The Experts below are selected from a list of 315 Experts worldwide ranked by ideXlab platform

You-jin Jeon - One of the best experts on this subject based on the ideXlab platform.

  • Protective effect of fucoxanthin isolated from Sargassum siliquastrum on UV-B induced Cell Damage
    Journal of Photochemistry and Photobiology B: Biology, 2009
    Co-Authors: Soo-jin Heo, You-jin Jeon
    Abstract:

    Fucoxanthin is a carotenoid isolated from Sargassum siliquastrum and is considered to be one of major active compound of marine algae. In this study, we investigated and confirmed the protective effect of fucoxanthin on UV-B induced Cell injury in human fibroblast via 2′,7′-dichlorodihydrofluorescein diacetate (DCFH-DA), 3-(4,5-dimethylthiazol-2-yl)2,5-diphenyltetrazolium bromide (MTT), and comet assays. IntraCellular ROS generated by exposure to UV-B radiation, which was significantly decreased by addition with various concentrations of fucoxanthin. Cell survival rate was increased with fucoxanthin pre-treated Cells, which was reached around 81.47% at 100 μM, and the inhibitory effect of Cell Damage exhibited dose-dependent manner. Moreover, fucoxanthin having protective properties was demonstrated via Hoechst 33342/PI staining. Hence, on the basis of the above-mentioned studies, fucoxanthin has the ability to protect against oxidative stress induced by UV-B radiation and which might be applied to antioxidant and cosmeceutical industries. © 2008 Elsevier B.V. All rights reserved.

  • cytoprotective effect of fucoxanthin isolated from brown algae sargassum siliquastrum against h2o2 induced Cell Damage
    European Food Research and Technology, 2008
    Co-Authors: Seokchun Ko, Sungmyung Kang, Hahksoo Kang, You-jin Jeon
    Abstract:

    In this study, the cytoprotective effect of fucoxanthin, which was isolated from Sargassum siliquastrum, against oxidative stress induced DNA Damage was investigated. Fucoxanthin, a kind of carotenoid, was pretreated to the medium and the protective effect was evaluated via 2′,7′-dichlorodihydrofluorescein diacetate, 3-(4,5-dimethylthiazol-2-yl)2,5-diphenyltetrazolium bromide, and comet assays. IntraCellular reactive oxygen species were over produced by addition of hydrogen peroxide (H2O2), but the production was significantly reduced by the treatment with fucoxanthin. The fucoxanthin strongly enhanced Cell viability against H2O2 induced oxidative Damage and the inhibitory effect of Cell Damage was a dose-dependent manner. Furthermore, a protective effect against oxidative stress-induced Cell apoptosis was also demonstrated via nuclear staining with Hoechst dye. These results clearly indicate that fucoxanthin isolated from S. siliquastrum possesses prominent antioxidant activity against H2O2-mediated Cell Damage and which might be a potential therapeutic agent for treating or preventing several diseases implicated with oxidative stress.

Gro V. Amdam - One of the best experts on this subject based on the ideXlab platform.

  • vitellogenin recognizes Cell Damage through membrane binding and shields living Cells from reactive oxygen species
    Journal of Biological Chemistry, 2013
    Co-Authors: Heli Havukainen, Daniel Munch, Anne Baumann, Shi Zhong, Oyvind Halskau, Michelle Krogsgaard, Gro V. Amdam
    Abstract:

    Abstract Large lipid transfer proteins are involved in lipid transportation and diverse other molecular processes. These serum proteins include vitellogenins, which are egg yolk precursors and pathogen pattern recognition receptors, and apolipoprotein B, which is an anti-inflammatory cholesterol carrier. In the honey bee, vitellogenin acts as an antioxidant, and elevated vitellogenin titer is linked to prolonged life span in this animal. Here, we show that vitellogenin has Cell and membrane binding activity and that it binds preferentially to dead and Damaged Cells. Vitellogenin binds directly to phosphatidylcholine liposomes and with higher affinity to liposomes containing phosphatidylserine, a lipid of the inner leaflet of Cell membranes that is exposed in Damaged Cells. Vitellogenin binding to live Cells, furthermore, improves Cell oxidative stress tolerance. This study can shed more light on why large lipid transfer proteins have a well conserved α-helical domain, because we locate the lipid bilayer-binding ability of vitellogenin largely to this region. We suggest that recognition of Cell Damage and oxidation shield properties are two mechanisms that allow vitellogenin to extend honey bee life span.

