• 제목/요약/키워드: Light-induced degradation

검색결과 109건 처리시간 0.025초

Photodegradation of 17α-ethynylestradiol in nitrate aqueous solutions

  • Ren, Dong;Bi, Tingting;Gao, Shumei;Li, Xukun;Huang, Bin;Pan, Xuejun
    • Environmental Engineering Research
    • /
    • 제21권2호
    • /
    • pp.188-195
    • /
    • 2016
  • $17{\alpha}$-Ethynylestradiol (EE2) has gotten growing concerns due to its widely detected in the environment and high estrogenic potency. However, the knowledge on the photochemical behaviors of EE2 in natural waters is still limited. Herein, the photodegradation and estrogenic potency variation of EE2 induced by nitrate were studied using a sunlight simulator consisted by a 300 W medium pressure mercury lamp and 290 nm cut-off filters. It was found that EE2 could be photodegraded at a rate of $0.0193h^{-1}$ in pure aqueous solutions, and the photodegradation of EE2 could be significantly promoted by nitrate. The photodegradation removal rate of EE2 was increased from 9% in Milli-Q water to 85% in 2.0 mM nitrate solutions. Reactive species scavenging experiments demonstrated that the photogenerated $HO{\bullet}$ contributed about 55% to EE2 degradation. Fe(III), Cl- and dissolved humic acid (DHA) could inhibit the photodegradation of EE2 by competing the incident light and photogenerated $HO{\bullet}$, while $HCO_3{^-}$ had no influence on EE2 photodegradation. EE2 was determined to be phototransformed into organic chemicals without estrogenic potency by GC-MS and MCF-7 cell proliferation toxicity tests. These findings could extend our knowledge on the photochemical behaviors of steroid estrogens and provide information for ecological risk assessment.

Potential Role of Ursodeoxycholic Acid in Suppression of Nuclear Factor Kappa B in Microglial Cell Line (BV-2)

  • Joo, Seong-Soo;Won, Tae-Joan;Lee, Do-Ik
    • Archives of Pharmacal Research
    • /
    • 제27권9호
    • /
    • pp.954-960
    • /
    • 2004
  • Expression of the NF-$textsc{k}$B-dependent genes responsible for inflammation, such as TNF-$\alpha$, IL-1$\beta$, and nitric oxide synthase (NOS), contributes to chronic inflammation which is a major cause of neurodegenerative diseases (i.e. Alzheimer's disease). Although NF-$textsc{k}$B plays a biphasic role in different cells like neurons and microglia, controlling the activation of NF-$textsc{k}$B is important for its negative feedback in either activation or inactivation. In this study, we found that ursodeoxycholic acid (UDCA) inhibited I$textsc{k}$B$\alpha$ degradation to block expression of the NF-$textsc{k}$B-dependent genes in microglia when activated by $\beta$-amyloid peptide (A$\beta$). We also showed that when microglia is activated by $A\beta$42, the expression of A20 is suppressed. These findings place A20 in the category of ' protective ' genes, protecting cells from pro-inflammatory reper-toires induced in response to inflammatory stimuli in activated microglia via NF-$textsc{k}$B activation. In light of the gene and proteins for NF-$textsc{k}$B-dependent gene and inactivator for NF-$textsc{k}$B (I$textsc{k}$B$\alpha$), the observations now reported suggest that UDCA plays a role in supporting the attenuation of the production of pro-inflammatory cytokines and NO via inactivation of NF-$textsc{k}$B. Moreover, an NF-$textsc{k}$B inhibitor such as A20 can collaborate and at least enhance the anti-inflammatory effect in microglia, thus giving a potent benefit for the treatment of neurodegenerative diseases such as AD.uch as AD.

