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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

Identifikátory výsledku

  • Kód výsledku v 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>

  • Výsledek na webu

    <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>

Alternativní jazyky

  • Jazyk výsledku

    angličtina

  • Název v původním jazyce

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

  • Popis výsledku v původním jazyce

    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.

  • Název v anglickém jazyce

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

  • Popis výsledku anglicky

    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.

Klasifikace

  • Druh

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

  • CEP obor

  • OECD FORD obor

    10608 - Biochemistry and molecular biology

Návaznosti výsledku

  • Projekt

    <a href="/cs/project/GA16-14631S" target="_blank" >GA16-14631S: Studium procesů spojených s peroxidací lipidů v modelových lidských buněčných liniích</a><br>

  • Návaznosti

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

Ostatní

  • Rok uplatnění

    2018

  • Kód důvěrnosti údajů

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

Údaje specifické pro druh výsledku

  • Název periodika

    Mutation Research - Genetic Toxicology and Environmental Mutagenesis

  • ISSN

    1383-5718

  • e-ISSN

  • Svazek periodika

    827

  • Číslo periodika v rámci svazku

    mar

  • Stát vydavatele periodika

    NL - Nizozemsko

  • Počet stran výsledku

    9

  • Strana od-do

    50-58

  • Kód UT WoS článku

    000428494500006

  • EID výsledku v databázi Scopus

    2-s2.0-85041483440