Nickel ferrite nanoparticles (NPs) have received much attention for their potential applications in biomedical fields such as magnetic resonance imaging,
drug delivery and
cancer hyperthermia. However, little is known about the toxicity of
nickel ferrite NPs at the cellular and molecular levels. In this study, we investigated the cytotoxic responses of
nickel ferrite NPs in two different types of human cells (i.e., liver HepG2 and breast MCF-7).
Nickel ferrite NPs induced dose-dependent cytotoxicity in both types of cells, which was demonstrated by 3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenyltetrazoliumbromide (MTT),
neutral red uptake (NRU) and
lactate dehydrogenase (LDH) assays.
Nickel ferrite NPs were also found to induce oxidative stress, which was evident by the depletion of
glutathione and the induction of
reactive oxygen species (ROS) and lipid peroxidation. The mitochondrial membrane potential due to
nickel ferrite NP exposure was also observed. The
mRNA levels for the tumor suppressor gene p53 and the apoptotic genes bax,
CASP3 and CASP9 were up-regulated, while the anti-apoptotic gene bcl-2 was down-regulated following
nickel ferrite NP exposure. Furthermore, the activities of apoptotic
enzymes (caspase-3 and caspase-9) were also higher in both types of cells treated with
nickel ferrite NPs. Cytotoxicity induced by
nickel ferrite was efficiently prevented by N-acetyl
cysteine (ROS scavenger) treatment, which suggested that oxidative stress might be one of the possible mechanisms of
nickel ferrite NP toxicity. We also observed that MCF-7 cells were slightly more susceptible to
nickel ferrite NP exposure than HepG2 cells. This study warrants further investigation to explore the potential mechanisms of different cytotoxic responses of
nickel ferrite NPs in different cell lines.