• 한국산학기술학회논문지
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• 제15권4호
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• pp.2189-2198
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• 2014

본 연구는 제초제 음독 중에서 가장 치명률이 높은 파라쿼트 중독의 독성 감소를 위하여 파라쿼트 독성 기전으로 알려진 파라쿼트 유도성 활성산소종을 감소시키기 위해 기존의 항산화제들 치료제와는 달리, 사전에 산소 농도를 줄여서 파라쿼트에 의한 활성 산소종 발생 자체를 줄이는 저농도 산소요법의 유용성을 연구하였다. 이를 위해 백서를 활용하여 생존률 및 파라쿼트에 의한 활성 산소종의 영향을 가장 빠르고 많이 받는 폐조직의 육안적 조직학적 변화를 비교 분석함으로써 세포 독성 상황에서 저농도 산소요법의 효과를 분석하였다. 그 결과 저농도 산소요법을 처리한 군에서 유의한 생존률 증가와 함께 H&E Stain결과에서는 염증세포 증가 및 Aveolar space에 부종 소견이 저농도 산소요법을 함께 시행한 군에서 완화된 소견을 확인할 수 있었다. 또한 파라쿼트의 독성기전의 핵심인 산화스트레스발생 분석을 시행한 결과, MDA assay, Glutathione assay 및 SOD Assay모두에서 파라쿼트는 산화스트레스를 증가하지만 파라쿼트와 함께 저농도 산소요법을 처리한 경우 산화 스트레스가 감소함을 증명하였다. 이를 통해 본 연구는 임상에서 파라쿼트 중독에 대한 새로운 치료 대안으로서의 기초 연구로서 활용이 기대된다.

• 대한약리학회지
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• 제27권2호
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• pp.197-205
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• 1991

Adriamycin (Doxorubicin HCl)의 혈관밖 유출에 따른 조직의 손상, 특히 피부괴양 및 괴사 기전을 규명하기 위한 연구의 일환으로 흰쥐 피부세포를 이용한 in vitro 실험에서 adriamycin에 의한 산소라디칼 생성 및 그와 관련된 세포독성 기전으로 지질과산화를 검토하였다. Adriamycin은 흰쥐 태자 피부의 배양세포에서 lactic dehydrogenase(LDH) 유리를 용량 및 시간 의존적으로 증가 시켰으며, NADPH 및 NADH 첨가 조건에서 $superoxide\;anion(O^-\;_2{\cdot})$ 생성을 현저히 증가시켰다. Adriamycin은 지질과산화 반응의 척도인 malondialdehyde(MDA) 생성을 역시 NADPH, NADH 존재하에서 용량의존적으로 증가시켰고, 산소라디칼 제거물질들인 superoxide dismutase (SOD), catalase 및 thiourea와 항산화물질인 butylated hydroxytoluene(BHT), ${\alpha}-tocopherol$은 MDA 생성증가를 현저히 억제하였다. 1, 3,-bis(2-chloroethyl)-1-nitrosourea(BCNU)를 처리하여 산화성 공격에 대한 방어기전의 하나인 glutahione 체계를 억제할 경우 adriamycin에 의한 MDA 생성은 더욱 현저히 증가하였고, 이는 역시 항산화 물질들에 의하여 억제되었다. 이상의 연구성적에서 adriamycin은 산소라디칼 생성의 증가와 그에 따른 지질과산화를 촉진하므로서 피부세포에 손상을 줄 것으로 사료되었다.

• 한국어병학회지
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• 제12권1호
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• pp.32-41
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• 1999

오존처리 해수중에 함유하는 잔류 옥시던트(TRO)가 양식 넙치의 생존, 혈액성상과 삼투질 농도, 산소소비 및 아가미 조직에 미치는 독성 영향을 조사하였다. TRO에 노출된 넙치의 48-hr 및 96-hr $LC_{50}$은 각각 26.4 와 22.3ppb이었고, 47ppb에서는 3시간 이내에 모두 치사하였으나 13ppb에서는 96시간 동안 폐사발생이 없었다. TRO 24~39ppb 농도범위에 노출된 넙치의 hematocrit, 헤모글로빈, 적혈구 수, 혈중 sodium과 chloride 이온 및 삼투압 농도는 TRO 농도가 높을수록 유의하게 증가하였고, 아가미 조직은 아가미 상피층이 모세혈관으로부터 박리되고, 괴사와 상피새포의 증생이 관찰되었다. 산소소비율은 TRO 농도가 높고, 노출이 계속될수록 감소하였다. 13ppb에서는 아가미 조직과 생리상태에 미치는 변화는 관찰되지 않았으나 혈당은 유의하게 증가하였다. 그러나 활성탄으로 TRO를 제거한 대조구에서는 오존의 독성 영향은 관찰되지 않았다. 잔류오존에 노출된 넙치는 삼투질 농도의 생리적 불균형 및 아가미 손상과 상피세포의 증생에 의한 산소섭취 부족이 치사를 유발하는 것으로 나타났다. 본 연구의 결과 해산어 양식장에서 오존을 사용할 경우에는 오존처리수중의 TRO는 제거하여야 하며, 비록 저농도라도 장기간 노출되면 양식어류의 생존과 생리상태에 미치는 영향은 현저할 것으로 평가되었다.