SiO2 완충층 두께에 따른 비정질 InGaZnO Pseudo-MOS Field Effect Transistor의 신뢰성 평가 (Effect of SiO2 Buffer Layer Thickness on the Device Reliability of the Amorphous InGaZnO Pseudo-MOS Field Effect Transistor)

  • 이세원;황영현;조원주
    • 한국전기전자재료학회논문지
    • /
    • 제25권1호
    • /
    • pp.24-28
    • /
    • 2012
  • In this study, we fabricated an amorphous InGaZnO pseudo-MOS transistor (a-IGZO ${\Psi}$-MOSFET) with a stacked $Si_3N_4/SiO_2$ (NO) gate dielectric and evaluated reliability of the devices with various thicknesses of a $SiO_2$ buffer layer. The roles of a $SiO_2$ buffer layer are improving the interface states and preventing degradation caused by the injection of photo-created holes because of a small valance band offset of amorphous IGZO and $Si_3N_4$. Meanwhile, excellent electrical properties were obtained for a device with 10-nm-thick $SiO_2$ buffer layer of a NO stacked dielectric. The threshold voltage shift of a device, however, was drastically increased because of its thin $SiO_2$ buffer layer which highlighted bias and light-induced hole trapping into the $Si_3N_4$ layer. As a results, the pseudo-MOS transistor with a 20-nm-thick $SiO_2$ buffer layer exhibited improved electrical characteristics and device reliability; field effective mobility(${\mu}_{FE}$) of 12.3 $cm^2/V{\cdot}s$, subthreshold slope (SS) of 148 mV/dec, trap density ($N_t$) of $4.52{\times}1011\;cm^{-2}$, negative bias illumination stress (NBIS) ${\Delta}V_{th}$ of 1.23 V, and negative bias temperature illumination stress (NBTIS) ${\Delta}V_{th}$ of 2.06 V.

Pectic-Oligoshaccharides from Apples Induce Apoptosis and Cell Cycle Arrest in MDA-MB-231 Cells, a Model of Human Breast Cancer

  • Delphi, Ladan;Sepehri, Houri;Khorramizadeh, Mohammad Reza;Mansoori, Fatemeh
    • Asian Pacific Journal of Cancer Prevention
    • /
    • 제16권13호
    • /
    • pp.5265-5271
    • /
    • 2015
  • Background: The effects of plant products on cancer cells has become a field of major importance. Many substancesmay induce apoptosis in anti-cancer treatment. Pectins, a family of complex polysaccharides, and their degradation products may for exasmple exert apoptotic effects in cancer cells. Apples and citrus fruits are the main sources of pectin which can be applied for anti-cancer research. The present study concerned an intact form of pectic-oligoshaccharide named pectic acid (poly galactronic acid). Materials and Methods: Inhibition of cell proliferation assays (MTT), light microscopy, fluorescence microscopy (acridin orange/ethidium bromide), DNA fragmentation tests, cell cycle analysis, annexin PI and Western blotting methods were applied to evaluate apoptosis. Results: The results indicated that pectic acid inhibited cell growth and reduced cell attachment after 24h incubation. This did not appear to be due to necrosis, since morphological features of apoptosis were detected with AO/EB staining and cell cycling was blocked in the sub-G1 phase. Annexin/PI and DNA fragmentation findings indicated that apoptosis frequency increased after 24h incubation with pectic acid. In addition, the data showed pectic acid induced caspase-dependent apoptosis. Conclusions: These data indicate that apple pectic acid without any modification could trigger apoptosis in MDA-MB-231 human breast cancer cells and has potential to improve cancer treatment as a natural product.

Evaluating the Catalytic Effects of Carbon Materials on the Photocatalytic Reduction and Oxidation Reactions of TiO2

  • Khan, Gulzar;Kim, Young Kwang;Choi, Sung Kyu;Han, Dong Suk;Abdel-Wahab, Ahmed;Park, Hyunwoong
    • Bulletin of the Korean Chemical Society
    • /
    • 제34권4호
    • /
    • pp.1137-1144
    • /
    • 2013
  • $TiO_2$ composites with seven different carbon materials (activated carbons, graphite, carbon fibers, single-walled carbon nanotubes, multi-walled carbon nanotubes, graphene oxides, and reduced graphene oxides) that are virgin or treated with nitric acid are prepared through an evaporation method. The photocatalytic activities of the as-prepared samples are evaluated in terms of $H_2$ production from aqueous methanol solution (photo-catalytic reduction: PCR) and degradation of aqueous pollutants (phenol, methylene blue, and rhodamine B) (photocatalytic oxidation: PCO) under AM 1.5-light irradiation. Despite varying effects depending on the kinds of carbon materials and their surface treatment, composites typically show enhanced PCR activity with maximum 50 times higher $H_2$ production as compared to bare $TiO_2$. Conversely, the carbon-induced synergy effects on PCO activities are insignificant for all three substrates. Colorimetric quantification of hydroxyl radicals supports the absence of carbon effects. However, platinum deposition on the binary composites displays the enhanced effect on both PCR and PCO reactions. These differing effects of carbon materials on PCR and PCO reactions of $TiO_2$ are discussed in terms of physicochemical properties of carbon materials, coupling states of $TiO_2$/carbon composites, interfacial charge transfers. Various surface characterizations of composites (UV-Vis diffuse reflectance, SEM, FTIR, surface area, electrical conductivity, and photoluminescence) are performed to gain insight on their photocatalytic redox behaviors.

