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    Wyświetlanie 1-3 z 3
    Tytuł:
    Curcumin induces cell death without oligonucleosomal DNA fragmentation in quiescent and proliferating human CD8+ cells
    Autorzy:
    Magalska, Adriana
    Brzezinska, Agnieszka
    Bielak-Zmijewska, Anna
    Piwocka, Katarzyna
    Mosieniak, Grażyna
    Sikora, Ewa
    Powiązania:
    https://bibliotekanauki.pl/articles/1041209.pdf
    Data publikacji:
    2006
    Wydawca:
    Polskie Towarzystwo Biochemiczne
    Tematy:
    CD8+
    cell death
    DNA degradation
    curcumin
    Opis:
    Cytotoxic CD8+ cells play an important role in determining host response to tumor, thus chemotherapy is potentially dangerous as it may lead to T cells depletion. The purpose of this study was to elucidate the propensity of quiescent and proliferating human CD8+ cells to undergo cell death upon treatment with curcumin, a natural dye in Phase I of clinical trials as a prospective chemopreventive agent. Methods: We treated human quiescent or proliferating CD8+ cells with 50 µM curcumin or irradiated them with UVC. Cell death symptoms such as decreased cell viability, chromatin condensation, activation of caspase-3 and specific DFF40/CAD endonuclease and oligonucleosomal DNA fragmentation were analyzed using MTT test, microscopic observation, Western blotting and flow cytometry. Results: Curcumin decreased cell viability, activated caspase-3 and decreased the level of DFF45/ICAD, the inhibitor of the DFF40/CAD endonuclease. However, this did not lead to oligonucleosomal DNA degradation. In contrast, UVC-irradiated proliferating, but not quiescent CD8+ cells revealed molecular and morphological changes characteristic for apoptosis, including oligonucleosomal DNA fragmentation. Curcumin can induce cell death in normal human lymphocytes both quiescent and proliferating, without oligonucleosomal DNA degradation which is considered as a main hallmark of apoptotic cell death. Taking into account the role of CD8+ cells in tumor response, their depletion during chemotherapy could be particularly undesirable.
    Źródło:
    Acta Biochimica Polonica; 2006, 53, 3; 531-538
    0001-527X
    Pojawia się w:
    Acta Biochimica Polonica
    Dostawca treści:
    Biblioteka Nauki
    Artykuł
    Tytuł:
    Antiviral Activities of Zn2+ Ions for Viral Prevention, Replication, Capsid Protein in Intracellular Proliferation of Viruses
    Autorzy:
    Ishida, Tsuneo
    Powiązania:
    https://bibliotekanauki.pl/articles/1177895.pdf
    Data publikacji:
    2018
    Wydawca:
    Przedsiębiorstwo Wydawnictw Naukowych Darwin / Scientific Publishing House DARWIN
    Tematy:
    Capsid protein
    DNA/RNA virus
    HIV
    RNA degradation
    ROS
    Replication
    Zinc finger
    Opis:
    In zinc homeostasis, zinc transporters ZIP and ZnT show tissue specificity and developmental and stimulus responsive expression patterns. The course of the life cycles of viral infections is governed by complex interactions between the virus and the host cellular system. Viruses depend on a host cell for their protein synthesis that the virus must first bind to the host cell, and then the virus enters in the cytoplasm which the genome is liberated from the protective capsid and, either in the nucleus or in the cytoplasm. The use of cellular zinc metalloproteases is effective for virus entry and coronavirus fusion. Molecular aspects of dengue virus genome uncoating and the fate of the capsid protein and RNA genome early during infection were investigated and found that capsid is degraded after viral internalization by the host ubiquitin-proteasome system. These results provide the first insights for antiviral intervention into dengue virus uncoating by Zn-binding degradation and enzyme inhibition of nucleocapsid, capsid protein, viral genome. AZPs inhibit virus DNA replication. Increasing the intracellular Zn2+ concentration with zinc-ionophores like pyrithione can efficiently impair the replication of a variety of RNA viruses, including poliovirus and influenza virus. ZAP is a host antiviral factor that specifically inhibit the replication of certain viruses, including HIV-1, Sindbis virus, and Ebola virus. ZAP specifically binds to the viral mRNA and recruits the cellular RNA degradation machinery to degrade the target RNA, while molecular mechanism by which ZAP inhibits target RNA expression and regulation of antiviral activity have been remained unclear. ROS as byproducts play an important role in cell signaling and regulate hormone action, growth factors, cytokines, transcription, apoptosis, iron transport, immunomodulation, and neuromodulation which many retroviruses, DNA and RNA viruses can cause cell death by generating oxidative stress in infected cells.
