Abstract
Wide application of TiO2 nanoparticles (nTiO(2)) and ubiquitous lead (Pb) pollution in natural environment enhance the chance of co-exposure of humans to Pb and nTiO(2). We investigated the effects of nTiO(2) on Pb-induced toxicity in human lung epithelial (A549) cells. Results showed that nTiO(2) 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 (nTiO(2) + Pb), nTiO(2) effectively attenuated the cytotoxicity, oxidative stress and apoptotic responses of Pb in A549 cells. Cellular uptake experiments demonstrated that nTiO(2) increased the bioaccumulation of Pb in cells. However, due to strong adsorption of Pb on nTiO(2), free Pb ions were not available even inside the cells. Hence, nTiO(2) significantly prevented the bioavailability and toxicity of Pb in A549 cells. This is the first report providing insight into understanding the mechanism of nTiO(2) mediated prevention against Pb-induced toxicity in human cells. This study warranted further research on co-exposure effects of nTiO(2) and Pb at in vivo mammalian models.