• 한국어병학회지
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• 제16권2호
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• pp.91-102
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• 2003

The present study was investigated the effects of chlorine dioxide ($CIO_2$) on the rcspimtory metabolism of olive flounder (Parolichlhys olivaceus) imtermittently exposed to seawater chlorinated by $CIO_2$:. Oxygen consumption of flounder before and after once or twice $CIO_2$-treatment with 12 hr- or/and 24 hr-interval were serially measured with automatic intenniteent-flow respirometer system (AIRS). The oxygen consumption rates of flowKier exposed to 0.10 and 0.20 ppm$CIO_2$, were not different from the control fish prior to the once or twice chlorinations . On the other hand, the respiratory metabolic rates of flounder exposed to 0.30 ppm$CIO_2$ were significantly increased 15% and 22 - 23% after the once and twice chlorinations compared to the control fish. respectively. The flounder exposed In 0.40 and 0.50 ppm$CIO_2$: died within 4 hr and I hr. respectively. The elevation( respiratory metabolism in flounder exposed toO.30 ppm$CIO_2$ and above is considered due to physiological stress caused by $CIO_2$ exposure.

• 대한임상독성학회지
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• 제18권1호
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• pp.34-41
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• 2020

Purpose: This study evaluated aggressive hyperbaric oxygen therapy (HBOT) by understanding various exposure routes of acute carbon monoxide (CO) poisoning, the risk factors causing acute cardiovascular, and neurological toxicity caused by poisoning. Methods: A retrospective study was conducted based on the medical records of 417 acute CO poisoning patients who visited the emergency care unit from March 2017 to August 2019. The exposure routes, HBOT performance, age, sex, medical history (hypertension, diabetes mellitus, ischemic heart disease, heart failure), intentionality, loss of consciousness (LOC), intake with alcohol or sedatives, and initial test results (carboxyhemoglobin (COHb), troponin-I, electrocardiography, echocardiography, brain MRI) were examined. Comparative analysis of the clinical information was conducted between the groups that showed acute cardiovascular toxicity and neurological toxicity, and groups that did not. Results: Among 417 patients diagnosed with acute CO poisoning, 201 cases (48.2%) were intentional, and charcoal briquette was the most common route (169 patients (40.5%)). Two hundred sixteen cases (51.8%) were accidental, and fire was the most common route (135 patients (32.4%)). The exposure route was more diverse with accidental poisoning. Three hundred ninety-nine patients were studied for acute cardiovascular toxicity, and 62 patients (15.5%) were confirmed to be positive. The result was statistically significant in intentionality, LOC, combined sedatives, initial COHb, HTN, and IHD. One hundred two patients were studied for acute neurological toxicity, which was observed in 26 patients (25.5%). The result was statistically significant in age and LOC. Conclusion: Active HBOT should be performed to minimize damage to the major organs by identifying the various exposure routes of CO poisoning, risk factors for acute cardiovascular toxicity (intentionality, LOC, combined sedatives, initial COHb, HTN, IHD), and the risk factors for acute neurological toxicity (age, LOC).

• 대한예방의학회:학술대회논문집
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• 대한예방의학회 1999년도 제51차 추계 학술대회 연제집
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• pp.308-309
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• 1999

• 한국자원식물학회지
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• 제21권6호
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• pp.435-439
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• 2008

Due to the fact that tocopherols and tocotrienols have antioxidant and anticancer properties, the commercial utilization of unsaponifiable fractions in rice bran is increasing. These nutraceutical compounds, however, are fairly unstable and readily break down when exposed to oxygen or lighting conditions. To compare the relative sensitivity of vit E isomers to heat and oxygen, concentrated unsaponifiable fractions extracted from crude rice bran oil were exposed to various temperature, oxygen (nitrogen-balanced), and bathing solvent conditions and resultant concentration changes in ${\alpha}$- and ${\gamma}$-tocopherols (T) and tocotrienols (T3) were evaluated. Each isomer exhibited different heat stability. Among them, ${\alpha}$-T3 degraded more rapidly compared to other vit E isomers while ${\alpha}$-T was the most stable isomer. Oxygen level also showed significant impact on each isomer's stability where severe reductions of ${\gamma}$-T (by 20%) and ${\gamma}$-T3 (by 29%) were observed under 2% oxygen conditions, while under 0% oxygen conditions no degradation could be observed even after exposure to $95^{\circ}C$ for 4 hours. When various blending solvents were mixed with concentrated unsaponifiable fractions, organic solvents such as isooctane and hexane were more effective in maintaining the stability of ${\gamma}$- T3 compared to edible oils, among which com oil was more efficient than soybean and rice bran oils.

