• 제목/요약/키워드: NO formation pathway

검색결과 85건 처리시간 0.029초

NOx 제거용 저온 플라즈마 반응기에서의 플라즈마 화학 및 입자 성장 (The Plasma Chemistry and Particle Growth in the Low Temperature Plasma Reactor for removal of NOx)

  • 김동주;김교선
    • 산업기술연구
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    • 제19권
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    • pp.331-341
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    • 1999
  • We analyzed theoretically the removal efficiency and the particle growth inside the pulse corona discharge reactor to remove $NO_x$ and investigated the effects of process variables such as the NO and $NH_3$ input concentrations. Most of NO is converted into $NO_2$ and $HNO_3$ and the $HNO_3$ reacts with $NH_3$ to form the $NH_4NO_3$ particles. About 6.4% of NO is converted into $HNO_2$ which form the $NH_4NO_2$ particles by reaction with $NH_3$. Some of $NO_2$ follows the reaction pathway to form $NO_3$ and $N_2O_5$. The amount of particles formed inside the reactor is basically determined by the input $NH_3$ concentration. The ratio of NO to $NH_3$ affects the reactor length for particle formation significantly. The higher the input concentrations of NO and $NH_3$ are, the faster the particles grow.

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N -Nitrosodimethylamine의 자외선 광분해 시 질소산화물 생성에 미치는 반응성 화학종의 형성 (The Formation of Reactive Species on the Nitrogen Oxide in the Ultraviolet Photolysis of N-Nitrosodimethylamine)

  • 권중근;김종오;권범근
    • 한국지반환경공학회 논문집
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    • 제13권2호
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    • pp.75-81
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    • 2012
  • NDMA는 잠재적인 발암 물질로 잘 알려져 있기 때문에 UV를 활용한 처리기술과 분해경로에 대해 많은 연구가 이루어졌다. 그러나 NDMA가 ${NO_2}^-$, ${NO_3}^-$ 와 같은 산화물을 형성하는 메커니즘은 아직 명확하게 알려져 있지 않다. 본 연구에서는 NDMA의 광반응에 의해 생성되는 핵심 반응기들을 검토하였다. 주요 반응기들에 대한 연구는 질소 산화물들의 형성과 메탄올과 NDMA의 광분해에 의해 형성되는 미지의 반응기들 사이에서의 반응을 통하여 간접적으로 수행하였다. NDMA의 직접적인 UV 광반응에 의해서 생성된 $ONOO^-$ 가 질소 산화물(중간생성물)들의 산화로 인한 ${NO_2}^-$${NO_3}^-$ 의 핵심 반응기인 것으로 확인되었다.

The impaired redox status and activated nuclear factor-erythroid 2-related factor 2/antioxidant response element pathway in wooden breast myopathy in broiler chickens

  • Pan, Xiaona;Zhang, Lin;Xing, Tong;Li, Jiaolong;Gao, Feng
    • Animal Bioscience
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    • 제34권4호
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    • pp.652-661
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    • 2021
  • Objective: Wooden breast (WB) is a novel myopathy affecting modern broiler chickens, which causes substantial economic losses in the poultry industry. The objective of this study was to evaluate the effect of WB abnormality on meat quality, redox status, as well as the expression of genes of the nuclear factor-erythroid 2-related factor 2 (Nrf2) pathway. Methods: A total of 80 broilers (Ross 308, 42 days of age, about 2.6 kg body weight) raised at Jiujin farm (Suqian, Jiangsu, China) were used. Twelve unaffected (no detectable hardness of the breast area) and twelve WB-affected (diffuse remarkable hardness in the breast muscle) birds were selected from the commercial broiler farm according to the criteria proposed by previous studies. Results: The results indicated that WB showed histological lesions characterized by fiber degeneration and fibrosis, along with an increase of muscle fiber diameter (p<0.05). Moreover, higher pH value, lightness, yellowness, drip loss and cooking loss were observed in the WB group (p<0.05). Compared with the normal breast (NOR) group, the WB group showed higher formation of reactive oxygen species (p<0.05), increased level of oxidation products and antioxidant activities (p<0.05), accompanied with mitochondrial damages and lower mitochondrial membrane potential (p<0.05). Meanwhile, the relative mRNA expressions of Nrf2 and its downstream antioxidant genes including heme oxygenase-1, NAD(P)H qui none dehydrogenase 1, glutathione peroxidase, superoxide dismutase, and glutamate-cysteine ligase were higher than those of the NOR group (p<0.05). Conclusion: In conclusion, WB myopathy impairs meat quality by causing oxidative damages and mitochondrial dysfunction in broilers, even though the activated Nrf2/antioxidant response element pathway provides protection for the birds.