• BMB Reports
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• 제40권6호
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• pp.1039-1049
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• 2007

Overdoses of acetaminophen cause hepato-renal oxidative stress. The present study was undertaken to investigate the protective effect of a 43 kDa protein isolated from the herb Cajanus indicus, against acetaminophen-induced hepatic and renal toxicity. Male albino mice were treated with the protein for 4 days (intraperitoneally, 2 mg/kg body wt) prior or post to oral administration of acetaminophen (300 mg/kg body wt) for 2 days. Levels of different marker enzymes (namely, glutamate pyruvate transaminase and alkaline phosphatase), creatinine and blood urea nitrogen were measured in the experimental sera. Intracellular reactive oxygen species production and total antioxidant activity were also determined from acetaminophen and protein treated hepatocytes. Indices of different antioxidant enzymes (namely, superoxide dismutase, catalase, glutathione-S-transferase) as well as lipid peroxidation end-products and glutathione were determined in both liver and kidney homogenates. In addition, Cytochrome P450 activity was also measured from liver microsomes. Finally, histopathological studies were performed from liver sections of control, acetaminophen-treated and protein pre- and post-treated (along with acetaminophen) mice. Administration of acetaminophen increased all the serum markers and creatinine levels in mice sera along with the enhancement of hepatic and renal lipid peroxidation. Besides, application of acetaminophen to hepatocytes increased reactive oxygen species production and reduced the total antioxidant activity of the treated hepatocytes. It also reduced the levels of antioxidant enzymes and cellular reserves of glutathione in liver and kidney. In addition, acetaminophen enhanced the cytochrome P450 activity of liver microsomes. Treatment with the protein significantly reversed these changes to almost normal. Apart from these, histopathological changes also revealed the protective nature of the protein against acetaminophen induced necrotic damage of the liver tissues. Results suggest that the protein protects hepatic and renal tissues against oxidative damages and could be used as an effective protector against acetaminophen induced hepato-nephrotoxicity.

• 한국작물학회:학술대회논문집
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• 한국작물학회 2017년도 9th Asian Crop Science Association conference
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• pp.187-187
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• 2017

Cadmium (Cd) pollution is rapidly increasing in worldwide due to industrialization and urbanization. In addition to its negative effects on the environment, Cd pollution adversely affects human health. Rice (Oryza sativa L.) is an important agricultural crop worldwide, including South Korea, and studies have examined its ability to alleviate Cd uptake from the soil into plants. However, information about the relationship between sulfur (S) and antioxidants in rice seedlings is still limited with regard to Cd phytotoxicity. We therefore investigated the changes in reactive oxygen species (ROS) and antioxidants in rice (Oryza sativa L. 'Dongjin') seedlings exposed to toxic Cd, S treatment, or both. The exposure of rice seedlings to $30{\mu}M$ Cd inhibited plant growth; increased the contents of superoxide, hydrogen peroxide, and malondialdehyde (MDA); and induced Cd uptake by the roots, stems, and leaves. Application of S to Cd-stressed seedlings decreased Cd-induced oxidative stress by increasing the capacity of the glutathione (GSH)-ascorbate (AsA) cycle, promoted S assimilation by increasing cysteine, GSH, and AsA contents in treated plants, and decreased Cd transfer from the roots to the stems and leaves. In conclusion, S application of plants under Cd stress promoted Cys and GSH biosynthesis and GSH-AsA cycle activity, thereby lowering the rate of Cd transfer to plant shoots and promoting the scavenging of the ROS that resulted from Cd toxicity, thus alleviating the overall Cd toxicity. Therefore, these results provide insights into the role of S in regulating the tolerance, uptake, and translocation of Cd in rice seedlings. The results of this study indicate that S application should have potential as a tool for mitigating Cd-stress in cereal crops, especially rice.