Soo-jin Heo - One of the best experts on this subject based on the ideXlab platform.

  • Protective effect of fucoxanthin isolated from Sargassum siliquastrum on UV-B induced Cell Damage
    Journal of Photochemistry and Photobiology B: Biology, 2009
    Co-Authors: Soo-jin Heo, You-jin Jeon
    Abstract:

    Fucoxanthin is a carotenoid isolated from Sargassum siliquastrum and is considered to be one of major active compound of marine algae. In this study, we investigated and confirmed the protective effect of fucoxanthin on UV-B induced Cell injury in human fibroblast via 2′,7′-dichlorodihydrofluorescein diacetate (DCFH-DA), 3-(4,5-dimethylthiazol-2-yl)2,5-diphenyltetrazolium bromide (MTT), and comet assays. IntraCellular ROS generated by exposure to UV-B radiation, which was significantly decreased by addition with various concentrations of fucoxanthin. Cell survival rate was increased with fucoxanthin pre-treated Cells, which was reached around 81.47% at 100 μM, and the inhibitory effect of Cell Damage exhibited dose-dependent manner. Moreover, fucoxanthin having protective properties was demonstrated via Hoechst 33342/PI staining. Hence, on the basis of the above-mentioned studies, fucoxanthin has the ability to protect against oxidative stress induced by UV-B radiation and which might be applied to antioxidant and cosmeceutical industries. © 2008 Elsevier B.V. All rights reserved.

Ryuichiro Nishigaki - One of the best experts on this subject based on the ideXlab platform.

  • Ultrasonically induced Cell Damage enhanced by photofrin II: mechanism of sonodynamic activation.
    in Vivo, 2000
    Co-Authors: Yumita N, Umemura S, Ryuichiro Nishigaki
    Abstract:

    Ultrasonically induced Cell Damage and active oxygen generation with photofrin II (PF) were compared in the same in vitro insonation setup. Sarcoma 180 Cells suspended in air-saturated PBS were exposed to ultrasound for up to 60 seconds in the presence and absence of PF. The viability was determined by the Trypan Blue exclusion test. Ultrasonically induced active oxygen generation in the presence and absence of PF in air-saturated aqueous solutions of 50 mM 2,2,6,6-tetramethyl-4-piperidone was detected by electron spin resonance (ESR) spectrum. Significant enhancement of the rates of both ultrasonically induced Cell Damage and nitroxide generation was demonstrated with 20-80 micrograms/ml PF. Both rates correlated very well. The enhancement of both rates with PF was suppressed by 10 mM histidine. These results may suggest that ultrasonically generated active oxygen plays a primary role in ultrasonically induced Cell Damage in the presence of PF.

  • Sonodynamically induced Cell Damage with 4'-O-tetrahydropyranyladriamycin, THP.
    Anticancer Research, 1999
    Co-Authors: Nagahiko Yumita, Yukihiro Okano, Masahiro Kaneuchi, Koshiro Umemura, Ryuichiro Nishigaki, S. Umemura
    Abstract:

    Background. 4'-O-tetrahydropyranyladriamycin (THP) is a novel anthracycline derivative with cardiotoxicity significantly lower than ADM. In this study, the ultrasonically induced in vitro Cell damaging effect of THP was investigated. Materials and methods. Sarcoma 180 Cells suspended in air-saturated PBS were exposed to ultrasound for up to 60 s in the presence and absence of THP. The viability of the isolated Cells was determined by staining of the Cells with Trypan Blue dye. Results. The rate of inducing Cell Damage with ultrasound was doubled with 80 μM THP, while no Cell Damage was observed with THP alone. Conclusion. The enhancement of ultrasonically induced in vitro Cell Damage was demonstrated with THP. This enhancement was significantly inhibited by histidine, which may suggest a sonochemical mechanism.

