Abstract
Zinc oxide (ZnO) nanoparticles (NPs) are increasingly recognized for their utility in biological applications, including biosensor and medicine. However, little is known about the toxicity mechanisms of ZnO nanorods in human cells. This study was designed to investigate the possible mechanisms of apoptosis induced by ZnO nanorods in human alveolar adenocarcinoma (A549) cells. ZnO nanorod was found to induce cytotoxicity, reactive oxygen species (ROS) generation, oxidative stress and activities of caspase-3 & caspase-9 in a dose- and time-dependent manner. Western blot results showed that ZnO nanorods induced the expression of heat shock protein 70, a first-tier marker of cell damage and a cell-cycle checkpoint protein p53. Moreover, pro-apoptotic protein bax was upregulated and the antiapoptotic proteins, survivin and bcl-2, were downregulated in ZnO nanorod exposed cells. In conclusion, our data demonstrateas that ZnO nanorod induced apoptosis in A549 cells through ROS and oxidative stress via p53, survivin, bax/bcl-2 and caspase pathways.
This study describes the mechanisms of apoptosis induced by ZnO nanorods in human alveolar adenocarcinoma cells.
This paper mainly describes the possible mechanisms of apoptosis induced by ZnO nanorods in human lung alveolar adenocarcinoma (A549) cells. Results showed that ZnO nanorods altered the expressions of different proteins involved in cellular apoptosis. ZnO nanorods induced the expression of heat shock protein 70, the first tier biomarker of cellular damage and cell cycle checkpoint protein p53. Further, the expression level of anti-apoptotic protein survivin was down-regulated while the expression of bax/bcl-2 protein ratio, an indicator of apoptosis was up-regulated by ZnO nanorods. Overall, this study highlights that ZnO nanorod-induce apoptosis in A549 cells via p53, survivin and bax/bcl-2 pathways. [Display omitted]