• 한국환경농학회지
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• 제6권2호
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• pp.66-72
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• 1987

잉어(C. carpio), 송사리(O. latipes), 일본산 송사리(O. latipes)등 3종의 담수산어 류에 대한 30개 농약의 급성독성$(48hr-LC_{50})$을 평가하여 각 어종간 농약에 대한 감수성의 상관관계를 비교하였다. 어종간 농약감수성의 상관관계는 잉어와 송사리는 r=0.80, 잉어와 일본산 송사리는 r=0.89로 비교적 높은 편이나, 송사리와 일본산 송사리의 상관관계는 r=0.93으로 매우 높았다. 따라서 일본산 송사리의 실험결과로 잉어 및 송사리의 농약 감수성을 예측할 수 있을 것으로 생각되었다. 그리고 우리나라의 잉어에 대한 어독성실험 지침은 실험수조내의 DO가 2mg/1 정도까지 떨어지므로 실험지침에 대한 검토가 있어야 할 것이다.

• Toxicological Research
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• 제30권3호
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• pp.149-157
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• 2014

Smoking is one of the most serious but preventable causes of cardiovascular disease (CVD). Key aspects of pathological process associated with smoking include endothelial dysfunction, a prothrombotic state, inflammation, altered lipid metabolism, and hypoxia. Multiple molecular events are involved in smoking-induced CVD. However, the dysregulations of reactive oxygen species (ROS) generation and metabolism mainly contribute to the development of diverse CVDs, and NADPH oxidase (NOX) has been established as a source of ROS responsible for the pathogenesis of CVD. NOX activation and resultant ROS production by cigarette smoke (CS) treatment have been widely observed in isolated blood vessels and cultured vascular cells, including endothelial and smooth muscle cells. NOX-mediated oxidative stress has also been demonstrated in animal studies. Of the various NOX isoforms, NOX2 has been reported to mediate ROS generation by CS, but other isoforms were not tested thoroughly. Of the many CS constituents, nicotine, methyl vinyl ketone, and ${\alpha}$,${\beta}$-unsaturated aldehydes, such as, acrolein and crotonaldehyde, appear to be primarily responsible for NOX-mediated cytotoxicity, but additional validation will be needed. Human epidemiological studies have reported relationships between polymorphisms in the CYBA gene encoding p22phox, a catalytic subunit of NOX and susceptibility to smoking-related CVDs. In particular, G allele carriers of A640G and $-930^{A/G}$ polymorphisms were found to be vulnerable to smoking-induced cardiovascular toxicity, but results for C242T studies are conflicting. On the whole, evidence implicates the etiological role of NOX in smoking-induced CVD, but the clinical relevance of NOX activation by smoking and its contribution to CVD require further validation in human studies. A detailed understanding of the role of NOX would be helpful to assess the risk of smoking to human health, to define high-risk subgroups, and to develop strategies to prevent or treat smoking-induced CVD.

• Journal of Preventive Medicine and Public Health
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• 제27권1호
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• pp.84-106
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• 1994

Hyperbaric oxygen (HBO) therapy for carbon monoxide (CO) poisoning eventually inducing the hypoxia-reoxygenation condition, may produce oxygen free radicals, which forms 8-hydroxydeoxyguanosine (8-OH-dG) by attacking C-8 position of deoxyguanosine (dG) in DNA. Effects of oxygen partial pressure or duration of HBO therapy with or without CO poisoning on the tissue 8-OH-dG formation were investigated. Male Sprague-Dawley rats were grouped and exposed to air (control group), 4000 ppm of CO for 10 to 30 minutes (CO only group), air for 30 minutes after 30 minute exposure to 4000 ppm of CO(CO-air exposure group), HBO after 30 minute exposure to 4000 ppm of CO(CO-HBO group), or HBO therapy fo. $10{\sim}120$ minutes(HBO only group). The 8-OH-4G concentrations in the brain and the lung tissues were measured with high performance liquid chromatography and electrochemical detector (ECD). Average concentrations of the 8-OH-dG of each group were statistically compared. In the brain tissues, 8-OH-dG concentrations of the CO only group, the CO-air exposure group, and the CO-HBO group did not significantly differ from those of the control group. Similar insignificance was also found between the CO-HBO group and the HBO only groups. No appreciable dose-response relationship was observed between the 8-OH-dG concentration and the oxygen partial pressure or the duration of HBO. However, the 8-OH-dG concentrations of the 30 minute CO only group were higher than those of the CO-air exposure group (p-value<0.05). In the lung tissues, there were no significant differences between the 8-OH-dG concentrations of the control group and those of the CO only group, the CO-air exposure group, and the CO-HBO group. However, mean 8-OH-dG concentration of the CO-air exposure group was significantly higher than that of the CO only group under the same CO exposure condition(p-value<0.05). With the duration of CO exposure, the 8-OH-dG concentrations of the lung tissues decreased significantly (p-value<0.05). The concentrations of 8-OH-dG in the lung tissues proportionally increased with the duration of HBO, but no such relation was observed with the oxygen partial pressure. These results suggest that the brain may be more resistant to oxygen free radicals as compared with the lungs, and that oxygen toxicity following HBO may be affected by factors other than oxygen free radicals.

