A mechanism for nano-titanium dioxide-induced cytotoxicity in HaCaT cells under UVA irradiation

Abstract

Nano-TiO₂ has been reported to be an efficient photocatalyst, which is able to produce reactive oxygen species (ROS) under UVA irradiation. In this study, we investigated the effects of nano-TiO₂ on the cytotoxicity, induction of apoptosis, and the putative pathways of its actions in HaCaT cells. We show that nano-TiO₂ is a potent inducer of apoptosis and that it transduces the apoptotic signal via ROS generation, thereby inducing mitochondrial permeability transition (MPT) and activating Caspase-3 from HaCaT cells. ROS production, mitochondrial alteration, and subsequent apoptotic cell death in nano-TiO₂-treated cells were blocked by the MPT pore-blocker cyclosporin A. Taken together, our data indicate that nano-TiO₂ induces the ROS-mediated MPT and resultant Caspase-3 activation.

Graphical abstract

Nano-TiO₂ led to a significant decrease of cell viability mediated mitochondrial permeability transition (MPT) pore.

Key words:

• nano-titanium dioxide
• mitochondrial permeability transition pore
• reactive oxygen species
• human keratinocyte (HaCaT) cells
• UVA irradiation

Disclosure statement

No potential conflict of interest was reported by the authors.

Additional information

Funding

This work was supported by Natural Science Foundation of Hubei Province [No. 2011CDB372], Wuhan Planning Project of Science and Technology [No. 2014070404010203], Engineering training young people in Wuhan City medical backbone personnel (2014).