• 한국지하수토양환경학회지:지하수토양환경
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• 제9권1호
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• pp.12-27
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• 2004

본 연구에서는 벤젠을 대상으로 오염된 지하수를 생활용수로 사용했을 때 발생하는 실내오염도를 모사하고 실내에서 가능한 흡입, 섭취, 피부흡수와 같은 노출경로를 고려하여 노출시나리오를 자성하였다. 인체에 유입된 벤젠에 대하여 PBPK 모델을 이용하여 인체의 각 장기에 어떻게 분포하는지를 분석하였다. 결과에서 흡입과 섭취가 주요노출 경로였으며 남성이 여성보다 많은 호흡량으로 인해 보다 높은 노출속도를 유지하였다. 노출속도에 대한 피부흡수의 공헌도는 상대적으로 매우 작았다. 단기노출의 결과 오염물 노출에 대하여 SPT, RPT,간의 정맥혈 중 벤젠농도는 빠르게 증감하는 반면 지방의 경우는 느리게 반응하였고 많은 벤젠이 지방세포에 축적되어 정맥혈에는 적은 농도로 존재하였다. 장기간 노출에서 여성은 남성보다 전체적으로 2.1배 많은 벤젠을 체내에 축적하고 있는 것으로 나타났다. 장기간 노출에서 총유입벤젠의 98%가 호흡과 대사분해에 의해 제거되었다. 흡입경로는 벤젠이 호흡배출에 의해 69.8% 제거되었으며 섭취경로는 48.4%로 오염물이 유입되는 위치에 따라 각각의 제거기작의 공헌도가 다르게 나타났다. 본 연구의 결과는 실내오염에 따라 오염물이 체내에 흡수되고 분포ㆍ제거되는 현상을 이해하고 노출저감대책을 마련하는데 필요한 자료를 제공하고자 하였다.

• 방사선산업학회지
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• 제18권1호
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• pp.35-42
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• 2024

Demand for RW transportation is expected to increase due to the continuous generation of RW from nuclear power plants and facilities, decommissioning of plants, and saturation of spent fuel temporary storage facilities. The locational aspect of plants and radiation protection optimization for the public have led to an increasing demand for maritime transportation, necessitating to apprehend the overseas and domestic current status. Given the potential long-term radiological impact on the public in the event of a sinking accident, a pre-transportation exposure assessment is necessary. The objective of this study is to investigate the overseas and domestic RW maritime transportation current status and overseas dose assessment cases for the public in sinking accident. Selected countries, including Japan, UK, Sweden, and Korea, were examined for transport cases, Japan and the U.S were chosen for dose assessment case in sinking accidents. As a result of the maritime transportation case analysis, it was performed between nuclear power plants and reprocessing facilities, from plants to disposal or intermediate storage facilities. HLW and MOX fuel were transported using INF 3 shipments, and all transports were performed low speed of 13 kn or less. As a result of the dose assessment for the public in sinking accident, japan conducted an assessment for the sinking of spent fuel and vitrified HLW, and the U.S conducted for the sinking of spent fuel. Both countries considered external exposure through swimming and working at seashore, and internal exposure through seafood ingestion as exposure pathway. Additionally, Japan considered external exposure through working on board and fishing, and the U.S considered internal exposure through spray inhalation and desalinized water and salt ingestion. Internal exposure through seafood ingestion had the largest dose contribution. The average public exposure dose was 20 years after the sinking, 0.04 mSv yr^-1 for spent fuel and 5 years after the sinking, 0.03 mSv yr^-1 for vitrified HLW in Japan. In the U.S, it was 1.81 mSv yr^-1 5 years after the sinking of spent fuel. The results of this study will be used as fundamental data for maritime transportation of domestic RW in the future.

