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Oxidative damage and OGG1 expression induced by a combined effect of titanium dioxide nanoparticles and lead acetate in human hepatocytes

Du, Hairong, Zhu, Xiaoling, Fan, Chuangang, Xu, Song, Wang, Youjie, Zhou, Yikai
Environmental toxicology 2012 v.27 no.10 pp. 590-597
DNA adducts, cytotoxicity, dimethyl sulfoxide, glutathione, hepatocytes, humans, lead acetate, nanoparticles, oxidative stress, reactive oxygen species, superoxide dismutase, titanium dioxide
Titanium dioxide (TiO2) is a widely used nanomaterial that can cause biological damage through oxidative stress. At low concentrations, TiO2 can interact with lead acetate (PbAc) to produce different toxic responses, compared with TiO2 or PbAc alone. In this study, we utilized the following as indicators of toxic responses in human embryo hepatocytes (L02): reactive oxygen species (ROS), reduced glutathione (GSH), superoxide dismutase (SOD), and the DNA adducts 8‐hydroxydeoxyguanosine (8‐OHdG) and 8‐oxoguanine DNA glycosylase homolog 1 (OGG1). These were used to evaluate the oxidative stress of TiO2 (at 0.001, 0.01, 0.1, 1, and 10 μg mL−1) mixed with PbAc (1 μg mL−1) on L02 cells without photoactivation. Compared with the negative control (1‰ dimethyl sulfoxide), TiO2 mixed with PbAc induced increased release of ROS (at 0.001, 0.01, 0.1, 1, 10 μg mL−1 TiO2), intracellular SOD activity (at 0.1 and 0.01 μg mL−1 TiO2), GSH levels (at 0.01–1 μg mL−1 TiO2), 8‐OHdG levels (at 1 and 10 μg mL−1 TiO2), OGG1 expression (at 0.001–1 μg mL−1 TiO2), and cytotoxicity (at 0.1, 1, and 10 μg mL−1 TiO2) in L02 cells. There were no significant changes in ROS, GSH, SOD, 8‐OHdG, or OGG1 levels when L02 cells were treated with TiO2 alone or PbAc alone. These findings indicate that TiO2 and PbAc in combination induce cytotoxicity and oxidative stress in L02 cells in the absence of photoactivation. © 2011 Wiley Periodicals, Inc. Environ Toxicol, 2012.