  • Sonodynamically-induced Cell Damage with fluorinated anthracycline derivative, FAD104
    Cancer Letters, 1998
    Co-Authors: Nagahiko Yumita, S. Umemura, Yukihiro Okano, Masahiro Kaneuchi, Naoki Magario, Midori Ishizaki, Keiko Shimizu, Yasuko Sano, Koshiro Umemura, Ryuichiro Nishigaki
    Abstract:

    The ultrasonically-induced in vitro Cell damaging effect of fluorine-containing anthracycline derivative (FAD104) was investigated. Sarcoma 180 Cells suspended in air-saturated PBS were exposed to ultrasound for up to 60 s in the presence and absence of FAD104. The rate of inducing Cell Damage with ultrasound was doubled with 80 μM FAD104, while no Cell Damage was observed with FAD104 alone. This enhancement was significantly inhibited by histidine, which may suggest a sonochemical mechanism.

  • Sonodynamically-induced in vitro Cell Damage enhanced by adriamycin
    Cancer Letters, 1997
    Co-Authors: S. Umemura, Nagahiko Yumita, Yukihiro Okano, Masahiro Kaneuchi, Naoki Magario, Midori Ishizaki, Keiko Shimizu, Yasuko Sano, Koshiro Umemura, Ryuichiro Nishigaki
    Abstract:

    Abstract Sonodynamically-induced Cell Damage and active oxygen generation enhanced by adriamycin (ADM) were compared in the same in vitro insonation set-up. Significant enhancement of the rates of both ultrasonically-induced Cell Damage and nitroxide generation was demonstrated with 40–160 μ M ADM. Both rates correlated very well resulting in a correlation coefficient of more than 0.99. The enhancement of both rates was suppressed by 10 mM histidine. These results are consistent with the hypothesis that ultrasonically-generated active oxygen plays a major role in the sonodynamically-induced Cell Damage enhanced by ADM.

  • Mechanism of Cell Damage by Ultrasound in Combination with Hematoporphyrin
    Japanese Journal of Cancer Research, 1990
    Co-Authors: Shin-ichiro Umemura, Nagahiko Yumita, Ryuichiro Nishigaki, Koshiro Umemura
    Abstract:

    Abstract The mechanism of Cell Damage by ultrasound in combination with hematoporphyrin was studied. Mouse sarcoma 180 Cell suspensions were exposed to ultrasound for up to 60 s in the presence and absence of hematoporphyrin, with and without active oxygen scavengers. The Cell Damage enhancement by hematoporphyrin was suppressed by adding histidine but not by mannitol. The enhancement was doubled in rate by substitution of deuterium oxide medium for normal water. Sonoluminescence was produced in a saline solution under similar acoustic conditions and observed to have spectral components that can excite hematoporphyrin molecules. These results suggest that Cell Damage enhancement is probably mediated via singlet oxygen generated by ultrasonically activated hematoporphyrin.

Baozhong Zhao - One of the best experts on this subject based on the ideXlab platform.

  • phototoxicity of nano titanium dioxides in hacat keratinocytes generation of reactive oxygen species and Cell Damage
    Toxicology and Applied Pharmacology, 2012
    Co-Authors: Marilyn Ehrenshaft, Joan E Roberts, Peter P Fu, Ronald P Mason, Baozhong Zhao
    Abstract:

    Nano-sized titanium dioxide (TiO2) is among the top five widely used nanomaterials for various applications. In this study, we determine the phototoxicity of TiO2 nanoparticles (nano-TiO2) with different molecular sizes and crystal forms (anatase and rutile) in human skin keratinocytes under UVA irradiation. Our results show that all nano-TiO2 particles caused phototoxicity, as determined by the MTS assay and by Cell membrane Damage measured by the lactate dehydrogenase (LDH) assay, both of which were UVA dose- and nano-TiO2 dose-dependent. The smaller the particle size of the nano-TiO2 the higher the Cell Damage. The rutile form of nano-TiO2 showed less phototoxicity than anatase nano-TiO2. The level of photocytotoxicity and Cell membrane Damage is mainly dependent on the level of reactive oxygen species (ROS) production. Using polyunsaturated lipids in plasma membranes and human serum albumin as model targets, and employing electron spin resonance (ESR) oximetry and immuno-spin trapping as unique probing methods, we demonstrated that UVA irradiation of nano-TiO2 can induce significant Cell Damage, mediated by lipid and protein peroxidation. These overall results suggest that nano-TiO2 is phototoxic to human skin keratinocytes, and that this phototoxicity is mediated by ROS generated during UVA irradiation.