• 약학회지
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• 제54권5호
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• pp.392-397
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• 2010

The aim of present study was to investigate the possible influence and related mechanism of additional alcohol on the flavonoid- induced arterial relaxation. Agonist-induced vascular smooth muscle contractions involve the activation of thick or thin filament pathway. However, there are no reports addressing the question whether this pathway is involved in quercetin-induced relaxation cotreated with alcohol in rat aortae contracted with phorbol ester, fluoride or thromboxane $A_2$ mimetic U-46619. We hypothesized that cotreated alcohol plays a role in vascular relaxation evoked by quercetin in rat aortae. Endothelium-denuded arterial rings from male Sprague-Dawley rats were used and isometric contractions were recorded using a computerized data acquisition system. Quercetin inhibited phorbol ester, fluoride or thromboxane $A_2$-induced contraction regardless of endothelial function. However, alcohol didn't decrease any agonist-induced contraction. Interestingly, only in thromboxane $A_2$-induced contraction, synergistic results were observed in aortae denuded and cotreated with quercetin and alcohol suggesting that additional pathways different from antioxidation or endothelial nitric oxide synthesis might be involved in the vasorelaxation. In conclusion, in the agonists-contracted rat aortae, quercetin and alcohol together showed synergistic response regardless of endothelial function in an agonist-dependent manner.

• Journal of Microbiology and Biotechnology
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• 제29권10호
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• pp.1675-1681
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• 2019

Clostridium difficile toxin A is known to cause colonic epithelial cell apoptosis, which is considered the main causative event that triggers inflammatory responses in the colon, reflecting the concept that the essential role of epithelial cells in the colon is to form a physical barrier in the gut. We previously showed that toxin A-induced colonocyte apoptosis and subsequent inflammation were dependent on prostaglandin E2 ($PGE_2$) produced in response to toxin A stimulation. However, the molecular mechanism by which $PGE_2$ mediates cell apoptosis in toxin A-exposed colonocytes has remained unclear. Here, we sought to identify the signaling pathway involved in toxin A-induced, $PGE_2$-mediated colonocyte apoptosis. In non-transformed NCM460 human colonocytes, toxin A exposure strongly upregulated expression of Bak, which is known to form mitochondrial outer membrane pores, resulting in apoptosis. RT-PCR analyses revealed that this increase in Bak expression was attributable to toxin A-induced transcriptional upregulation. We also found that toxin A upregulation of Bak expression was dependent on $PGE_2$ production, and further showed that this effect was recapitulated by an Prostaglandin E2(PGE2) receptor-1 receptor agonist, but not by agonists of other EP receptors. Collectively, these results suggest that toxin A-induced cell apoptosis involves $PGE_2$-upregulation of Bak through the EP1 receptor.

• Journal of Plant Biotechnology
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• 제46권2호
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• pp.88-96
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• 2019

Terpenes constitute a large class of secondary metabolites in plants. The Oryza sativa terpene synthase is a vital gene in plant defense response. In this study, the molecular and physiological functions of Oryza sativa terpene synthase 30 (OsTPS30, LOC_Os08g07080) were investigated after exposure of the seeds and plants to gamma-rays. The OsTPS30 expression was slightly induced at 200 Gray (Gy), but was significantly induced at 400 Gy. The total terpenoid was synthesized more in OsTPS30-overexpressing (OX-OsTPS30) Arabidopsisthaliana plants than in wild-type (WT) plants. The OX-OsTPS30 plants exhibited resistance to gamma-rays, as compared to WT. The OX-OsTPS30 plants had significantly increased height and weight after gamma irradiation. Additionally, the activity of antioxidant enzymes was increased more in OX OsTPS30 plants than in WT plants after gamma irradiation. Furthermore, the OsTPS30-GFP fusion protein was mostly localized in the chloroplast, suggesting that OsTPS30 is putative MEP pathway-related terpene synthase.

• The Plant Pathology Journal
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• 제39권5호
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• pp.449-465
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• 2023

Plants are challenged by various pathogens throughout their lives, such as bacteria, viruses, fungi, and insects; consequently, they have evolved several defense mechanisms. In addition, plants have developed localized and systematic immune responses due to biotic and abiotic stress exposure. Animals are known to activate DNA damage responses (DDRs) and DNA damage sensor immune signals in response to stress, and the process is well studied in animal systems. However, the links between stress perception and immune response through DDRs remain largely unknown in plants. To determine whether DDRs induce plant resistance to pathogens, Arabidopsis plants were treated with bleomycin, a DNA damage-inducing agent, and the replication levels of viral pathogens and growth of bacterial pathogens were determined. We observed that DDR-mediated resistance was specifically activated against viral pathogens, including turnip crinkle virus (TCV). DDR increased the expression level of pathogenesis-related (PR) genes and the total salicylic acid (SA) content and promoted mitogen-activated protein kinase signaling cascades, including the WRKY signaling pathway in Arabidopsis. Transcriptome analysis further revealed that defense-and SA-related genes were upregulated by DDR. The atm-2atr-2 double mutants were susceptible to TCV, indicating that the main DDR signaling pathway sensors play an important role in plant immune responses. In conclusion, DDRs activated basal immune responses to viral pathogens.

