Abstract
Wide application of TiO2 nanoparticles (nTiO2) and ubiquitous lead (Pb) pollution in natural environment enhance the chance of co-exposure of humans to Pb and nTiO2. We investigated the effects of nTiO2 on Pb-induced toxicity in human lung epithelial (A549) cells. Results showed that nTiO2 was not toxic to A549 cells. Conversely, Pb-induced cytotoxicity and oxidative stress in A549 cells were evidenced by cell viability reduction, cell membrane damage, reactive oxygen species generation and depletion of antioxidants. The Pb was also found to alter the regulation of apoptotic genes and cell cycle. Interestingly, in co-exposure group (nTiO2 + Pb), nTiO2 effectively attenuated the cytotoxicity, oxidative stress and apoptotic responses of Pb in A549 cells. Cellular uptake experiments demonstrated that nTiO2 increased the bioaccumulation of Pb in cells. However, due to strong adsorption of Pb on nTiO2, free Pb ions were not available even inside the cells. Hence, nTiO2 significantly prevented the bioavailability and toxicity of Pb in A549 cells. This is the first report providing insight into understanding the mechanism of nTiO2 mediated prevention against Pb-induced toxicity in human cells. This study warranted further research on co-exposure effects of nTiO2 and Pb at in vivo mammalian models.
Published Version
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