Zinc oxide nanoparticles (ZnO NPs) are among the most widely used nanomaterials. They have multiple applications in cosmetics, textiles, paints, electronics and, recently, also in biomedicine. This extensive use of ZnO NPs notably increases the probability that both humans and wildlife are subjected to undesirable effects. Despite being among the most studied NPs from a toxicological point of view, much remains unknown about their ecotoxicological effects or how they may affect specific cell types, such as cells of the central nervous system. The main objective of this work was to investigate the effects of ZnO NPs on human glial cells and zebrafish embryo development and to explore the role of the released Zn²⁺ ions in these effects. The effects on cell viability on human A172 glial cells were assessed with an MTT assay and morphological analysis. The potential acute and developmental toxicity was assessed employing zebrafish (Danio rerio) embryos. To determine the role of Zn²⁺ ions in the in vitro and in vivo observed effects, we measured their release from ZnO NPs with flame atomic absorption spectrometry. Then, cells and zebrafish embryos were treated with a water-soluble salt (zinc sulfate) at concentrations that equal the number of Zn²⁺ ions released by the tested concentrations of ZnO NPs. Exposure to ZnO NPs induced morphological alterations and a significant decrease in cell viability depending on the concentration and duration of treatment, even after removing the overestimation due to NP interference. Although there were no signs of acute toxicity in zebrafish embryos, a decrease in hatching was detected after exposure to the highest ZnO NP concentrations tested. The ability of ZnO NPs to release Zn²⁺ ions into the medium in a concentration-dependent manner was confirmed. Zn²⁺ ions did not seem entirely responsible for the effects observed in the glial cells, but they were likely responsible for the decrease in zebrafish hatching rate. The results obtained in this work contribute to the knowledge of the toxicological potential of ZnO NPs.

Despite being one of the most studied nanomaterials, much remains unknown about the mechanism of action of zinc oxide (ZnO) nanoparticles (NP). The aim of this work was to evaluate the effects on cell viability caused by the exposure of glial cells to ZnO NP, and the role of Zn²⁺ in the observed effects. The impact of ZnO NP or Zn²⁺ ions on cell viability was assessed by MTT assay. The exposure to ZnO NP induced a significant decrease in cell viability. The presence of Zn²⁺ ions released from ZnO NP was not entirely responsible for the observed cytotoxic effects.

Cerium dioxide nanoparticles (CeO₂NP) show antioxidant enzyme-like properties and reactive oxygen species (ROS) scavenging activity, making them a promising material for potential therapeutic applications in neurodegenerative diseases. The objective of this work was to assess the biological behavior of CeO₂NP in human SH-SY5Y neuronal and A172 glial cells by means of the MTT assay and the γH2AX assay. Despite the significant dose- and time-dependent NP internalization by both cell lines, nanoceria generally presented scarce cytotoxicity or genotoxicity, essentially restricted to the highest NP doses and longest exposure times. In conclusion, a high biocompatibility of CeO₂NP was observed under the conditions tested.

Gold nanoparticles (AuNPs) are one of the most remarkable nanomaterials. Due to their small size, these NPs can cross the blood–brain barrier making them good candidates for the treatment of diseases related to the central nervous system. The main objective of the present work was to evaluate the influence of surface charge on the biological behaviour of AuNPs by assessing the cytotoxic—viability and morphological alterations—and genotoxic—double strand breaks—effects induced in neuronal cells exposed to AuNPs with different charges: cationic, anionic, and neutral. Different toxicological behaviours were obtained depending on the surface charge of the NPs.