Abstract

Nanosized titanium dioxide (nano-TiO2) is widely used in the chemical, electrical, and electronic industries. Nanosized TiO2 has been reported to be an efficient photocatalyst, which is able to produce reactive oxygen species (ROS) under UVA irradiation. In the present work, we evaluate the effect of mitochondrial respiratory chain on the generation of ROS and cytotoxicity in keratinocyte (HaCaT) cells induced by nano-TiO2 under UVA irradiation. HaCaT cells were pretreated with different inhibitors of mitochondrial respiratory chain and followed by treatment with 200 µg/mL nano-TiO2, then exposed to UVA (365 nm) for 1 hour and cultured for 24 hours. Our results demonstrated that the complexes I and III of the mitochondrial respiratory chain are the major site in the ROS generation induced by nano-TiO2 Our results also demonstrated that the uncouplers of mitochondrial oxidative phosphorylation resulted in obvious changes in the production of intracellular ROS induced by nano-TiO2 The ROS sources of lipoxygenase, cyclooxygenase, and nicotinamide adenine dinucleotide phosphate oxidase had no significant effect on the ROS production. To some extent, nitric oxide synthase had effect on the ROS production. These results indicated that mitochondrial respiratory chain may be the main source of intracellular ROS production induced by nano-TiO2.

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