Barium titanate (BaTiO3) nanoparticles (BT NPs) have shown exceptional characteristics such as high dielectric constant and suitable ferro-, piezo-, and pyro-electric properties. Thus, BT NPs have shown potential to be applied in various fields including electro-optical devices and biomedicine. However, very limited knowledge is available on the interaction of BT NPs with human cells. This work was planned to study the interaction of BT NPs with human lung carcinoma (A549) cells. Results showed that BT NPs decreased cell viability in a dose- and time-dependent manner. Depletion of mitochondrial membrane potential and induction of caspase-3 and -9 enzyme activity were also observed following BT NP exposure. BT NPs further induced oxidative stress indicated by induction of pro-oxidants (reactive oxygen species and hydrogen peroxide) and reduction of antioxidants (glutathione and several antioxidant enzymes). Moreover, BT NP-induced cytotoxicity and oxidative stress were effectively abrogated by N-acetyl-cysteine (an ROS scavenger), suggesting that BT NP-induced cytotoxicity was mediated through oxidative stress. Intriguingly, the underlying mechanism of cytotoxicity of BT NPs was similar to the mode of action of ZnO NPs. At the end, we found that BT NPs did not affect the non-cancerous human lung fibroblasts (IMR-90). Altogether, BT NPs selectively induced cytotoxicity in A549 cells via oxidative stress. This work warrants further research on selective cytotoxicity mechanisms of BT NPs in different types of cancer cells and their normal counterparts.

Graphene-based nanocomposites have attracted enormous interest in nanomedicine and environmental remediation, owing to their unique characteristics. The increased production and widespread application of these nanocomposites might raise concern about their adverse health effects. In this study, for the first time, we examine the cytotoxicity and oxidative stress response of a relatively new nanocomposite of cerium oxide-reduced graphene oxide (CeO2-RGO) in human lung epithelial (A549) cells. CeO2-RGO nanocomposites and RGO were prepared by a simple hydrothermal method and characterized by relevant analytical techniques. Cytotoxicity data have shown that RGO significantly induces toxicity in A549 cells, evident by cell viability reduction, membrane damage, cell cycle arrest, and mitochondrial membrane potential loss. However, CeO2-RGO nanocomposites did not cause statistically significant toxicity as compared to a control. We further observed that RGO significantly induces reactive oxygen species generation and reduces glutathione levels. However, CeO2-RGO nanocomposites did not induce oxidative stress in A549 cells. Interestingly, we observed that CeO2 nanoparticles (NPs) alone significantly increase glutathione (GSH) levels in A549 cells as compared to a control. The GSH replenishing potential of CeO2 nanoparticles could be one of the possible reasons for the biocompatible nature of CeO2-RGO nanocomposites. Our data warrant further and more advanced research to explore the biocompatibility/safety mechanisms of CeO2-RGO nanocomposites in different cell lines and animal models.

Due to unique physicochemical properties, magnesium oxide nanoparticles (MgO NPs) have shown great potential for various applications, including biomedical and environmental remediation. Moreover, the physiochemical properties of MgO NPs can be tailored by metal ion doping that can be utilized in photocatalytic performance and in the biomedical field. There is limited study on the photocatalytic activity and biocompatibility of silver (Ag)-doped MgO NPs. This study was planned for facile synthesis, characterization, and photocatalytic activity of pure and silver (Ag)-doped MgO NPs. In addition, cytotoxicity of pure and Ag-doped MgO NPs was assessed in human normal umbilical vein endothelial cells (HUVECs). Pure MgO NPs and Ag-doped (1, 2, 5, and 7.5 mol%) MgO NPs were prepared via a simple sol-gel procedure. X-ray diffraction (XRD), scanning electron microscopy (SEM), transmission electron microscopy (TEM), Fourier transform infrared (FTIR), photoluminescence (PL), and X-ray photoelectron spectroscopy (XPS) were used to characterize the prepared samples. XRD results showed the preparation of highly crystalline NPs with no impurity peaks. TEM and SEM studies indicate smooth surfaces with almost spherical morphology of MgO NPs, and Ag-doping did not change the morphology. Elemental composition study suggested that Ag is uniformly distributed in MgO particles. Intensity of the PL spectra of MgO NPs decreased with increasing the concentration of Ag dopants. In comparison to pure MgO NPs, Ag-MgO NPs showed higher degradation of methylene blue (MB) dye under UV irradiation. The improved photocatalytic activity of Ag-MgO NPs was related to the effect of dopant concentration on reducing the recombination between electrons and holes. Cytotoxicity studies showed good biocompatibility of pure and Ag-doped MgO NPs with human normal umbilical vein endothelial cells (HUVECs). These results highlighted the potential of Ag-doped MgO NPs in environmental remediation.

In spite of the potential preclinical advantage of Gd2O3 nanoparticles (designated here as GO NPs) over gadolinium-based compounds in MRI, recent concerns of gadolinium deposits in various tissues undergoing MRI demands a mechanistic investigation. Hence, we chose human to measure umbilical vein endothelial cells (HUVECs) that line the vasculature and relevant biomarkers due to GO NPs exposure in parallel with the NPs of ZnO as a positive control of toxicity. GO NPs, as measured by TEM, had an average length of 54.8 ± 29 nm and a diameter of 13.7 ± 6 nm suggesting a fiber-like appearance. With not as pronounced toxicity associated with a 24-h exposure, GO NPs induced a concentration-dependent cytotoxicity (IC50 = 304 ± 17 µg/mL) in HUVECs when exposed for 48 h. GO NPs emerged as significant inducer of lipid peroxidation (LPO), reactive oxygen species (ROS), mitochondrial membrane potential (MMP) and autophagic vesicles in comparison to that caused by ZnO NPs at its IC50 for the same exposure time (48 h). While ZnO NPs clearly appeared to induce apoptosis, GO NPs revealed both apoptotic as well as necrotic potentials in HUVECs. Intriguingly, the exogenous antioxidant NAC (N-acetylcysteine) co-treatment significantly attenuated the oxidative imbalance due to NPs preventing cytotoxicity significantly.