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Effect of acrylamide on BEAS-2B normal human lung cells: Cytotoxic, oxidative, apoptotic and morphometric analysis

•Acrylamide induces dose-dependent toxic effect on BEAS-2B normal lung cells.•Apoptotic hallmarks and signs are observable after acrylamide treatment.•Nrf2 translocates to nucleus and Nrf-2 expression increases following acrylamide injection.•IC50 and IC75 of acrylamide for BEAS-2B cells are 2.0 and...

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Published in:Acta histochemica 2019-07, Vol.121 (5), p.595-603
Main Authors: Kacar, Sedat, Sahinturk, Varol, Kutlu, Hatice Mehtap
Format: Article
Language:English
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Summary:•Acrylamide induces dose-dependent toxic effect on BEAS-2B normal lung cells.•Apoptotic hallmarks and signs are observable after acrylamide treatment.•Nrf2 translocates to nucleus and Nrf-2 expression increases following acrylamide injection.•IC50 and IC75 of acrylamide for BEAS-2B cells are 2.0 and 2.75 mM, respectively.•BEAS-2B cells are very sensitive to acrylamide treatment when compared to other cell lines. Due to the broad toxic relevance of acrylamide, many measures have been taken since the 1900s. These measures increased day by day when acrylamide was discovered in foods in 2002, and its toxic spectrum was found to be wider than expected. Therefore, in some countries, the products with higher acrylamide content were restricted. On the other hand, the effects of acrylamide on the respiratory system cells have yet to be well understood. In this study, we aimed at investigating the effect of acrylamide on lung epithelial BEAS-2B cells. Initially, the cytotoxic effect of acrylamide on BEAS-2B was determined by MTT assay. Then, cellular oxidative stress was measured. Flow cytometry analysis was conducted for Annexin-V and caspase 3/7. Furthermore, Bax, Bcl-2 and Nrf-2 proteins were evaluated by immunocytochemistry. Finally, acrylamide-induced cellular morphological changes were observed under confocal and TEM microscopes. According to MTT results, the IC50 concentration of acrylamide was 2.00 mM. After acrylamide treatment, oxidative stress increased dose-dependently. Annexin V-labelled apoptotic cells and caspase 3/7 activity were higher than untreated cells in acrylamide-treated cells. Immunocytochemical examination revealed a marked decrease in Bcl-2, an increase in Bax and Nrf-2 protein staining upon acrylamide treatment. Furthermore, in confocal and TEM microscopy, apoptotic hallmarks were pronounced. In the present study, acrylamide was suggested to display anti-proliferative activity, decrease viability, induce apoptosis and oxidative stress and cause morphological changes in BEAS-2B cells.
ISSN:0065-1281
1618-0372
DOI:10.1016/j.acthis.2019.05.005