A mechanism for nano-titanium dioxide-induced cytotoxicity in HaCaT cells under UVA irradiation. Issue 8 (3rd August 2015)

• Record Type: Journal Article
• Authors: Xue, Chengbin; Luo, Wen; Yang, Xiang liang
• Is Part Of: Bioscience, biotechnology, and biochemistry. Volume 79:Issue 8(2015)
• Page Start: 1384
• Page End: 1390
• Publication Date: 2015-08-03
• Subjects: nano-titanium dioxide -- mitochondrial permeability transition pore -- reactive oxygen species -- human keratinocyte (HaCaT) cells -- UVA irradiation; Biotechnology -- Periodicals; Biochemistry -- Periodicals; 660.6
• DOI: 10.1080/09168451.2015.1023248
• Languages: English
• ISSNs: 0916-8451

Abstract

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.