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Short-term and Long-term Exposure of the MucilAir (TM) Model to Polycyclic Aromatic Hydrocarbons

Identifikátory výsledku

  • Kód výsledku v IS VaVaI

    <a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F00216208%3A11310%2F19%3A10396038" target="_blank" >RIV/00216208:11310/19:10396038 - isvavai.cz</a>

  • Nalezeny alternativní kódy

    RIV/68378041:_____/19:00518514

  • Výsledek na webu

    <a href="https://verso.is.cuni.cz/pub/verso.fpl?fname=obd_publikace_handle&handle=QIYpXU12UK" target="_blank" >https://verso.is.cuni.cz/pub/verso.fpl?fname=obd_publikace_handle&handle=QIYpXU12UK</a>

  • DOI - Digital Object Identifier

    <a href="http://dx.doi.org/10.1177/0261192919841484" target="_blank" >10.1177/0261192919841484</a>

Alternativní jazyky

  • Jazyk výsledku

    angličtina

  • Název v původním jazyce

    Short-term and Long-term Exposure of the MucilAir (TM) Model to Polycyclic Aromatic Hydrocarbons

  • Popis výsledku v původním jazyce

    Cells grown in monocultures are widely used to model lung tissue. As a result of these culture conditions, these cells exhibit poor morphological similarity to those present in in vivo lung tissue. MucilAir, a 3-D in vitro model comprising human basal, goblet and ciliated cells, represents a fully differentiated respiratory epithelium that can be used as an alternative and a more realistic system. The aim of our study was to compare the effects of short-term and long-term exposure to two polycyclic aromatic hydrocarbons (PAHs) - benzo[a]pyrene (B[a]P) and 3-nitrobenzanthrone (3-NBA) - using MucilAir as a model of human lung tissue. Two concentrations (0.1 M and 1 M) were tested at three time points (24 hours, 7 days and 28 days). Several aspects were assessed: cytotoxicity (lactate dehydrogenase (LDH) release), integrity of the cell layer (transepithelial electrical resistance (TEER)), induction of oxidative stress (reactive oxygen species production) and changes in the expression of selected genes involved in PAH metabolism (CYP1A1 and AKR1C2) and the antioxidant response (ALDH3A1, SOD1, SOD2, GPX1, CAT, HMOX1 and TXNRD1). The results showed that exposure to B[a]P caused a spike in LDH release at day 5. Exposure to 3-NBA caused a number of spikes in LDH release, starting at day 5, and a decrease in TEER after 11 days. CYP1A1 gene expression was upregulated after the 7-day and 28-day B[a]P exposures, as well as after the 24-hour and 7-day 3-NBA exposures. HMOX1 and SOD1 were downregulated after both 24-hour PAH treatments. HMOX1 was upregulated after a 1-week exposure to 3-NBA. There were no significant changes in the messenger RNA (mRNA) levels of AKR1C2, ALDH3A1, TXNRD1, SOD2, GPX1 or CAT. These results illustrate the potential use of this 3-D in vitro lung tissue model in studying the effects of chronic exposure to PAHs.

  • Název v anglickém jazyce

    Short-term and Long-term Exposure of the MucilAir (TM) Model to Polycyclic Aromatic Hydrocarbons

  • Popis výsledku anglicky

    Cells grown in monocultures are widely used to model lung tissue. As a result of these culture conditions, these cells exhibit poor morphological similarity to those present in in vivo lung tissue. MucilAir, a 3-D in vitro model comprising human basal, goblet and ciliated cells, represents a fully differentiated respiratory epithelium that can be used as an alternative and a more realistic system. The aim of our study was to compare the effects of short-term and long-term exposure to two polycyclic aromatic hydrocarbons (PAHs) - benzo[a]pyrene (B[a]P) and 3-nitrobenzanthrone (3-NBA) - using MucilAir as a model of human lung tissue. Two concentrations (0.1 M and 1 M) were tested at three time points (24 hours, 7 days and 28 days). Several aspects were assessed: cytotoxicity (lactate dehydrogenase (LDH) release), integrity of the cell layer (transepithelial electrical resistance (TEER)), induction of oxidative stress (reactive oxygen species production) and changes in the expression of selected genes involved in PAH metabolism (CYP1A1 and AKR1C2) and the antioxidant response (ALDH3A1, SOD1, SOD2, GPX1, CAT, HMOX1 and TXNRD1). The results showed that exposure to B[a]P caused a spike in LDH release at day 5. Exposure to 3-NBA caused a number of spikes in LDH release, starting at day 5, and a decrease in TEER after 11 days. CYP1A1 gene expression was upregulated after the 7-day and 28-day B[a]P exposures, as well as after the 24-hour and 7-day 3-NBA exposures. HMOX1 and SOD1 were downregulated after both 24-hour PAH treatments. HMOX1 was upregulated after a 1-week exposure to 3-NBA. There were no significant changes in the messenger RNA (mRNA) levels of AKR1C2, ALDH3A1, TXNRD1, SOD2, GPX1 or CAT. These results illustrate the potential use of this 3-D in vitro lung tissue model in studying the effects of chronic exposure to PAHs.

Klasifikace

  • Druh

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

  • CEP obor

  • OECD FORD obor

    30104 - Pharmacology and pharmacy

Návaznosti výsledku

  • Projekt

  • Návaznosti

    I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace

Ostatní

  • Rok uplatnění

    2019

  • Kód důvěrnosti údajů

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

Údaje specifické pro druh výsledku

  • Název periodika

    ATLA - Alternatives to Laboratory Animals

  • ISSN

    0261-1929

  • e-ISSN

  • Svazek periodika

    47

  • Číslo periodika v rámci svazku

    1

  • Stát vydavatele periodika

    GB - Spojené království Velké Británie a Severního Irska

  • Počet stran výsledku

    10

  • Strana od-do

    9-18

  • Kód UT WoS článku

    000473691700004

  • EID výsledku v databázi Scopus

    2-s2.0-85068771642