사독의 인체 폐암세포(A549)에 대한 Natural Killer 세포 세포독성 촉진 효과 (Snake Venom-enhanced Cytotoxic Effect of Natural Killer Cells on A549 Human Lung Cancer Cell Growth)

  • 이지인;송호섭
    • Journal of Acupuncture Research
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    • 제32권1호
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    • pp.79-88
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    • 2015
  • Objectives : The purpose of this research was to investigate the cytotoxic effect of Natural Killer(NK)-92 cell and Snake Venom, and to elucidate its mechanism on human lung carcinoma cell A549. Methods : In order to figure out whether Snake Venom enhances the cytotoxic effect of NK-92 cell in A549 cell, Cell Viability Assay was conducted. Also, in order to observe the changes of Caspase-3 and Caspase-8, both of which are proteinases that advance apoptosis, and the changes of TNRF and DR3, which are Death Receptors of the extrinsic pathway of apoptosis, Western Blot Analysis was conducted. By conducting RT-PCR analysis, we have tried to confirm Perforin, Granzyme B, and GADPH, all of which are cytotoxic-related proteins. Lastly, in order to observe the effect of Snake Venom on NO formation within human lung carcinoma cells, NO determination was conducted. Results : 1. After conducting Cell Viability Assay, Snake Venom enhanced the cytotoxic effect of NK-92 cell and inhibited the growth of A549. 2. Western Blot Analysis caused proteinases Caspase-3 and Caspase-8, which advance apoptosis, to increase in the combined treatment group, but not in treatment groups that focused only on either Snake Venom or NK-92 cell in A549 lung carcinoma cells. 3. Western Blot Analysis caused an expression of TNFR2 and DR3, both of which are Death Receptors of the apoptosis extrinsic pathway, in the combined treatment group, but not intreatment groups that focused only on either Snake Venom or NK-92 cell in A549 human lung carcinoma cells. 4. After conducting NO determination, NO formation within A549 cell showed no significant changes in both treatment groups that focused NK-92 cell and combined treatment group. 5. After conducting RT-PCR, the expression of Granzyme B and Perforin, which are cytotoxic-related proteins within A549 human lung carcinoma cells, showed growth in the combined treatment group, but not the treatment group that focused only on NK-92 cell. Conclusion : It has been indicated that, when it comes to the A549 cell, Snake Venom enhances the increase of Death Receptor expression and continuous apoptosis reaction, leading to the enhancement of the cancer cell cytotoxic effect of the NK-92 cell. It is expected that Snake Venom can be used with the NK-92 cell for further lung cancer treatment.

Ginsenoside Rg1 ameliorates chronic intermittent hypoxia-induced vascular endothelial dysfunction by suppressing the formation of mitochondrial reactive oxygen species through the calpain-1 pathway

  • Fang Zhao;Meili Lu;Hongxin Wang
    • Journal of Ginseng Research
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    • 제47권1호
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    • pp.144-154
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    • 2023
  • Background: As the major pathophysiological feature of obstructive sleep apnea (OSA), chronic intermittent hypoxia (CIH) is vital for the occurrence of cardiovascular complications. The activation of calpain-1 mediates the production of endothelial reactive oxygen species (ROS) and impairs nitric oxide (NO) bioavailability, resulting in vascular endothelial dysfunction (VED). Ginsenoside Rg1 is thought to against endothelial cell dysfunction, but the potential mechanism of CIH-induced VED remains unclear. Methods: C57BL/6 mice and human coronary artery endothelial cells (HCAECs) were exposed to CIH following knockout or overexpression of calpain-1. The effect of ginsenoside Rg1 on VED, oxidative stress, mitochondrial dysfunction, and the expression levels of calpain-1, PP2A and p-eNOS were detected both in vivo and in vitro. Results: CIH promoted VED, oxidative stress and mitochondrial dysfunction accompanied by enhanced levels of calpain-1 and PP2A and reduced levels of p-eNOS in mice and cellular levels. Ginsenoside Rg1, calpain-1 knockout, OKA, NAC and TEMPOL treatment protected against CIH-induced VED, oxidative stress and mitochondrial dysfunction, which is likely concomitant with the downregulated protein expression of calpain-1 and PP2A and the upregulation of p-eNOS in mice and cellular levels. Calpain-1 overexpression increased the expression of PP2A, reduced the level of p-eNOS, and accelerated the occurrence and development of VED, oxidative stress and mitochondrial dysfunction in HCAECs exposed to CIH. Moreover, scavengers of O2·-, H2O2, complex I or mitoKATP abolished CIH-induced impairment in endothelial-dependent relaxation. Conclusion: Ginsenoside Rg1 may alleviate CIH-induced vascular endothelial dysfunction by suppressing the formation of mitochondrial reactive oxygen species through the calpain-1 pathway.