Autophagy localization and cytoprotective role in cisplatin-induced acute kidney injury

  • Karunasagara, Shanika;Hong, Geum-Lan;Jung, Da-Young;Ryu, Si-Yun;Jung, Ju-Young
    • 대한수의학회지
    • /
    • 제59권3호
    • /
    • pp.133-139
    • /
    • 2019
  • Autophagy is a fundamental cellular process that maintains homeostasis and cell integrity, under stress conditions. Although the involvement of autophagy in various conditions has been elucidated, the role of autophagy in renal structure is not completely clarified. Our aim was to investigate the cytoprotective effect of autophagy against acute kidney injury (AKI) through cisplatin deteriorative pathway, which leads to AKI via renal cell degradation. For in vivo experiments, male Sprague Dawley rats were divided in to 2 groups (n = 6/group) as control, Cis-5D. Following a single intraperitoneal injection of cisplatin, rats were sacrificed after 5 days. Blood urea nitrogen (BUN), creatinine (Cr) and histological alterations were examined. Further, expression of key regulators of autophagy, light-clain 3 (LC3), p62, and Beclin1, was evaluated by immunohistochemistry (IHC). The rats exhibited severe renal dysfunction, indicated by elevated BUN, Cr. Hematoxylin and eosin staining revealed histological damages in cisplatin-treated rats. Furthermore, IHC analysis revealed increased expression of LC3, Beclin1 and decreased expression of p62. Furthermore, expression of aforementioned autophagy markers was restricted to proximal tubule. Taken together, our study demonstrated that cisplatin can cause nephrotoxicity and lead to AKI. This phenomenon accelerated autophagy in renal proximal tubules and guards against AKI.

오메프라졸의 안정화를 위한 에칠렌디아민 복합체 개발 (Ethylenediamine Complex for Stabilization of Omeprazole)

  • 오세종;김은영;김길수;김윤정;이계주
    • Journal of Pharmaceutical Investigation
    • /
    • 제25권1호
    • /
    • pp.9-17
    • /
    • 1995
  • To stabilize omeprazole(OMP), ethylenediamine(ED) complex of omeprazole(OMPED) was prepared by reaction between OMP and ED in methanol, and the complex formation was confirmed by the instrumental analysis, i.e., IR, DSC, EA, NMR, MS and XRD. The rates of decomposition of OMP and OMPED in aqueous solution and the shelf lives at standard temperature were measured by accelerated stability analysis. The results are summarized as follows; The mole ratio of OMP and ED in OMPED complex is 1:1, the energy of formation within OMPED might be combined between polar imidazole group of OMP with induced a dipole amine group in the readily polarizable ED molecule. At standard temperature the degradation rate constant of OMP in aqueous solution is $2.540{\times}10^{-2}\;hr^{-1}$ and the shelf life is 4.15 hrs, and in the case of OMPED the degradation rate constant is $7.986{\times}10^{-4}\;hr^{-1}$ and the shelf life is 131.96 hrs. So, the OMPED has about 31 times longer shelf life than OMP. The activation energy of OMP and OMPED are 5.23 and 18.55 kcal $mole^{-1}$ respectively. The stability of OMP is dependent chiefly on pH in the solutions and it decomposes readily in acidic medium by hydrogen ion catalized reaction but becomes stable beyond pH 9.0. In case of the ED-complex, OMPED is stable in neutral as well as in dilute acidic solutions even in pH 6, OMPED is very stable to light(UV), that is, the rate constant and shelf life of OMP are $k=1.0188{\times}10^{-2}\;day^{-1}$, $T_{90%}=4.5 \;days$, on the other hand, the those of OMPED are $k=7.138{\times}10^{-4}\;day^{-1}$, $T_{90%}=64.1\;days$, respectively. From the above results, it is thought that new dosage forms could be developed by using the OMPED as a potential OMP complex.