• Tuberculosis and Respiratory Diseases
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• 제41권3호
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• pp.222-230
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• 1994

연구배경 : Paraquat는 광범위 제초제로서 널리 사용하고 있으나, 중독시 치명적인 중독 증상을 일으킨다. 특히 폐에서는 진행성 불가역성 폐섬유종을 일으키는데, 이의 기전으로 산소유리기와 관계가 있으나 아직은 생화학적 기전이 명확하지 않다. paraquat에 의한 산소유리기가 생기면 glutathione의 변화와 G6PDH, SOD, catalase 및 glutathione peroxidase등의 효소 활성의 변화가 생길 것으로 생각되며, 특히 catalase가 많이 관여할 것으로 생각되어진다. 방법 : Catalase 억제제인 aminotriazole을 사용하여 paraquat만 쓰는 것과 paraquat와 aminotriazole을 같이 투여할때 생쥐의 생존율을 알아보고, 실험군을 정상대조군, Group A(aminotriazole투여군), Group B(paraquat 투여군), Group C(paraquat와 amino-triazole 병합투여군) 4군으로 나누어 폐조직에서 glutathione량, G6PDH, SOD, catalase 및 glutathione peroxidase활성도를 측정하여 비교했다. 결과 : Paraquat와 aminotriazole 병합 투여군의 생존율이 paraquat투여군보다 현저히 감소하였고, paraquat 투여로 인하여 폐 glutathione량은 정상대조군에 비해 20%정도 감소 되었으나, aminotriazole의 투여로 인한 폐 glutathione량의 변화는 없었다. Paraquat투여로 폐 SOD, catalase 및 glutathione peroxidase활성이 모두 유의한 감소를 나타냈는데, 특히 catalase가 가장 큰 효소활성 감소를 나타냈으며, paraquat와 aminotriazole병합투여군에서는 catalase와 glutathione peroxidase활성이 paraquat단독투여군에 비하여 유의한 효소활성감소를 나타냈고, SOD는 효소활성의 변화가 감지되지 않았다. 결론 : Paraquat투여시 catalase활성이 유의하게 감소되는 점으로 보아 paraquat독성이 catalase활성과 밀접하게 연관되는 것으로 사료되며, 또한 paraquat의 독성이 aminotriazole의 병합 투여로 더욱 증가되어 나타나는데, 이러한 결과는 aminotriazole투여로 catalase활성의 감소가 크게 나타나나 glutathione량의 변화는 없는 점으로 보아 aminotriazole투여에 의한 paraquat독성의 증가는 총 폐 glutathione량의 변화에 의한 영향보다는 catalase활성감소에 의한 결과로 생각된다. Paraquat와 aminotriazole를 병합 투여하여 catalase활성이 억제되면 증가된 과산화수소로 hydroxyl radicals이 생성되고, 이에 의한 폐 세포손상이 유발되어 나타나는 것으로 사료된다.

• 한국양식학회지
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• 제11권3호
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• pp.285-294
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• 1998

When Cochlodinium polykrikoides came into the culture tanks through influent cultivated water during the red tides, hundred thousands of commercial flounders were concomitantly killed and many culturists suffered from a great deal of financial loss in the east coast of Korea. It is charactrized by high sinking rate after sunset and the formatino of clump which results in oxygen deficiency by its respiration at tank bottom under condition. We investigated the efficacy of hydrogen peroxide and chlorine dioxide, known to form radicals, for extermination of red tide organism C. polykrikoides. When C. polykrikoides seawater with a density of 6,000 cells/$m\ell$ was treated with 14, 28 and $42mg/\ell$ of hydrogen peroxide, its survival rate was markedly decreased to 9.8, 0.8 and 0.3% respectively immediately after 6 hours of treatments whereas when it was treated with 1.5, 2.1 and $3.0mg/\ell$ chlorine dioxide, its survival rate showed 87.7, 81.3 and 80.1 and 80.1% respectively at the same treatment time. Hydrogen peroxide was the effective agent since it has scarcely injured the cultured olive flounder when exposed to the tested concentration range of $14~28mg/\ell$ with the extermination of almost3 C. polykrikoides during the experimental period of 5 days and has shown the oxygen increase of approximately $1.23mg/\ell$ 2 hours immediately after the flounder by C. polykrikoides in the land-based culture tank is assumed to be not by the toxicity of itself but by oxygen dificiency from the rapid respiration of dinoflagellate clump sunken to the tank bottom.