Inflammatory mediators accelerate metabolism of benzo[a]pyrene in rat alveolar type II cels: the role of enhanced cytochrome P450 1B1 expression

Kód výsledku v IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F00216224%3A14310%2F13%3A00081939" target="_blank" >RIV/00216224:14310/13:00081939 - isvavai.cz</a>

Výsledek na webu

<a href="http://dx.doi.org/10.1016/j.tox.2013.09.001" target="_blank" >http://dx.doi.org/10.1016/j.tox.2013.09.001</a>

DOI - Digital Object Identifier

<a href="http://dx.doi.org/10.1016/j.tox.2013.09.001" target="_blank" >10.1016/j.tox.2013.09.001</a>

Jazyk výsledku

angličtina

Název v původním jazyce

Inflammatory mediators accelerate metabolism of benzo[a]pyrene in rat alveolar type II cels: the role of enhanced cytochrome P450 1B1 expression

Popis výsledku v původním jazyce

Long-term deregulated inflammation represents one of the key factors contributing to lung cancer etiology. Previously, we have observed that tumor necrosis factor-alpha (TNF-alpha), a major pro-inflammatory cytokine, enhances genotoxicity of benzo[a]pyrene (B[a]P), a highly carcinogenic polycyclic aromatic hydrocarbon, in rat lung epithelial RLE-6TN cells, a model of alveolar type II cells. Therefore, we analyzed B[a]P metabolism in RLE-6TN cells under inflammatory conditions, simulated using either recombinant INF-alpha, or a mixture of inflammatory mediators derived from activated alveolar macrophage cell line. Inflammatory conditions significantly accelerated BaP metabolism, as evidenced by decreased levels of both parent B[a]P and its metabolites.INF-alpha altered production of the metabolites associated with dihydrodiol-epoxide and radical cation pathways of B[a]P metabolism, especially B[a]P-dihydrodiols, and B[a]P-diones.

Název v anglickém jazyce

Inflammatory mediators accelerate metabolism of benzo[a]pyrene in rat alveolar type II cels: the role of enhanced cytochrome P450 1B1 expression

Popis výsledku anglicky

Long-term deregulated inflammation represents one of the key factors contributing to lung cancer etiology. Previously, we have observed that tumor necrosis factor-alpha (TNF-alpha), a major pro-inflammatory cytokine, enhances genotoxicity of benzo[a]pyrene (B[a]P), a highly carcinogenic polycyclic aromatic hydrocarbon, in rat lung epithelial RLE-6TN cells, a model of alveolar type II cells. Therefore, we analyzed B[a]P metabolism in RLE-6TN cells under inflammatory conditions, simulated using either recombinant INF-alpha, or a mixture of inflammatory mediators derived from activated alveolar macrophage cell line. Inflammatory conditions significantly accelerated BaP metabolism, as evidenced by decreased levels of both parent B[a]P and its metabolites.INF-alpha altered production of the metabolites associated with dihydrodiol-epoxide and radical cation pathways of B[a]P metabolism, especially B[a]P-dihydrodiols, and B[a]P-diones.

Druh

J_x - Nezařazeno - Článek v odborném periodiku (Jimp, Jsc a Jost)

CEP obor

FR - Farmakologie a lékárnická chemie

OECD FORD obor

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Projekt

—

Návaznosti

S - Specificky vyzkum na vysokych skolach

Rok uplatnění

2013

Kód důvěrnosti údajů

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

Název periodika

Toxicology

ISSN

0300-483X

e-ISSN

—

Svazek periodika

314

Číslo periodika v rámci svazku

1

Stát vydavatele periodika

IE - Irsko

Počet stran výsledku

9

Strana od-do

30-38

Kód UT WoS článku

000209429700004

EID výsledku v databázi Scopus

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