  • PDF

Ultrastructural changes of Haematococcus pluvialis (Chlorophyta) in process of astaxanthin accumulation and cell damage under condition of high light with acetate

  • He, Bangxiang;Hou, Lulu;Zhang, Feng;Cong, Xiaomei;Wang, Zhendong;Guo, Yalin;Shi, Jiawei;Jiang, Ming;Zhang, Xuecheng;Zang, Xiaonan
    • ALGAE
    • /
    • 제35권3호
    • /
    • pp.253-262
    • /
    • 2020
  • Haematococcus pluvialis is a commercial microalga that can produce high quantities of astaxanthin. Under induced conditions, some important changes in the subcellular structures related to astaxanthin accumulation were observable. For example, a large number of astaxanthin granules, oil structures and starch granules appeared in the thick-walled cells; Astaxanthin granules gradually dissolved into the oil structures and spread throughout the entire cell with the fusion and diffusion process of oil structures during the middle and late stages of induction; The plastoglobules were closed to the newly formed structures, and some plastoglobules would abnormally increase in size under stress. Based on observations of cell damage, the degradation of membrane structures, such as chloroplasts, was found to be the primary form of damage during the early stage of induction. During the middle stage of induction, some transparent holes were exposed in the dissolving astaxanthin granules in the cytoplasm. In thick-walled cells, these transparent holes were covered by oil substances dissolving astaxanthin, thereby avoiding further damage to cells. Given the relatively few oil structures, in non-thick-walled cells, the transparent holes expanded to form multiple transparent areas, eventually resulting in the rupture and death of cells. These results suggested that the high level of synthesis and the wide range diffusion of oil explained the expansion of astaxanthin in H. pluvialis.

비정질 실리콘 태양전지에 대한 장시간 성능예측: 확장지수함수 모형 및 컴퓨터 모의실험 (Long-term performance of amorphous silicon solar cells by the stretched exponential defect kinetics)

  • 김지회;박상현;유종훈
    • 한국신재생에너지학회:학술대회논문집
    • /
    • 한국신재생에너지학회 2011년도 춘계학술대회 초록집
    • /
    • pp.105.2-105.2
    • /
    • 2011
  • 화비정질 실리콘의 빛에 의한 노화현상 (light-induced degradation; LID)은 이미 1977년 보고된 Staebler-Wronski 효과에 의해서 확인된 바 있다. 이는 비정질 실리콘이 빛에 노출될 때, 이미 포함되어 있는 수소원자가 빛 에너지에 의해서 이동하게 되고, 이로 인해서 생성 또는 소멸되는 댕글링 본드 때문에 일어난다. 특히, 일상적인 태양광의 노출 하에서 태양전지의 장시간 성능을 예측하는데 물리적인 이해의 부족 및 기술 환경적인 어려움이 있고, 이러한 요인들은 안정된 태양전지를 개발하는데 장해요인으로 나타난다. 그러므로 비정질 실리콘 태양전지가 장시간 태양광에 노출되어 시간이 지남에 따라서 "성능이 어떻게 변하는지?" 그리고 "이에 대한 원인은 무엇인지?" 등은 여전히 과학적으로 풀어야할 숙제로 남아있다. 본 논문에서는 비정질 실리콘으로 구성된 태양전지가 태양광에 노출될 때 시간이 지남에 따라서 (1) 성능이 어떻게 변하는지, (2) LID의 변화는 언제 안정화되는지, 그리고 (3) 성능변화에 대한 원인은 무엇인지에 대해서 논의한다. 본 논문은 장시간 빛에 노출되는 비정질 실리콘 태양전지의 성능예측에 관해서 연구하였다. 결함밀도의 운동학적 모형을 통해서 태양광 노출에 대한 태양전지 성능변화를 예측하는데 초점을 맞추었고, 이를 위해서 태양전지에 조사되는 태양광 세기, 주변온도, 등이 고려되었다. 특히, 전하운반자의 수명이 결함밀도에 의해서 결정되기 때문에 비정질 실리콘 태양전지의 빛에 대한 노화현상 (LID)이 확장지수함수 (stretched-exponential) 완화법칙을 따르는 결함밀도에 의해서 물리적으로 설명된다. 한편 이와 같은 물리적 계산의 유용성을 확인하기 위해서 동일한 태양전지에 대해서 AMPS-1D 컴퓨터 프로그램을 사용하였고, 이를 통해서 비정질 실리콘 태양전지의 빛에 대한 노화현상을 물리적 및 정량적으로 이해하였다. 본 연구에 적용되는 태양전지는 비정질 실리콘으로 구성된 pin 구조 (glass/$SnO_2$/a-SiC:H:B/a-Si:H/a-Si:H:P/ITO)로서 다음과 같은 특성을 갖는다: 에너지 띠간격~1.72 eV, 두께~400 nm, 내부전위~1.05 V, 초기 fill factor~0.71, 초기 단락전류~16.4 mA/$cm^2$, 초기 개방전압 0.90 V, 초기 변환효율 10.6 %. 우리는 이와 같은 연구를 통해서 과학적으로 비정질 실리콘의 빛에 의한 노화현상을 이해하고, 기술적으로 효율 및 경제성이 높은 태양전지의 개발에 도전한다.