• 한국지하수토양환경학회지:지하수토양환경
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• 제21권6호
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• pp.56-66
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• 2016

Generally, the contribution of crop-intake pathway (CIP) is remarkable in human health assessment (HHA) of heavy metal contamination. Although the crop exposure concentrations (Cp) should directly be used for calculating the average daily dose (ADD) of CIP, the soil exposure concentration (Cs) multiplied by soil-crop bio-concentration factor (BCF) has frequently been used instead of using Cp values. Thus, the BCF values are significant in the HHA, and care should be taken to ensure the reasonable acquisition of BCF values. Meanwhile, the BCF values are known to be significantly affected by analytical methods. Nevertheless, they have been calculated from the concentrations of soil and crop analyzed by only one method: total digestion (aqua regia extraction). For this reason, this study was initiated to seek appropriate soil analysis methods for effective computation of the ADD of CIP. The concentrations of 5 metal contaminants (As, Cd, Cu, Pb, and Zn) in 127 soil samples obtained from 4 abandoned metal mine areas were analyzed by several methods including total digestion and partial digestions using 0.1/1 N HCl, 1M $NH_4NO_3$, 0.1 M $NaNO_3$, and 0.01M $CaCl_2$. The heavy metal concentrations in 127 crop samples (rice grains) were analyzed by total digestion as well. Using the concentrations of soils and crops, the BCF values of each contaminant were calculated according to the kind of soil extraction methods applied. Finally, the errors between Cp and $C_s{\times}BCF$ were computed to evaluate the relevance of each method. The results indicate that the partial extraction using 0.1 N and 1 N HCl was superior or equivalent to total digestion. In addition, the 0.1M $NaNO_3$ method combined with total digestion is recommended for improving the reliability of BCF values.

• Journal of Microbiology and Biotechnology
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• 제27권1호
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• pp.197-205
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• 2017

Exposure of Jurkat T cell clone (J/Neo cells) to acacetin (5,7-dihydroxy-4'-methoxyflavone), which is present in barnyard millet (Echinochloa esculenta (A. Braun)) grains, caused cytotoxicity, enhancement of apoptotic $sub-G_1$ rate, Bak activation, loss of mitochondrial membrane potential (${\Delta}{\Psi}m$), activation of caspase-9 and caspase-3, degradation of poly(ADP-ribose) polymerase, and FITC-Annexin V-stainable phosphatidylserine exposure on the external surface of the cytoplasmic membrane without accompanying necrosis. These apoptotic responses were abrogated in Jurkat T cell clone (J/Bcl-xL) overexpressing Bcl-xL. Under the same conditions, cellular autophagic responses, including suppression of the Akt-mTOR pathway and p62/SQSTM1 down-regulation, were commonly detected in J/Neo and J/Bcl-xL cells; however, formation of acridine orange-stainable acidic vascular organelles, LC3-I/II conversion, and Beclin-1 phosphorylation (Ser-15) were detected only in J/Neo cells. Correspondingly, concomitant treatment with the autophagy inhibitor (3-methyladenine or LY294002) appeared to enhance acacetin-induced apoptotic responses, such as Bak activation, ${\Delta}{\Psi}m$ loss, activation of caspase-9 and caspase-3, and apoptotic $sub-G_1$ accumulation. This indicated that acacetin could induce apoptosis and cytoprotective autophagy in Jurkat T cells simultaneously. Together, these results demonstrate that acacetin induces not only apoptotic cell death via activation of Bak, loss of ${\Delta}{\Psi}m$, and activation of the mitochondrial caspase cascade, but also cytoprotective autophagy resulting from suppression of the Akt-mTOR pathway. Furthermore, pharmacologic inhibition of the autophagy pathway augments the activation of Bak and resultant mitochondrial damage-mediated apoptosis in Jurkat T cells.

