The effect of Fe₂O₃ and ZnO nanoparticles on cytotoxicity and glucose metabolism in lung epithelial cells

Abstract

Metallic nanoparticles (NPs) have potential applications in industry and medicine, but they also have the potential to cause many chronic pulmonary diseases. Mechanisms for their cytotoxicity, glucose and energy metabolism responses need to be fully explained in lung epithelial cells after treatment with metallic nanoparticles. In our study, two different metallic nanoparticles (Fe2O3 and ZnO) and two cell‐based assays (BEAS‐2B and A549 cell lines) were used. Our findings demonstrate that ZnO nanoparticles, but not Fe2O3 nanoparticles, induce cell cycle arrest, cell apoptosis, reactive oxygen species (ROS) production, mitochondrial dysfunction and glucose metabolism perturbation, which are responsible for cytotoxicity. These results also suggest that the glucose metabolism and bioenergetics had a great potential in evaluating the cytotoxicity and thus were very helpful in understanding their underlying molecular mechanisms. Copyright © 2015 John Wiley & Sons, Ltd.

Differential Cytotoxicity Induced by Transition Metal Oxide Nanoparticles is a Function of Cell Killing and Suppression of Cell Proliferation

“…In contrast, exposure to NiO NPs led to a significant increase in G 0 /G 1 and a decrease in G 2 /M in BEAS-2B cells [34]. Exposure to NiO NPs caused BEAS-2B cells arrest in the G 2 /M phase, while ZnO and Fe 2 O 3 did not affect the cell cycle [34,35]. It is important to be aware of the fact that NPs composed of the same elements may have quite different physical and chemical properties, such as surface charge, surface area, dissolution of ions, morphology, and crystalline structure, in different studies.…”

Cytotoxic effects of ZnO nanoparticles on mouse testicular cells

“…9,10 Several studies have reported the cytotoxic and genotoxic potential of ZnO NPs using in vitro assays in immune cells, lung epithelial, and cancer cells. [11][12][13][14] Johnson et al showed that the exposure of immune cells to ZnO NPs resulted in increased levels of the autophagosome protein LC3A and, consequently, autophagic death, which were inhibited by blocking autophagy and reactive oxygen species (ROS) production. 11 Sharma et al reported that ZnO NPs induced DNA damage in human epidermal cells, even at low concentrations, which may have been mediated by lipid peroxidation and oxidative stress.…”

“…13 Other studies showed that ZnO NPs were cytotoxic for human lung epithelial cells and induced cell-cycle arrest, cell apoptosis, ROS production, mitochondrial dysfunction, and perturbation of glucose metabolism in such cells. 14,15 Increasing evidence has shown that the cytotoxicity of ZnO NPs is mediated by the generation of oxidative stress, involving the induction of lipid peroxidation and ROS-dependent DNA damage. Ahamed et al reported that ZnO NPs induced apoptosis in A549 cells, a type II pulmonary epithelial cell line, through ROS and oxidative stress by the TP53, survivin, Bax/Bcl-2, and caspase pathways.…”

Zinc Oxide Nanoparticles Influence Microflora in Ileal Digesta and Correlate Well with Blood Metabolites

“…Lai et al (2015) discovered that ZnO NPs (mean diameter 63.1 nm) located in lung cell mitochondria cause mitochondrial dysfunction and are a major source of ROS; in turn, the level of ROS affects energy metabolism. They also found that glucose consumption and lactate production were reduced at the concentration of 10 μg/ml.…”

“…The augmentation of reactive oxygen species (ROS) and Zn 2+ are the greatest potential causes of ZnO NP cytotoxicity (Wang et al, 2014). Furthermore, ZnO NPs have some influence on metabolism as evidenced by metabolites in mouse urine (Yan et al, 2012) and disturbed glucose metabolism in lung epithelial cells (Lai et al, 2015). …”