PKC Downstream of PI3-Kinase Regulates Peroxynitrite Formation for Nrf2-Mediated GSTA2 Induction

  • Kim, Sang-Geon;Kim, Sun-Ok
    • Archives of Pharmacal Research
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    • 제27권7호
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    • pp.757-762
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    • 2004
  • The protective adaptive response to electrophiles and reactive oxygen species is mediated by the induction of phase II detoxifying genes including glutathione S-transferases (GSTs). NF-E2-related factor-2 (Nrf2) phosphorylation by protein kinase C (PKC) is a critical event for its nuclear translocation in response to oxidative stress. Previously, we have shown that peroxynitrite plays a role in activation of Nrf2 and Nrf2 binding to the antioxidant response element (ARE) via the pathway of phosphatidylinositol 3-kinase (PI3-kinase) and that nitric oxide synthase in hepatocytes is required for GSTA2 induction. In view of the importance of PKC and Pl3-kinase in Nrf2-mediated GST induction, we investigated the role of these kinases in peroxynitrite formation for GSTA2 induction by oxidative stress and determined the relationship between PKC and PI3-kinase. Although PKC activation by phorbol 12-myristate-13-acetate (PMA) did not increase the extents of constitutive and inducible GSTA2 expression, either PKC depletion by PMA or PKC inhibition by staurosporine significantly inhibited GSTA2 induction by tert-butylhydroquinone (t-SHa) a prooxidant chemical. Therefore, the basal PKC activity is req- uisite for GSTA2 induction. 3-Morpholinosydnonimine (SIN-1), which decomposes and yields peroxynitrite, induced GSTA2, which was not inhibited by PKC depletion, but slightly enhanced by PKC activation, suggesting that PKC promotes peroxynitrite formation for Nrf2-mediated GSTA2 induction. Treatment of cells with S-nitroso-N-acetyl-penicillamine (SNAP), an exogenous NO donor, in combination with t-BHQ may produce peroxynitrite. GSTA2 induction by SNAP + t-BHQ was not decreased by PKC depletion, but rather enhanced by PKC activation, showing that the activity of PKC might be required for peroxynitrite formation. LY294002 a P13-kinase inhibitor blocked GSTA2 induction by t-BHQ, which was reversed by PMA-induced PKC activation. These results provide evidence that PKC may playa role in formation of peroxynitrite that activates Nrf2 for GSTA2 induction and that PKC may serve an activator for GSTA2 induction downstream of PI3-kinase.

Evaluation on Anticancer Effect Against HL-60 Cells and Toxicity in vitro and in vivo of the Phenethyl Acetate Isolated from a Marine Bacterium Streptomyces griseus

  • Lee, Ji-Hyeok;Zhang, Chao;Ko, Ju-Young;Lee, Jung-Suck;Jeon, You-Jin
    • Fisheries and Aquatic Sciences
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    • 제18권1호
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    • pp.35-44
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    • 2015
  • We previously identified Streptomyces griseus as an anti-cancer agent (Kim et al., 2014). In this study, we isolated compounds from S. griseus and evaluated their anticancer effect and toxicity in vitro and in vivo. Preparative centrifugal partition chromatography (CPC) was used to obtain three compounds, cyclo($_{\small{L}}$-[4-hydroxyprolinyl]-$_{\small{L}}$-leucine], cyclo($_{\small{L}}$-Phe-trans-4-hydroxy-$_{\small{L}}$-Pro) and phenethyl acetate (PA). We chose PA, which had the highest anticancer activity, as a target compound for further experiments. PA induced the formation of apoptotic bodies, DNA fragmentation, DNA accumulation in $G_0/G_1$ phase, and reactive oxygen species (ROS) formation. Furthermore, PA treatment increased Bax/Bcl-xL expression, activated caspase-3, and cleaved poly-ADP-ribose polymerase (PARP) in HL-60 cells. Simultaneous evaluation in vitro and in vivo, revealed that PA exhibited no toxicity in Vero cells and zebrafish embryos. We revealed, for the first time, that PA generates ROS, and that this ROS accumulation induced the Bcl signaling pathway.

마이크로 에멀젼 계면을 통과하는 광유발전자의 양자수득률 (Quantum Yield of Photoinduced Electron Transfer Across Microemulsion Interfaces)

  • 박용태
    • 대한화학회지
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    • 제27권3호
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    • pp.213-217
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    • 1983
  • 태양에너지의 한 저장방법으로 녹색식물의 광합성을 모방한 계, 마이크로 에멀젼(microemulsion)을 고안하였으며, 이때 광에 의해서 유발된 전자가 계면을 통하는 능력을 측정하였다. 광증감제로 류테니늄비피리딘 착물$[Ru(bipy)_3]^{2+}$을 사용, 전자공여체 EDTA와 함께 물층에, 전자수용체 $HV^{2+}$(Hexadecyl violagan)이 계면에 각각 존재할 때 광에 의한 전자전이에 따르는 $HV^+$ 형성수득률은 0.12이였다. 또 계면에 $BNA^+$(Benzyl nicotinamide)를 넣고 유층에 아조(azo) 화합물을 넣었을 때는 azobenzene이 환원되었는데, 이때 양자수득률이 줄었다. (${\Phi}$ = 0.0016) 양이온 마이크로 에멀젼과 음이온 마이크로에멀젼의 광유발 전자전이 능력을 비교하였다. 광증감제로 유기염료인 로즈벤갈(Rose bengal)을 시험하였는데, 류테니늄착물보다 낮지 않았지만 광유발 전자가 계면에 전이되는 것을 알았다.

