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TiO2 NPs induced hepatic injury in mammals: a mechanistic approach


The rapid advancement in nanotechnology has increased the production of metal oxide nanoparticles (NPs) especially TiO2 for consumer and industrial products. This has also increased the likelihood for their exposure to human. TiO2 NPs exposure to humans can occur through different routes, but will finally reach to liver through the circulatory system. Hence, the present study was planned to assess the effects of TiO2 NPs in mammalian liver and their possible mechanism.

Materials and methods

TiO2 NPs were characterized by transmission electron microscopy (TEM) and dynamic light scattering (DLS). Genotoxicity assessment of TiO2 NPs was carried out by fpg-modified Comet assay both in in vitro (HepG2 cells) and in vivo (mice liver). Additionally, to understand the mechanism of hepatotoxicity, biochemical parameters, oxidative stress markers, reactive oxygen species (ROS), and expression profile of different stress proteins, tumour suppressor apoptotic/antiapoptotic proteins were investigated.


TEM measurements and DLS analysis showed that TiO2 NPs were in nano size regime, stable and mono-dispersed in different exposure vehicles, making them suitable for in vitro and in vivo toxicity studies. Our data from in vitro and in vivo study exhibited that TiO2 NPs induced significant (p<0.05) oxidative DNA damage assessed by the fpg-Comet assay. This could be attributed to a concentration-dependent significant (p<0.05) increase of ROS generation as evident from the enhanced fluorescence intensity of DCFDA dye. A significant alteration in the level of different hepatic enzymes in TiO2 NPs treated mice was also observed.

Furthermore, immunoblot analysis revealed a significant increase in the expression profile of Hsp60, Hsp70, p53, BAX, Cyto-c, Apaf-1, caspase-9 and caspase-3 protein and a concomitant decrease in the level of antiapoptotic protein Bcl-2. Our data demonstrate the role of mitochondrial intrinsic pathway for TiO2 NP induced apoptosis in liver cells.


The present study using fpg-modified Comet assay, blood biochemical parameters, oxidative stress markers and immunoblot analysis confirmed that oxidative stress induced by TiO2 NPs trigger the DNA damage, which consequently initiates the expression of apoptotic proteins resulting in hepatic injury. Hence the use of such nanoparticles should be carefully monitored.


The financial assistance for the Centre for Nanotechnology Research and Applications (CENTRA) by The Gujarat Institute for Chemical Technology (Grant no. ILS/GICT/2013/003) is acknowledged.

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This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. The Creative Commons Public Domain Dedication waiver ( applies to the data made available in this article, unless otherwise stated.

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Shukla, R.K., Kumar, A., Vallabani, N.S. et al. TiO2 NPs induced hepatic injury in mammals: a mechanistic approach. Mol Cytogenet 7 (Suppl 1), P82 (2014).

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