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

Result code in IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F68378041%3A_____%2F19%3A00518514" target="_blank" >RIV/68378041:_____/19:00518514 - isvavai.cz</a>

Alternative codes found

RIV/00216208:11310/19:10396038

Result on the web

<a href="https://journals.sagepub.com/doi/10.1177/0261192919841484" target="_blank" >https://journals.sagepub.com/doi/10.1177/0261192919841484</a>

DOI - Digital Object Identifier

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

Result language

angličtina

Original language name

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

Original language description

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.

Czech name

—

Czech description

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Type

J_imp - Article in a specialist periodical, which is included in the Web of Science database

CEP classification

—

OECD FORD branch

30108 - Toxicology

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

I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace

Publication year

2019

Confidentiality

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

Name of the periodical

Alternatives to Laboratory Animals

ISSN

0261-1929

e-ISSN

—

Volume of the periodical

47

Issue of the periodical within the volume

1

Country of publishing house

GB - UNITED KINGDOM

Number of pages

10

Pages from-to

9-18

UT code for WoS article

000473691700004

EID of the result in the Scopus database

2-s2.0-85068771642