    Źródło:
    World Scientific News; 2018, 97; 28-50
    2392-2192
    Pojawia się w:
    World Scientific News
    Dostawca treści:
    Biblioteka Nauki
    Artykuł
    Tytuł:
    Antiviral Activities of Cu2+ Ions in Viral Prevention, Replication, RNA Degradation, and for Antiviral Efficacies of Lytic Virus, ROS-Mediated Virus, Copper Chelation
    Autorzy:
    Ishida, Tsuneo
    Powiązania:
    https://bibliotekanauki.pl/articles/1177808.pdf
    Data publikacji:
    2018
    Wydawca:
    Przedsiębiorstwo Wydawnictw Naukowych Darwin / Scientific Publishing House DARWIN
    Tematy:
    Capsid protein
    Copper chelation
    Copper homeostasis
    Copper oxide nanoparticles
    Cu2+ and Cu1+ ions
    DNA/RNA virus
    HSV
    ROS
    Viral replication
    mRNA degradation or decay
    Opis:
    Copper has been known for decades that marked changes of micronutrient homeostasis in the host are accompanied by infection or inflammation. Copper levels in the serum are significantly elevated in response to inflammation that copper accumulates at sites of inflammation. Easily oxidized copper oxide nanoparticles (CuONPs) are widely used as catalysts that the ability of CuONPs to reduce bacterial population and virus application is enhanced. The mechanism of copper-mediated inactivation of herpes simplex virus (HSV) is by which cupric ions oxidatively damage biomolecules. Virus-mediated subjugation and modulation of host lipids during infection that the life cycle of most viruses proceeds through a series of basic steps: binding and internalization, fusion, uncoating, of the viral genome, its replication, assembly of new particles, and budding or release of the newly made viruses. The HIV-1 protein Vpu is an 81-amino-acid (16-kDa) type I which the presence of Vpu leads to the degradation of BST-2 via an endosome-lysosome degradation pathway. Oxidative degradation by a Cu-metalloenzyme, and ubiquitin-mediated degradation of cellular proteins were exploited. Copper can disrupt the lytic cycle of the Coccolithovirus. Lysins represent a novel class of anti-infectives derived from bacteriophage which lysins are bacterial cell wall hydrolytic enzymes that selectively and rapidly kill specific bacteria. Regarding copper induced cellular toxicity, several mechanisms have been proposed based on the formations of ROS by free Cu ions as cupric and cuprous ions can participate in redox reactions. ROS (O2ˉ,･OH, OHˉ), Cu+ and H2O2 play the important roles for viral inactivations. Thujaplicin-copper chelates inhibit influenza virus-induced apoptosis. Pyrrolidine dithiocarbamate as a metal ion binding agent inhibits the activity of the viral proteases of polyprotein processing and RNA replication of HRV. Chelation enables metals are capable of ligand scavenging via complexation, since reverse transcriptase enzyme inhibits the growth and replication of RNA tumor viruses. Thus, copper complex and copper chelation enhance antiviral efficacy.
    Źródło:
    World Scientific News; 2018, 99; 148-168
    2392-2192
    Pojawia się w:
    World Scientific News
    Dostawca treści:
    Biblioteka Nauki
    Artykuł
      Wyświetlanie 1-3 z 3

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