Carbon black and titanium dioxide nanoparticles elicit distinct apoptotic pathways in bronchial epithelial cells

Salik Hussain,Karine Andreau,Francelyne Marano,Johan A Martens,Leen Cj Thomassen,Jocelyne Fleury,Armelle Baeza-Squiban,Sonja Boland,Ioana Ferecatu,Marie-Caroline Borot

doi:10.1186/1743-8977-7-10

Abstract

BackgroundIncreasing 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.ResultsDetailed time course studies revealed that both CB (13 nm) and TiO2(15 nm) NP exposed cells exhibit typical morphological (decreased cell size, membrane blebbing, peripheral chromatin condensation, apoptotic body formation) and biochemical (caspase activation and DNA fragmentation) features of apoptotic cell death. A decrease in mitochondrial membrane potential, activation of Bax and release of cytochrome c from mitochondria were only observed in case of CB NPs whereas lipid peroxidation, lysosomal membrane destabilization and cathepsin B release were observed during the apoptotic process induced by TiO2 NPs. Furthermore, ROS production was observed after exposure to CB and TiO2 but hydrogen peroxide (H2O2) production was only involved in apoptosis induction by CB NPs.ConclusionsBoth CB and TiO2 NPs induce apoptotic cell death in bronchial epithelial cells. CB NPs induce apoptosis by a ROS dependent mitochondrial pathway whereas TiO2 NPs induce cell death through lysosomal membrane destabilization and lipid peroxidation. Although the final outcome is similar (apoptosis), the molecular pathways activated by NPs differ depending upon the chemical nature of the NPs.

Highlights

Increasing environmental and occupational exposures to nanoparticles (NPs) warrant deeper insight into the toxicological mechanisms induced by these materials
carbon black (CB) has a large population of small aggregates (86 nm) in water, whereas in PBS and DMEM F-12 the dispersion of CB is heterogeneous with an average size of respectively 281 and 253 nm
For the titanium dioxide sample, small aggregates were present in the water and DMEM F-12 suspension, but in all media the size distribution was transmission electron microscopy (TEM) Sizeb

Summary

Introduction

Increasing environmental and occupational exposures to nanoparticles (NPs) warrant deeper insight into the toxicological mechanisms induced by these materials. Translocation of NPs from the lungs towards other organs has been demonstrated and possible consequences include inflammation, heart rate and function anomalies, homeostatic disturbances and oxidative. NP exposures can lead to disturbances in the cellular homeostatic mechanisms resulting either in adaptive cellular responses or cell death. NP-induced perturbations of cellular mechanisms might act as basis of different pathophysiological processes depending upon the concentration and duration of exposure[11]. Necrotic cell death occurs in different human pathologies like cerebral ischemia, myocardial infarction and acute organ failures. Apoptosis plays an important role in the pathogenesis of different respiratory disorders such as asthma, emphysema, and acute respiratory distress syndrome[13,14]

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