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

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.