Zinc oxide nanoparticles (ZnO-NPs) are increasingly used in sunscreens, food additives, pigments, rubber manufacture, and electronic materials. Several studies have shown that ZnO-NPs inhibit cell growth and induce apoptosis by the production of oxidative stress in a variety of human cancer cells. However, the anti-cancer property and molecular mechanism of ZnO-NPs in human gingival squamous cell carcinoma (GSCC) are not fully understood. In this study, we found that ZnO-NPs induced growth inhibition of GSCC (Ca9-22 and OECM-1 cells), but no damage in human normal keratinocytes (HaCaT cells) and gingival fibroblasts (HGF-1 cells). ZnO-NPs caused apoptotic cell death of GSCC in a concentration-dependent manner by the quantitative assessment of oligonucleosomal DNA fragmentation. Flow cytometric analysis of cell cycle progression revealed that sub-G1 phase accumulation was dramatically induced by ZnO-NPs. In addition, ZnO-NPs increased the intracellular reactive oxygen species and specifically superoxide levels, and also decreased the mitochondrial membrane potential. ZnO-NPs further activated apoptotic cell death via the caspase cascades. Importantly, anti-oxidant and caspase inhibitor clearly prevented ZnO-NP-induced cell death, indicating the fact that superoxide-induced mitochondrial dysfunction is associated with the ZnO-NP-mediated caspase-dependent apoptosis in human GSCC. Moreover, ZnO-NPs significantly inhibited the phosphorylation of ribosomal protein S6 kinase (p70S6K kinase). In a corollary in vivo study, our results demonstrated that ZnO-NPs possessed an anti-cancer effect in a zebrafish xenograft model. Collectively, these results suggest that ZnO-NPs induce apoptosis through the mitochondrial oxidative damage and p70S6K signaling pathway in human GSCC. The present study may provide an experimental basis for ZnO-NPs to be considered as a promising novel anti-tumor agent for the treatment of gingival cancer.

This study discussed the photoreduction of Cr(VI) ions in aqueous solutions by UV/TiO 2 photocatalytic processes under various operational factors. Experimental results showed that the removal rate of Cr(VI) increased with decreasing solution pH values and with increasing dosages of organic compounds, indicating that the recombination rate of electrons and h + can be retarded in the reaction systems by the addition of the scavenger, thus raising the reaction rate of Cr(VI). The relationship of the chemical reaction rate of Cr(VI), TiO 2 dosage, and changes of Cr(VI) concentration was expressed by the pseudo-first-order kinetic equation. Comparing the experimental results of two different doping metals in modified TiO 2 photoreduction systems, the removal rate of Cr(VI) by the Ag/TiO 2 process is larger, possibly because the electron transferring ability of Ag is superior to that of Cu. However, the photoreduction rates of Cr(VI) by modified UV/TiO 2 processes are worse than those by a nonmodified commercial UV/TiO 2 process.