Particulate Matter (PM 2.5 ) from Biomass Combustion Induces an Anti-Oxidative Response and Cancer Drug Resistance in Human Bronchial Epithelial BEAS-2B Cells

Regina Merk, Katharina Heßelbach, Anastasiya Osipova, Désirée Popadić, Wolfgang Schmidt-Heck, Gwang-Jin Kim, Stefan Günther, Alfonso García Piñeres, Irmgard Merfort and Matjaz Humar
Additional contact information
Regina Merk: Department of Pharmaceutical Biology and Biotechnology, Institute of Pharmaceutical Sciences, Albert Ludwigs University Freiburg, 79104 Freiburg, Germany
Katharina Heßelbach: Department of Pharmaceutical Biology and Biotechnology, Institute of Pharmaceutical Sciences, Albert Ludwigs University Freiburg, 79104 Freiburg, Germany
Anastasiya Osipova: Department of Pharmaceutical Biology and Biotechnology, Institute of Pharmaceutical Sciences, Albert Ludwigs University Freiburg, 79104 Freiburg, Germany
Désirée Popadić: Department of Pharmaceutical Biology and Biotechnology, Institute of Pharmaceutical Sciences, Albert Ludwigs University Freiburg, 79104 Freiburg, Germany
Wolfgang Schmidt-Heck: Department of Systems Biology and Bioinformatics, Leibniz Institute for Natural Product Research and Infection Biology-Hans-Knöll Institute (HKI), 07745 Jena, Germany
Gwang-Jin Kim: Department of Pharmaceutical Bioinformatics, Institute of Pharmaceutical Sciences, Albert-Ludwigs University Freiburg, 79104 Freiburg, Germany
Stefan Günther: Department of Pharmaceutical Bioinformatics, Institute of Pharmaceutical Sciences, Albert-Ludwigs University Freiburg, 79104 Freiburg, Germany
Alfonso García Piñeres: Centro de Investigación en Biología Celular y Molecular (CIBCM), Universidad de Costa Rica, 11501-2060 San José, Costa Rica
Irmgard Merfort: Department of Pharmaceutical Biology and Biotechnology, Institute of Pharmaceutical Sciences, Albert Ludwigs University Freiburg, 79104 Freiburg, Germany
Matjaz Humar: Department of Pharmaceutical Biology and Biotechnology, Institute of Pharmaceutical Sciences, Albert Ludwigs University Freiburg, 79104 Freiburg, Germany

IJERPH, 2020, vol. 17, issue 21, 1-22

Abstract: Nearly half of the world’s population relies on combustion of solid biofuels to cover fundamental energy demands. Epidemiologic data demonstrate that particularly long-term emissions adversely affect human health. However, pathological molecular mechanisms are insufficiently characterized. Here we demonstrate that long-term exposure to fine particulate matter (PM 2.5 ) from biomass combustion had no impact on cellular viability and proliferation but increased intracellular reactive oxygen species (ROS) levels in bronchial epithelial BEAS-2B cells. Exposure to PM 2.5 induced the nuclear factor erythroid 2-related factor 2 (Nrf2) and mediated an anti-oxidative response, including enhanced levels of intracellular glutathione (GSH) and nuclear accumulation of heme oxygenase-1 (HO-1). Activation of Nrf2 was promoted by the c-Jun N-terminal kinase JNK1/2, but not p38 or Akt, which were also induced by PM 2.5 . Furthermore, cells exposed to PM 2.5 acquired chemoresistance to doxorubicin, which was associated with inhibition of apoptosis and elevated levels of GSH in these cells. Our findings propose that exposure to PM 2.5 induces molecular defense mechanisms, which prevent cellular damage and may thus explain the initially relative rare complications associated with PM 2.5 . However, consistent induction of pro-survival pathways may also promote the progression of diseases. Environmental conditions inducing anti-oxidative responses may have the potential to promote a chemoresistant cellular phenotype.

Keywords: particulate matter from biomass combustion; Nrf2; anti-oxidative response; glutathione; cancer drug resistance (search for similar items in EconPapers)
JEL-codes: I I1 I3 Q Q5 (search for similar items in EconPapers)
Date: 2020
References: View references in EconPapers View complete reference list from CitEc
Citations: View citations in EconPapers (1)

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