Author:

Keywords:

lysosomal membrane permeabilization, oxidative stress, engineered nanoparticles, ultrafine particles, gold nanoparticles, caspase activation, death, mitochondrial, inhibition, lung, Science & Technology, Life Sciences & Biomedicine, Toxicology, LYSOSOMAL MEMBRANE PERMEABILIZATION, OXIDATIVE STRESS, ENGINEERED NANOPARTICLES, CASPASE ACTIVATION, MITOCHONDRIAL, INHIBITION, LUNG, EXPOSURE, DEATH, MECHANISMS, Apoptosis, Bronchi, Caspases, Cell Line, Cell Membrane, Cell Size, Cell Survival, Chromatin, Cytochromes c, DNA Fragmentation, Humans, Hydrogen Peroxide, Lipid Peroxidation, Lysosomes, Membrane Potential, Mitochondrial, Metal Nanoparticles, Mitochondria, Reactive Oxygen Species, Respiratory Mucosa, Soot, Titanium, bcl-2-Associated X Protein, 0303 Macromolecular and Materials Chemistry, 0304 Medicinal and Biomolecular Chemistry, 1199 Other Medical and Health Sciences, 3206 Medical biotechnology, 3404 Medicinal and biomolecular chemistry

Abstract:

Background: Increasing environmental and occupational exposures to nanoparticles (NPs) warrant deeper insight into the toxicological mechanisms induced by these materials. The present study was designed to characterize the cell death induced by carbon black (CB) and titanium dioxide (TiO2) NPs in bronchial epithelial cells (16HBE14o-cell line and primary cells) and to investigate the implicated molecular pathways.