  • PDF

Downregulation of $\textrm{NF}_{-{\kappa}}\textrm{B}$ activation in human keratinocytes by melanogenic inhibitors

  • Ahn, Kwang-Seok;Lee, Jinseon;Kim, Yeong-Shik
    • 대한화장품학회:학술대회논문집
    • /
    • 대한화장품학회 2003년도 IFSCC Conference Proceeding Book I
    • /
    • pp.780-803
    • /
    • 2003
  • Exposure of skin cells, particularly keratinocytes to various nuclear factor-kappaB ($\textrm{NF}_{-{\kappa}}\textrm{B}$) activators [e.g. tumor necrosis factor-$\alpha$, interleukin-1, lipopolysaccharides, and ultraviolet light] leads to phosphorylation and degradation of the inhibitory protein, $\textrm{I}_{{\kappa}}\textrm{B}$. Liberated $\textrm{NF}_{-{\kappa}}\textrm{B}$ is translocated into the nucleus where it can change or alter expression of target genes, resulting in the secretion of extracellular signaling molecules including melanotrophic factors affecting melanocyte. In order to demonstrate the possible role of $\textrm{NF}_{-{\kappa}}\textrm{B}$ activation on the synthesis of melanotrophic factors from the keratinocytes, the activities of $\textrm{NF}_{-{\kappa}}\textrm{B}$ induced by melanogenic inhibitors (MIs) were determined in human HaCaT keratinocytes transfected with $\textrm{pNF}_{-{\kappa}}\textrm{B}$-SEAP-NPT plasmid. Transfectant cells released the secretory alkaline phosphatase (SEAP) as a transcription reporter in response to the $\textrm{NF}_{-{\kappa}}\textrm{B}$ activity and contain the neomycin phosphotransferase (NPT) gene for the dominant selection marker for geneticin resistance. MIs such as niacinamide, kojic acid, hydroquinone, resorcinol, arbutin, and glycolic acid were preincubated with transfectant HaCaT cells for 3 h and then ultraviolet B (UVB) was irradiated. $\textrm{NF}_{-{\kappa}}\textrm{B}$ activation was measured with the SEAP reporter gene assay using a fluorescence detection method. Of the Mis tested, kojic acid ($IC_{50}$/ = 60 $\mu$M) was found to be the most potent inhibitor of UVB-upregulating $\textrm{NF}_{-{\kappa}}\textrm{B}$ activation in transfectant HaCaT cells, which is followed by niacinamide ($IC_{50}$/= 540 $\mu$M). Pretreatment of the transfectant HaCaT cells with the Mis, especially kojic acid and niacinamide, effectively lowered $\textrm{NF}_{-{\kappa}}\textrm{B}$ binding measured by electrophoretic mobility shift assay. Furthermore, these two inhibitors remarkably reduced the secretion level of IL-6, one of melanotrophic factors, triggered by UV-radiation of the HaCaT cells. These observations suggest that Mis working at the in vivo level might act partially through the modulation of the synthesis of melanotrophic factors in keratinocyte.

  • PDF