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Kinetics of ROS generation induced by polycyclic aromatic hydrocarbons and organic extracts from ambient air particulate matter in model human lung cell lines

The result's identifiers

  • Result code in IS VaVaI

    <a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F68378041%3A_____%2F18%3A00493296" target="_blank" >RIV/68378041:_____/18:00493296 - isvavai.cz</a>

  • Result on the web

    <a href="http://dx.doi.org/10.1016/j.mrgentox.2018.01.006" target="_blank" >http://dx.doi.org/10.1016/j.mrgentox.2018.01.006</a>

  • DOI - Digital Object Identifier

    <a href="http://dx.doi.org/10.1016/j.mrgentox.2018.01.006" target="_blank" >10.1016/j.mrgentox.2018.01.006</a>

Alternative languages

  • Result language

    angličtina

  • Original language name

    Kinetics of ROS generation induced by polycyclic aromatic hydrocarbons and organic extracts from ambient air particulate matter in model human lung cell lines

  • Original language description

    Polycyclic aromatic hydrocarbons /PAHs/ associated with particulate matter /PM/ may induce oxidative damage via reactive oxygen species /ROS/ generation. However, the kinetics of ROS production and the link with antioxidant response induction has not been well studied. To elucidate the differences in oxidative potential of individual PAH compounds and extractable organic matter /EOM/ from PM containing various PAH mixtures, we studied ROS formation and antioxidant response /total antioxidant capacity /TAC/ and expression of HMOXI and TXNRD1/ in human alveolar basal epithelial cells /A549 cells/ and human embryonic lung fibroblasts /HEL12469 cells/. We treated the cells with three concentrations of model PAHs /benzo/a/pyrene, B/a/P, 3-nitrobenzanthrone, 3-NBA/ and EOM from PM < 2.5 mu m /PM2.5/. ROS levels were evaluated at 8 time intervals /30 min-24 h/. In both cell lines, B/a/P treatment was associated with a time-dependent decrease of ROS levels. This trend was more pronounced in HEL12469 cells and was accompanied by increased TAC. A similar response was observed upon 3-NBA treatment in HEL12469 cells. In A549 cells, however, this compound significantly increased superoxide levels. This response was accompanied by the decrease of TAC as well as HMOXI and TXNRD1 expression. In both cell lines, a short-time exposure to EOMs tended to increase ROS levels, while a marked decrease was observed after longer treatment periods. This was accompanied by the induction of HMOX1 and TXNRD1 expression in HEL12469 cells and increased TAC in A549 cells. In summary, our data indicate that in the studied cell lines B/a/P and EOMs caused a time-dependent decrease of intracellular ROS levels, probably due to the activation of the antioxidant response. This response was not detected in A549 cells following 3-NBA treatment, which acted as a strong superoxide inducer. Pro-oxidant properties of EOMs are limited to short-time exposure periods.

  • Czech name

  • Czech description

Classification

  • Type

    J<sub>imp</sub> - Article in a specialist periodical, which is included in the Web of Science database

  • CEP classification

  • OECD FORD branch

    10608 - Biochemistry and molecular biology

Result continuities

  • Project

    <a href="/en/project/GA16-14631S" target="_blank" >GA16-14631S: The study of processes associated with lipid peroxidation in model human cell lines</a><br>

  • Continuities

    P - Projekt vyzkumu a vyvoje financovany z verejnych zdroju (s odkazem do CEP)

Others

  • Publication year

    2018

  • Confidentiality

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

Data specific for result type

  • Name of the periodical

    Mutation Research - Genetic Toxicology and Environmental Mutagenesis

  • ISSN

    1383-5718

  • e-ISSN

  • Volume of the periodical

    827

  • Issue of the periodical within the volume

    mar

  • Country of publishing house

    NL - THE KINGDOM OF THE NETHERLANDS

  • Number of pages

    9

  • Pages from-to

    50-58

  • UT code for WoS article

    000428494500006

  • EID of the result in the Scopus database

    2-s2.0-85041483440