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어머니의 특성에 따른 아동의 애착안정성 형성 발달경로 (A Developmental Pathway of Child Attachment Security through Maternal Characteristics)

  • 이경혜
    • 아동학회지
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    • 제23권1호
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    • pp.153-171
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    • 2002
  • 영아기의 애착형성이 어머니의 특성에 따른 상호작용에 의해 안정애착 혹은 불안정 애착으로 발달된다는 이론이 널리 알려지면서 불안정 애착에 대한 예방과 치료중재의 필요성이 고취되어졌음에도 불구하고, 가장 결정적인 문제인 어머니의 어떤 특성들이 아동의 불안정애착 형성에 직접적인 영향을 미치는가에 대한 연구는 거의 전무한 실정이다. 이에 따라 본 연구는 어머니와 아동간의 세대간 애착순환을 재검증함과 동시에 어머니의 양육스트레스가 어머니-아동 불안정 애착전이를 예방 및 중재시킬 수 있는 매개변인이 되는지를 검증하고자 한다. 영아기 이후의 애착형성에 대한 이해를 확장시키기 위한 시도에서, 30개월에 달한 아동과 어머니 53쌍이 조사 관찰되어졌고, 이는 아동발달의 관점에서 이 아동들이 49개월에 달했을 때 다시 조사 관찰되어졌다. 아동양육과 관련된 어머니 특성들을 측정하기 위하여 the Attachment Style Questionnaire와 the Parental Stress Inventory를 사용하였고, 아동애착안정성을 측정하기 위하여 the Separation-Reunion Classifications (1차)와 the Attachment Q-set (2차)이 사용되어졌으며, 이를 분석하기 위해 Amos structural equation 통계분석법이 사용되었다. 이에 따른 본 연구결과는, 아동애착안정성은 어머니 애착유형과 유의미하게 관련되어 있다는 것을 증명하였고, 단 이러한 관계는 어머니 스트레스 형태를 통하여 전달 형성된다는 것을 입증하였다. 더욱이 본 연구는 어머니-아동 애착 형성의 순환에 있어서 직접적인 경로가 없다는 것을 밝혀 줌으로서, 세대간 불안정애착 유형 순환 붕괴의 가능성을 제시하였다.

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Anti-inflammatory Effect of Biotin and Plant extracts

  • Y. J. Joo;S. W. Jung;Kim, B. R.;Kim, I. Y.;Lee, J. D.;H. C. Ryoo;Lee, S. H.
    • 대한화장품학회:학술대회논문집
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    • 대한화장품학회 2003년도 IFSCC Conference Proceeding Book I
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    • pp.601-610
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    • 2003
  • Biotin is a water-soluble vitamin used as a skin conditioning agent and promotes the formation of intercellular lipid layers through increased lipid synthesis, which improves the skin's natural barrier function. The anti-inflammatory effects of biotin have been investigated using in vitro assay models, such as MTT assay, measurements of concentrations of nitric oxide(NO), prostaglandin E2(PGE$_2$), and inhibition rate of 5-lipoxygenase(5-LOX). In comparison with biotin, other plant extracts were tested at the same time which were kudzu vine extract, sage extract, paeonia extract, and dipotassium glycyrrhetinate. Nitric oxide is a signal molecule with functions such as neurotransmission, local vascular relaxation, and anti-inflammation in many physiological and pathological processes. NO can cause apoptosis and necrosis of target cells such as keratinocytes and is generated from L-arginine by nitric oxide synthase (NOS). Prostanoids, including prostaglandins and thromboxanes, are generated by the phospholipase $A_2$/cyclooxygenase(COX) pathway, and leukotrienes are generated by the 5-lipoxygenase pathway from arachidonic acid. Prostaglandin E2 recently have been shown to be beneficial in the resolution of tissue injury and inflammation, also has been implicated as an immunosuppressive agent and plasma levels of PGE$_2$ are elevated in patients sustaining thermal injury. Lipoxygenase metabolites from arachidonic acid have been implicated in inflammation, anti-inflammatory activity of the raw materials was evaluated in vitro by the offered inhibition of lipoxygenase.

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