• 폴리머
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• 제35권6호
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• pp.565-573
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• 2011

Poly(methyl methacrylate)/aluminum hydroxide(PMMA/AH) 컴포지트의 기계적 강도를 향상시키기 위해 그래핀 산화물(GO)을 충전제로 사용하여 나노컴포지트를 제조하였다. GO는 흑연을 Hummers법으로 산화한 후 열처리에 의해 박리시켜 제조하였다. PMMA/AH 컴포지트 매트릭스와의 계면혼화성을 향상시키기 위해 산소 플라즈마를 사용하여 노출 시간을 0분에서 70분까지 변화를 주어가며 GO 표면을 개질시켰다. 노출 시간이 50분까지 증가함에 따라 산소 플라즈마 처리한 GO를 충전제로 사용한 나노컴포지트는 PMMA/AH 컴포지트에 비해 굴곡강도, 굴곡탄성률, Rockwell 경도, Barcol 경도, Izod 충격강도 모두 현저히 증가하였다. 적절한 조건에서 산소 플라즈마 처리된 GO는 PMMA/AH 컴포지트 매트릭스와의 계면접착력이 매우 우수함을 파단면 모폴로지로부터 확인하였다. 하지만 GO의 함량이 0.07 phr 이상으로 증가하면 충전제의 분산이 균일하지 못하여 나노컴포지트의 기계적 강도는 오히려 감소하는 경향을 나타내었다.

• 한국가스학회지
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• 제17권4호
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• pp.18-25
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• 2013

맨홀 또는 환기가 부족한 공간에서 작업 중 유해 가스나 산소결핍에 의한 질식 또는 급성중독에 의한 건강장해나 사망사고가 빈번히 발생되고 있다. 따라서 유해가스에 의한 급성중독이나 산소결핍에 의한 유해농도 규명과 재해발생시 원인규명 자료로 활용하고자 산소결핍과 유해가스 노출에 따른 사망농도 시험하고자 하였다. 특히 산소결핍 상황에서 유해가스의 영향에 대해서도 시험하였으며, 국내외에서 발생된 관련 각종 사고 사례 조사를 통하여 동종재해를 예방하고자 하였다. 자료를 조사한 결과 산소결핍 또는 유해가스 노출에 의한 사망 재해는 하절기(6-8월)에 전체의 50%가 발생하고, 업종은 건설업 40%, 장소는 맨홀 50%, 원인은 산소결핍이 가장 많았으며(40%), 기타 가스($H_2S$, CO, $N_2$, Ar 등) 및 환경적 요인(내부 온도, 바닥 물 익사)도 크게 작용하였다. 동물실험 결과 산소결핍에 의한 치사 산소농도는 5%수준이었으며 Dose-Response의 통계처리결과 과반수치사농도 $LC_{50}$(rat, 4hr)는 5.5%로 산출되었다. 또한 산소결핍(6%수준) 상황에서 다른 유해물질이 혼합 될 경우 미치는 치사농도 시험 결과 $H_2S$ 20 ppm에서 40%치사, CO는 600 ppm에서 20%치사, 톨루엔은 1,000 ppm에서도 사망 예가 증가하지 않았다. 즉, $H_2S$, CO 등은 치사농도에 민감하게 반응하는 유해물질로의 상승작용을 했다.

• 한국식품과학회지
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• 제37권6호
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• pp.951-956
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• 2005

Bifidobacteria의 효과적인 이용을 위해서는 산소에 내성을 갖는 균주를 선발하는 연구 외에도 산소 스트레스에 대한 방어 기작에 대한 기초적인 연구가 필요하다. 인체로부터 분리된 산소 내성 bifidobacteria는 산소제거활성을 가지고 있었으며 이는 열처리 및 극단적인 pH(pH 2.0)하에서 산소제거활성이 소실되는 것으로 보아 효소가 관여 할 가능성을 확인하였다. 또한 산소제거활성을 보이는 주된 효소를 탐색해본 결과 NADH를 공급하였을 때만 산소제거활성을 보여 NADH oxidase가 주된 역할을 하는 효소임을 알 수 있었다. 또한 산소 내성 균주는 높은 NADH peroxidase 활성을 보유한 것으로 보아 NADH oxidase의 작용에 의해 생성되는 $H_2O_2$는 NADH peroxidase에 의해 무독화 되는 것으로 판단되었다. 배양 중 산소를 공급하여 산소스트레스를 주었을 경우 NADH oxidase와 NADH peroxidase 활성이 1시간 이내에 급격히 증가하였고 산소 공급 후 2시간 동안 배양액 중 용존 산소가 크게 증가하지 않았다. 산소공급 후 2시간 이상이 경과하면 NADH oxidase와 NADH peroxidase활성이 감소하고 용존 산소가 급격히 증가하였고 산소스트레스에 대한 방어 체계가 붕괴되는 현상이 관찰되었다. 즉, 산소 내성 bifidobacteria는 일정 한계까지는 환경중의 산소를 NADH oxidase로 제거하고 생성되는 $H_2O_2$는 NADH peroxidase에 의해 제거시키는 방어 체계를 갖고 있음을 알 수 있었다.

