Research

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

Salik Hussain^1,2 , Leen CJ Thomassen³ , Ioana Ferecatu¹ , Marie-Caroline Borot¹ , Karine Andreau¹ , Johan A Martens³ , Jocelyne Fleury⁴ , Armelle Baeza-Squiban¹ , Francelyne Marano¹ and Sonja Boland¹

¹  Université Paris Diderot - Paris 7, Unit of Functional and Adaptive Biology (BFA) CNRS EAC 4413, Laboratory of Molecular and Cellular Responses to Xenobiotics, 75205 Paris, France

²  Department of Pathology, University of Veterinary and Animal Sciences, Lahore, Pakistan

³  Center for Surface Chemistry & Catalysis, Katholieke Universiteit Leuven, Kasteelpark Arenberg 23, 3001 Heverlee, Belgium

⁴  INSERM, Unité 955, 94000 Créteil, France

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Particle and Fibre Toxicology 2010, 7:10doi:10.1186/1743-8977-7-10

Published:	16 April 2010

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.

Results

Detailed 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.

Conclusions

Both 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.