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Oxidative damage and OGG1 expression induced by a combined effect of titanium dioxide nanoparticles and lead acetate in human hepatocytes
Author(s) -
Du Hairong,
Zhu Xiaoling,
Fan Chuangang,
Xu Song,
Wang Youjie,
Zhou Yikai
Publication year - 2012
Publication title -
environmental toxicology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.813
H-Index - 77
eISSN - 1522-7278
pISSN - 1520-4081
DOI - 10.1002/tox.20682
Subject(s) - oxidative stress , reactive oxygen species , chemistry , superoxide dismutase , glutathione , dna damage , cytotoxicity , biochemistry , antioxidant , microbiology and biotechnology , enzyme , dna , biology , in vitro
Titanium dioxide (TiO 2 ) is a widely used nanomaterial that can cause biological damage through oxidative stress. At low concentrations, TiO 2 can interact with lead acetate (PbAc) to produce different toxic responses, compared with TiO 2 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 TiO 2 (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), TiO 2 mixed with PbAc induced increased release of ROS (at 0.001, 0.01, 0.1, 1, 10 μg mL −1 TiO 2 ), intracellular SOD activity (at 0.1 and 0.01 μg mL −1 TiO 2 ), GSH levels (at 0.01–1 μg mL −1 TiO 2 ), 8‐OHdG levels (at 1 and 10 μg mL −1 TiO 2 ), OGG1 expression (at 0.001–1 μg mL −1 TiO 2 ), and cytotoxicity (at 0.1, 1, and 10 μg mL −1 TiO 2 ) in L02 cells. There were no significant changes in ROS, GSH, SOD, 8‐OHdG, or OGG1 levels when L02 cells were treated with TiO 2 alone or PbAc alone. These findings indicate that TiO 2 and PbAc in combination induce cytotoxicity and oxidative stress in L02 cells in the absence of photoactivation. © 2011 Wiley Periodicals, Inc. Environ Toxicol, 2012.