Abstract
Diesel exhaust particles (DEPs) and non-exhaust particles from abrasion are two main representative sources of air pollution to which humans are exposed daily, together with emerging nanomaterials, whose emission is increasing considerably. In the present work, we aimed to investigate whether DEPs, metal oxide nanoparticles (MeO-NPs), and their mixtures could affect alveolar cells. The research was focused on whether NPs induced different types of death in cells, and on their effects on cell motility and migration. Autophagy and cell cycles were investigated via cytofluorimetric analyses, through the quantification of the autophagic biomarker LC3B and PI staining, respectively. Cellular ultrastructures were then observed via TEM. Changes in cell motility and migration were assessed via transwell migration assay, and by the cytofluorimetric analysis of E-cadherin expression. A colony-forming efficiency (CFE) assay was performed in order to investigate the interactions between cells inside the colonies, and to see how these interactions change after exposure to the single particles or their mixtures. The results obtained suggest that NPs can either reduce the toxicity of DEPs (CuO) or enhance it (ZnO), through a mechanism that may involve autophagy as cells’ response to stressors and as a consequence of particles’ cellular uptake. Moreover, NPs can induce modification of E-cadherin expression and, consequentially, of colonies’ phenotypes.
Highlights
Several epidemiological studies have suggested that the carcinogenic potential of particulate matter (PM) and UFPs, including diesel-combustionderived particles, is mainly related to their small size and to the amount of polycyclic aromatic hydrocarbons (PAHs) and toxic metals that are adsorbed on the soot core [3,4]
We aimed to investigate whether diesel exhaust particles (DEPs), metal oxide nanoparticles (MeO-NPs), and their mixtures could affect human lung adenocarcinoma cell line (A549) functionality and morphology, by assessing cellular apoptosis and necrosis, oxidative stress response, and DNA damage, while focusing on NP-induced autophagy and its ability to modulate cells’ motility and migration
The differences observed were attributed to the amount of Cu2+ and Zn2+ ions released from NPs, either alone or in co-presence with DEPs
Summary
The inhalation of airborne ultrafine particles (UFPs,
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