Treating experimental tumors growing in the legs of mice with irradiation and intraperitoneal injection of ${\beta}$-Lap suppressed the growth of the tumors in a manner more than additive. Collectively, ${\beta}$-Lap is a potentially useful anti-cancer drug, particularly in combination with radiotherapy.

• Journal of Radiation Protection and Research
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• 제24권1호
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• pp.17-22
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• 1999

이온화방사선이 동물 생식세포에 미치는 생화학적 및 형태학적 영향을 알아보기 위해 본 연구를 시행하였다. 미성숙 생쥐 (ICR, 3 주령)에 $\gamma$선을 선량 $LD_{80(30)}$으로 전신조사하였다. 방사선 조사 후 6 시간, 12 시간, 1 일, 그리고 2 일 후에 난소를 적출하였다. 난소에서 추출한 과립세포의 세포주기를 DNA에 대한 유세포 분석으로 분석하였다. 세포자연사를 확인할 수 있는 $A_0$ 세포주기는 이온화방사선이 조사된 실험군에서 대조군에 비해 현저히 높은 값을 보였다. 이온화방사선을 조사한 후 6 시간 군에서 TUNEL 면역조직화학 염색도를 나타낸 난포의 수가 대조군에 비해 현저히 증가하였다. 따라서, 본 실험의 결과 방사선 조사에 의해 유발되는 난포의 퇴화는 6 시간 이내에 급성으로 진행되는 과립세포의 세포자연사에 의해 매개됨을 알 수 있었다. 유세포분석기를 이용한 세포주기 평가는 방사선에 의해 유발되는 세포자연사 기작의 이해와 퇴화난포의 정량화를 위한 수단이 될 수 있다.