• 한국산업보건학회지
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• 제29권2호
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• pp.141-158
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• 2019

Objectives: An adverse outcome pathway is a biological pathway that disturbs homeostasis and causes toxicity. It is a conceptual framework for organizing existing biological knowledge and consists of the molecular initiating event, key event, and adverse output. The AOP concept provides intuitive risk identification that can be helpful in evaluating the carcinogenicity of chemicals and in the prevention of cancer through the assessment of chemical carcinogenicity predictions. Methods: We reviewed various papers and books related to the application of AOPs for the prevention of occupational cancer. We mainly used the internet to search for the necessary research data and information, such as via Google scholar(http://scholar.google.com), ScienceDirect(www.sciencedirect.com), Scopus(www.scopus. com), NDSL(http: //www.ndsl.kr/index.do) and PubMed(http://www.ncbi.nlm.nih.gov/pubmed). The key terms searched were "adverse outcome pathway," "toxicology," "risk assessment," "human exposure," "worker," "nanoparticle," "applications," and "occupational safety and health," among others. Results: Since it focused on the current state of AOP for the prediction of toxicity from chemical exposure at work and prospects for industrial health in the context of the AOP concept, respiratory and nanomaterial hazard assessments. AOP provides an intuitive understanding of the toxicity of chemicals as a conceptual means, and it works toward accurately predicting chemical toxicity. The AOP technique has emerged as a future-oriented alternative to the existing paradigm of chemical hazard and risk assessment. AOP can be applied to the assessment of chemical carcinogenicity along with efforts to understand the effects of chronic toxic chemicals in workplaces. Based on these predictive tools, it could be possible to bring about a breakthrough in the prevention of occupational and environmental cancer. Conclusions: The AOP tool has emerged as a future-oriented alternative to the existing paradigm of chemical hazard and risk assessment and has been widely used in the field of chemical risk assessment and the evaluation of carcinogenicity at work. It will be a useful tool for prediction, and it is possible that it can help bring about a breakthrough in the prevention of occupational and environmental cancer.

• Toxicological Research
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• 제28권2호
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• pp.107-112
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• 2012

Polychlorinated biphenyls (PCBs) are persistent and bioaccumulative environmental pollutants. Recently, it is suggested that neurotoxic effects such as motor dysfunction and impairment in memory and learning have been associated with PCB exposure. However, structure relationship of PCB congeners with neurotoxic effects remains unknown. Since PKC signaling pathway is implicated in the modulation of motor behavior as well as learning and memory and the role of PKC are subspecies-specific, we attempted to study the effects of structurally distinct PCBs on the total PKC activity as well as subspecies of PKC in cerebellar granule cell culture model. Cells were exposed to 0, 25 and 50 ${\mu}M$ of PCB-126, PCB-169, PCB-114, PCB-157, PCB-52 and PCB-4 for 15 min. Cells were subsequently analyzed by [$^3H$] phorbol ester binding assay or immunoblotted against PKC-${\alpha}$ and -${\varepsilon}$ monoclonal antibodies. While non-dioxin-like-PCB (PCB-52 and PCB-4) induced a translocation of PKC-${\alpha}$ and -${\varepsilon}$ from cytosol to membrane fraction, dioxin-like PCBs (PCB-126, -169, -114, -157) had no effects. [$^3H$] Phorbol ester binding assay also revealed structure-dependent increase similar to translocation of PKC isozymes. While PCB-4 induced translocation of PKC-${\alpha}$ and -${\varepsilon}$ was inhibited by ROS inhibitor, the pattern of translocation was not affected in presence of AhR inhibitor. It is suggested that PCB-4-induced PKC activity may not be mediated via AhR-dependent pathway. Taken together, our findings suggest that chlorination of ortho-position in PCB may be a critical structural moiety associated with neurotoxic effects, which may be preferentially mediated via non-AhR-dependent pathway. Therefore, the present study may contribute to understanding the neurotoxic mechanism of PCBs as well as providing a basis for establishing a better neurotoxic assessment.