| Summary: | Widespread application of silica nanoparticles (nSiO<sub>2</sub>) and ubiquitous metalloid arsenic (As) may increase their chances of co-exposure to human beings in daily life. Nonetheless, studies on combined effects of nSiO<sub>2</sub> and As in human cells are lacking. We investigated the co-exposure effects of nSiO<sub>2</sub> and As in human liver (HepG2) and human fibroblast (HT1080) cells. Results showed that nSiO<sub>2</sub> did not cause cytotoxicity. However, exposure of As caused oxidative stress and apoptosis in both types of cells. Interesting results were that co-exposure of a non-cytotoxic concentration of nSiO<sub>2</sub> significantly augmented the As induced toxicity in both cells. Intracellular level of As was higher in the co-exposure group (nSiO<sub>2</sub> + As) than the As group alone, suggesting that nSiO<sub>2</sub> facilitates the cellular uptake of As. Co-exposure of nSiO<sub>2</sub> and As potentiated oxidative stress indicated by pro-oxidants generation (reactive oxygen species, hydrogen peroxide and lipid peroxidation) and antioxidants depletion (glutathione level, and glutathione reductase, superoxide dismutase and catalase activities). In addition, co-exposure of nSiO<sub>2</sub> and As also potentiated mitochondria-mediated apoptosis suggested by increased expression of <i>p53</i>, <i>bax</i>, <i>caspase-3</i> and <i>caspase-9</i> genes (pro-apoptotic) and decreased expression of <i>bcl-2</i> gene (anti-apoptotic) along with depleted mitochondrial membrane potential. To the best of our knowledge, this is the first study showing that co-exposure of nSiO<sub>2</sub> and As induced augmentation of oxidative stress and mitochondria-mediated apoptosis in HepG2 and HT1080 cells. Hence, careful attention is required for human health assessment following combined exposure to nSiO<sub>2</sub> and As.
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