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In vitro stress response induced by sulfur mustard in lung fibroblasts NHLF and human pulmonary epithelial cells A-549

Identifikátory výsledku

  • Kód výsledku v IS VaVaI

    <a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F60162694%3AG44__%2F20%3A00556085" target="_blank" >RIV/60162694:G44__/20:00556085 - isvavai.cz</a>

  • Výsledek na webu

    <a href="https://link.springer.com/article/10.1007/s00204-020-02845-9" target="_blank" >https://link.springer.com/article/10.1007/s00204-020-02845-9</a>

  • DOI - Digital Object Identifier

    <a href="http://dx.doi.org/10.1007/s00204-020-02845-9" target="_blank" >10.1007/s00204-020-02845-9</a>

Alternativní jazyky

  • Jazyk výsledku

    angličtina

  • Název v původním jazyce

    In vitro stress response induced by sulfur mustard in lung fibroblasts NHLF and human pulmonary epithelial cells A-549

  • Popis výsledku v původním jazyce

    Sulfur mustard [bis(2-chloroethyl) sulfide; SM] is a highly poisonous chemical warfare agent. The mechanism of its cytotoxicity affects several pathways, which cause cell damage or death. The main organ affected in case of exposure to both aerosol and vapor is lungs. The present study focuses on time- and concentration-dependent changes in human lung fibroblasts NHLF and lung epithelial cell line A-549. The cells were treated with SM at the concentrations of 5, 10 and 100 mu M and signs of stress response were evaluated during 1-72 h post-treatment. Parameters for testing included cell viability and morphology, loss of transmembrane mitochondrial potential, apoptosis, oxidative stress, changes in the cell cycle, and ATM kinase activation. The cytotoxic effect of SM resulted in a time-dependent decrease in viability of A-459 associated with apoptosis more markedly than in NHLF. We did not observe any generation of reactive oxygen species by SM. SM at concentrations of 5 and 10 mu M induced the S-phase cell cycle arrest at both cell lines. On the other hand, 100 mu M caused nonspecific cell cycle arrest. ATM kinase was activated transiently. The results indicate that NHLF cells are less prone to toxic damage by SM in case of cell viability, apoptosis and loss of transmembrane mitochondrial potential. The analysis provides a time-related cytotoxic profile of A-549 and NHLF cells for further investigation into the prevention of SM toxic effects and their potential treatment.

  • Název v anglickém jazyce

    In vitro stress response induced by sulfur mustard in lung fibroblasts NHLF and human pulmonary epithelial cells A-549

  • Popis výsledku anglicky

    Sulfur mustard [bis(2-chloroethyl) sulfide; SM] is a highly poisonous chemical warfare agent. The mechanism of its cytotoxicity affects several pathways, which cause cell damage or death. The main organ affected in case of exposure to both aerosol and vapor is lungs. The present study focuses on time- and concentration-dependent changes in human lung fibroblasts NHLF and lung epithelial cell line A-549. The cells were treated with SM at the concentrations of 5, 10 and 100 mu M and signs of stress response were evaluated during 1-72 h post-treatment. Parameters for testing included cell viability and morphology, loss of transmembrane mitochondrial potential, apoptosis, oxidative stress, changes in the cell cycle, and ATM kinase activation. The cytotoxic effect of SM resulted in a time-dependent decrease in viability of A-459 associated with apoptosis more markedly than in NHLF. We did not observe any generation of reactive oxygen species by SM. SM at concentrations of 5 and 10 mu M induced the S-phase cell cycle arrest at both cell lines. On the other hand, 100 mu M caused nonspecific cell cycle arrest. ATM kinase was activated transiently. The results indicate that NHLF cells are less prone to toxic damage by SM in case of cell viability, apoptosis and loss of transmembrane mitochondrial potential. The analysis provides a time-related cytotoxic profile of A-549 and NHLF cells for further investigation into the prevention of SM toxic effects and their potential treatment.

Klasifikace

  • Druh

    J<sub>imp</sub> - Článek v periodiku v databázi Web of Science

  • CEP obor

  • OECD FORD obor

    30108 - Toxicology

Návaznosti výsledku

  • Projekt

  • Návaznosti

    I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace

Ostatní

  • Rok uplatnění

    2020

  • Kód důvěrnosti údajů

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

Údaje specifické pro druh výsledku

  • Název periodika

    Archives of Toxicology

  • ISSN

    0340-5761

  • e-ISSN

    1432-0738

  • Svazek periodika

    94

  • Číslo periodika v rámci svazku

    10

  • Stát vydavatele periodika

    DE - Spolková republika Německo

  • Počet stran výsledku

    11

  • Strana od-do

    3503-3514

  • Kód UT WoS článku

    000549697000004

  • EID výsledku v databázi Scopus

    2-s2.0-85087983321