• Toxicological Research
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• 제27권3호
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• pp.161-166
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• 2011

Carbon black, a particulate form of pure elemental carbon, is an industrial chemical with the high potential of occupational exposure. Although the relationship between exposure to particulate matters (PM) and cardiovascular diseases is well established, the cardiovascular risk of carbon black has not been characterized clearly. In this study, the cytotoxicity of carbon black to vascular smooth muscle and endothelial cells were examined to investigate the potential vascular toxicity of carbon black. Carbon black with distinct particle size, N330 (primary size, 28~36 nm) and N990 (250~350 nm) were treated to A-10, rat aortic smooth muscle cells and human umbilical vein endothelial cell line, ECV304, and cell viability was assessed by lactate dehydrogenase (LDH) leakage assay. Treatment of carbon black N990 resulted in the significant reduction of viability in A-10 cells at 100 ${\mu}g$/ml, the highest concentration tested, while N330 failed to cause cell death. Cytotoxicity to ECV304 cells was induced only by N330 at higher concentration, 200 ${\mu}g$/ml, suggesting that ECV304 cells were relatively resistant to carbon black. Treatment of 100 ${\mu}g$/ml N990 led to the elevation of reactive oxygen species (ROS) detected by dichlorodihydrofluorescein (DCF) in A-10 cells. Pretreatment of antioxidants, N-acetylcysteine (NAC) and sulforaphane restored decreased viability of N990-treated A-10 cells, and N-acetylcysteine, but not sulforaphane, attenuated N990-induced ROS generation in A-10 cells. Taken together, present study shows that carbon black is cytotoxic to vascular cells, and the generation of reactive oxygen contributes to the development of cytotoxicity. ROS scavenging antioxidant could be a potential strategy to attenuate the toxicity induced by carbon black exposure.

• 한국어병학회지
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• 제21권1호
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• pp.67-79
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• 2008

This study was conducted to find out biological response of bivalves exposed to tributyltin chloride(TBTCl). The results of the study confirmed that TBTCl induce the reduction of oxygen consumption rateand histopathological feature in the gill structure of equilateral venus, Gomphina veneriformis. The experi-mental groups consisted of a control and 3 TBTCl exposure groups (0.4, 0.6 and 0.8 yg TBTCl L') and theexperimental period was 36 weeks. For histological analysis, gill tissues were fixed in Bouin's fluid andthen stained H-E stain, AB-PAS (PH 2.5) reaction and Masson's trichrome stain after having serially sec-tioned the tissue by paraffin method at thickness of 4-6 (an. The oxygen consumption rate was not signifi-cantly different between the control and exposure groups at 4 weeks, but in all exposure groups at 28 weeks,it was significantly different to the control. Gill of G. veneriformis had demibranch that attached two sheetsof lamellae and a lamella was composed of numerous filaments, numbering 25 on average. The frontal fila-ment zone had three types of cilia; frontal, latero-frontal and lateral depending on locations while the lateralcilia were the longest and largest in number. The mucous cells observed in filaments were more abundant in(542c) in AB-PAS (PH 2.5) reaction. Gill exposed to TBTCl was extended hemolymph sinus and increased hemocytes at 4 weeks, and then it showed increases of mucous cells and partially disappearance of frontalcilia. In the group of 0.8 yg TBTCl L' at 12 weeks, hypertrophy of frontal and latero-frontal epithelia wasobserved. Also it observed m decrease of mucous cell containing weekly acid mucosubstance and appearedpartially destruction muscle fiber bundle, In the groups of 0.4 and 0.6 ug TBTCl L' at 36 weeks, it appearedpartially modification of epithelia and in 0.8 us TBTCl L' group, observed filaments that come out chiti-nous rod from disappearance of frontal and latero-frontal epithelia.

• Environmental Analysis Health and Toxicology
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• 제21권1호
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• pp.71-79
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• 2006

Epidemiologic studies have showed a close correlation between arsenic exposure and heart disease such as, cardiovascular problem, ischemic heart disease, infarction, atherosclerosis and hypertension in human. It may increase the mortality of high risk group with heart disease. Regarding the mechanism studies of heart failure, blood vessel, vascular smooth muscle cells and endothelial cells have long been focused as the primary targets in arsenic exposure but there are only a few studies on the cardiomyocytes. In this study, the generation of oxidative stress by low dose of arsenic trioxide was investigated in rat cardiomyocytes. By direct measurement of reactive oxygen species and fluorescent microscopic observation using fluorescent dye 2',7'-dichlorofluorescin diacetate, reactive oxygen species were found to be generated without cell death, where cells are treated with 0.1 ppm arsenic for 24 hours. With the induction of reactive oxygen species, GSH level was decreased by the same treatment. However, DNA damage did not seem to be serious by DAPI staining, while high dose of arsenic (2 ppm for 24 hrs) caused fragmentation of DNA. To identify the molecular biomarkers of low-dose arsenic exposure, gene expression was also investigated with whole genome microarray. As results, 9,022 genes were up-regulated including heme oxygenase-l and glutathione S-transrerase, which are well-known biomarkers of oxidative stress. 9,404 genes were down-regulated including endothelial type gp 91-phox gene by the treatment of 0.1 ppm arsenic for 24 hours. This means that biological responses of cardiomyocytes may be altered by ROS induced by low level arsenic without cell death, and this alteration may be detected clearly by molecular biomarkers such as heme oxygenase-1.