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Benzo[a]pyrene and tumor necrosis factor-alpha coordinately increase genotoxic damage and the production of proinflammatory mediators in alveolar epithelial type II cells

The result's identifiers

  • Result code in IS VaVaI

    <a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F00027162%3A_____%2F11%3A%230000813" target="_blank" >RIV/00027162:_____/11:#0000813 - isvavai.cz</a>

  • Alternative codes found

    RIV/68081707:_____/11:00366512 RIV/68378041:_____/11:00366512

  • Result on the web

  • DOI - Digital Object Identifier

Alternative languages

  • Result language

    angličtina

  • Original language name

    Benzo[a]pyrene and tumor necrosis factor-alpha coordinately increase genotoxic damage and the production of proinflammatory mediators in alveolar epithelial type II cells

  • Original language description

    Alveolar type II epithelial (AEII) cells regulate lung inflammatory response and, simultaneously, they are a target of environmental carcinogenic factors. We employed an in vitro model of rat AEII cells, the RLE-6TN cell line, in order to analyze the interactive effects of tumor necrosis factor-alpha (TNF-alpha), a cytokine which plays a key role in the initiation of inflammatory responses in the lung, and benzo[a]pyrene (BaP), a highly carcinogenic polycyclic aromatic hydrocarbon. TNF-alpha strongly augmented the formation of stable BaP diol epoxide-DNA adducts in AEII cells, which was associated with enhanced p53-Ser15 phosphorylation and decreased cell survival. The increased genotoxicity of BaP was associated with altered expression of cytochrome P450 (CYP) enzymes involved in its bioactivation, a simultaneous suppression of CYP1A1 and enhancement of CYP1B1 expression. Importantly, BaP and TNE-alpha acted synergistically to upregulate key inflammatory regulators in AEII cells, incl

  • Czech name

  • Czech description

Classification

  • Type

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

  • CEP classification

    DN - Environmental impact on health

  • OECD FORD branch

Result continuities

  • Project

    <a href="/en/project/GAP503%2F11%2F1227" target="_blank" >GAP503/11/1227: Interactions of inflammatory mediators and Ah receptor signaling in toxic effects of polycyclic aromatic hydrocarbons</a><br>

  • Continuities

    Z - Vyzkumny zamer (s odkazem do CEZ)

Others

  • Publication year

    2011

  • Confidentiality

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

Data specific for result type

  • Name of the periodical

    Toxicology Letters

  • ISSN

    0378-4274

  • e-ISSN

  • Volume of the periodical

    206

  • Issue of the periodical within the volume

    2

  • Country of publishing house

    IE - IRELAND

  • Number of pages

    9

  • Pages from-to

    121-129

  • UT code for WoS article

    000295298800002

  • EID of the result in the Scopus database