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Selenite induces DNA damage and specific mitochondrial degeneration in human bladder cancer cells

The result's identifiers

  • Result code in IS VaVaI

    <a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F00216208%3A11150%2F16%3A10324540" target="_blank" >RIV/00216208:11150/16:10324540 - isvavai.cz</a>

  • Result on the web

    <a href="http://dx.doi.org/10.1016/j.tiv.2015.12.011" target="_blank" >http://dx.doi.org/10.1016/j.tiv.2015.12.011</a>

  • DOI - Digital Object Identifier

    <a href="http://dx.doi.org/10.1016/j.tiv.2015.12.011" target="_blank" >10.1016/j.tiv.2015.12.011</a>

Alternative languages

  • Result language

    angličtina

  • Original language name

    Selenite induces DNA damage and specific mitochondrial degeneration in human bladder cancer cells

  • Original language description

    We have investigated the cytotoxicity and specific effects of selenite in human bladder cancer cell line RT-112 and its clonogenic variant RT-112 HB. Selenite inhibited cell growth and proliferation in both cell lines. Treated cells developed extensive vacuolization which was dose independent but occurring in differing time frames. Ultrastructure analysis revealed that the observed vacuoles are damaged mitochondria and potentially other sub cellular compartments. Selenite-specific effects on mitochondria were further confirmed by mitochondrial membrane potential analysis, changes in ATP production and generation of superoxide. Simultaneously, selenite induced DNA damage in treated cells with activation of p53, PARP-1 and JNK and suppressed autophagy. Cells ultimately died via a combination of apoptosis, necrosis and a distinct type of cell death featuring "vacuolar shrink age", loss of adherence and absence of secondary necrosis as well as other classical markers of either apoptosis or autophagy. The significant presence of so called necroptosis was also not confirmed as the specific inhibitor necrostatin-1 could not prevent cell death. These results thus confirm the toxicity of selenite in bladder cancer cells while pointing at potentially new mechanism of action of this compound in this model.

  • Czech name

  • Czech description

Classification

  • Type

    J<sub>x</sub> - Unclassified - Peer-reviewed scientific article (Jimp, Jsc and Jost)

  • CEP classification

    EB - Genetics and molecular biology

  • OECD FORD branch

Result continuities

  • Project

  • Continuities

    I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace

Others

  • Publication year

    2016

  • Confidentiality

    S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Data specific for result type

  • Name of the periodical

    Toxicology in Vitro

  • ISSN

    0887-2333

  • e-ISSN

  • Volume of the periodical

    32

  • Issue of the periodical within the volume

    Aprile

  • Country of publishing house

    GB - UNITED KINGDOM

  • Number of pages

    10

  • Pages from-to

    105-114

  • UT code for WoS article

    000372760900012

  • EID of the result in the Scopus database

    2-s2.0-84952837134