Nickel nanowires induce cell cycle arrest and apoptosis by generation of reactive oxygen species in HeLa cells

Toxicol Rep. 2014 May 16:1:114-121. doi: 10.1016/j.toxrep.2014.04.008. eCollection 2014.

Abstract

Nickel nanowires (Ni NWs) have great potential to be used as a living cell manipulation tool and developed into an anticancer agent. However, their candidacy as biomedical appliances need detailed human cell studies, such as study of the interaction between Ni NWs and tumor cells. The present study investigated the cytotoxicity of Ni NWs in HeLa cells. A dose-dependent inhibition of cell growth was observed by using the MTT assay. We demonstrated that Ni NWs induced oxidative stress by generation of reactive oxygen species (ROS). Apoptosis induction was evidenced by flow cytometry, annexin V binding assay and DAPI staining. DNA flow cytometric analysis indicated that Ni NWs significantly increased the percentages of cells in S phase compared with control cells. This process was accompanied by the loss of mitochondrial membrane potential. These results revealed that Ni NWs induced apoptosis in HeLa cells via ROS generation and cell cycle arrest.

Keywords: 2′,7′-Dichlorodihydrofluorescein diacetate (PubChem CID: 77718); 3,3′tetraethyl-imidacarbocyanine iodide (PubChem CID: 5353694); 5,5′,6,6′-Tetrachloro-1,1′; Apoptosis; Cell cycle arrest; Cytotoxicity; DAPI (PubChem CID: 2954); Dimethylformamide (PubChem CID: 6228); Ni NWs; Propidium iodide (PubChem CID: 104981); ROS; Sodium dodecyl sulfate (PubChem CID: 3423265); Thiazolyl blue (PubChem CID: 64965).