Aluminum enhances the oxidative damage of ZnO NMs in the human neuroblastoma SH-SY5Y cell line.

Bare and doped zinc oxide nanomaterials (ZnO NMs) are of great interest as multifunctional platforms for biomedical applications. In this study, we systematically investigate the physicochemical properties of Aluminum doped ZnO (AZO) and its bio-interactions with neuroblastoma (SH-SY5Y) and red blood (RBCs) cells. We provide a comprehensive chemical and structural characterization of the NMs. We also evaluated the biocompatibility of AZO NMs using traditional toxicity assays and advanced microscopy techniques. The toxicity of AZO NMs towards SH-SY5Y cells, decreases as a function of Al doping but is higher than the toxicity of ZnO NMs. Our results show that N-acetyl cysteine protects SH-SY5Y cells against reactive oxygen species toxicity induced by AZO NMs. ZnO and AZO NMs do not exert hemolysis in human RBCs at the doses that cause toxicity (IC50) in neuroblastoma cells. The Atomic force microscopy qualitative analysis of the interaction of SH-SY5Y cells with AZO NMs shows evidence that the affinity of the materials with the cells results in morphology changes and diminished interactions between neighboring cells. The holotomographic microscopy analysis demonstrates NMs' internalization in SH-SY5Y cells, changes in their chemical composition, and the role of lipid droplets in the clearance of toxicants.

Biocompatibility Evaluation of TiO2, Fe3O4, and TiO2/Fe3O4 Nanomaterials: Insights into Potential Toxic Effects in Erythrocytes and HepG2 Cells.

Nanomaterials such as titanium dioxide and magnetite are increasingly used in several fields, such as water remediation and agriculture. However, this has raised environmental concerns due to potential exposure to organisms like humans. Nanomaterials can cause adverse interactions depending on physicochemical characteristics, like size, morphology, and composition, when interacting with living beings. To ensure safe use and prevent the risk of exposure to nanomaterials, their biocompatibility must be assessed. In vitro cell cultures are beneficial for assessing nanomaterial-cell interactions due to their easy handling. The present study evaluated the biocompatibility of TiO2, Fe3O4, and TiO2/Fe3O4 nanomaterials thermally treated at 350 °C and 450 °C in erythrocytes and HepG2 cells. According to the hemolysis experiments, non-thermally treated NMs are toxic (>5% hemolysis), but their thermally treated counterparts do not present toxicity (<2%). This behavior indicates that the toxicity derives from some precursor (solvent or surfactant) used in the synthesis of the nanomaterials. All the thermally treated nanomaterials did not show hemolytic activity under different conditions, such as low-light exposure or the absence of blood plasma proteins. In contrast, non-thermally treated nanomaterials showed a high hemolytic behavior, which was reduced after the purification (washing and thermal treatment) of nanomaterials, indicating the presence of surfactant residue used during synthesis. An MTS cell viability assay shows that calcined nanomaterials do not reduce cell viability (>11%) during 24 h of exposure. On the other hand, a lactate dehydrogenase leakage assay resulted in a higher variability, indicating that several nanomaterials did not cause an increase in cell death as compared to the control. However, a holotomographic microscopy analysis reveals a high accumulation of nanomaterials in the cell structure at a low concentration (10 µg mL-1), altering cell morphology, which could lead to cell membrane damage and cell viability reduction.

Synthesis of TiO2-Cu2+/CuI Nanocomposites and Evaluation of Antifungal and Cytotoxic Activity.

Fungal infections have become a significant public health concern due to their increasing recurrence and harmful effects on plants, animals, and humans. Opportunistic pathogens (among others from the genera Candida and Aspergillus) can be present in indoor air, becoming a risk for people with suppressed immune systems. Engineered nanomaterials are novel alternatives to traditional antifungal therapy. In this work, copper(I) iodide (CuI) and a copper-doped titanium dioxide-copper(I) iodide (TiO2-Cu2+/CuI) composite nanomaterials (NMs)-were synthesized and tested as antifungal agents. The materials were synthesized using sol-gel (TiO2-Cu2+) and co-precipitation (CuI) techniques. The resulting colloids were evaluated as antifungal agents against Candida parapsilosis and Aspergillus niger strains. The NMs were characterized by XRD, HRTEM, AFM, and DLS to evaluate their physicochemical properties. The NMs present a high size dispersion and different geometrical shapes of agglomerates. The antifungal capacity of the NMs by the minimum inhibitory concentration (MIC) and minimum fungicidal concentration (MFC) was below 15 µg/mL against Candida parapsilosis and below 600 µg/mL against Aspergillus niger for both NMs. Holotomography microscopy showed that the NMs could penetrate cell membranes causing cell death through its rupture and reactive oxygen species (ROS) production. Cytotoxicity tests showed that NMs could be safe to use at low concentrations. The synthesized nanomaterials could be potential antifungal agents for biomedical or environmental applications.

Subchronic co-exposure to particulate matter and fructose-rich-diet induces insulin resistance in male Sprague Dawley rats.

Insulin resistance (IR) and metabolic disorders are non-pulmonary adverse effects induced by fine particulate matter (PM2.5) exposure. The worldwide pandemic of high fructose sweeteners and fat rich modern diets, also contribute to IR development. We investigated some of the underlying effects of IR, altered biochemical insulin action and Insulin/AKT pathway biomarkers. Male Sprague Dawley rats were subchronically exposed to filtered air, PM2.5, a fructose rich diet (FRD), or PM2.5 + FRD. Exposure to PM2.5 or FRD alone did not induce metabolic changes. However, PM2.5 + FRD induced leptin release, systemic hyperinsulinemia, and Insulin/AKT dysregulation in insulin-sensitive tissues preceded by altered AT1R levels. Histological damage and increased HOMA-IR were also observed from PM2.5 + FRD co-exposure. Our results indicate that the concomitant exposure to a ubiquitous environmental pollutant, such as PM2.5, and a metabolic disease risk factor, a FRD, can contribute to the metabolic disorder pandemic occurring in highly polluted locations.