Fabrication of Biogenic Silica Nanostructures from Sorghum bicolor Leaves for Food Industry Applications

Silicon - Due to the large production of sorghum, the generation of associated agricultural residues, which contain high contents of silica, is inevitable. Also, these agricultural residues are not...     

Morphological,Thermal, and Cytotoxicity Features Assessment of Starch–Myristic Acid Complex-Derived Nanostructured Materials

The present study investigates the morphological and cytotoxic properties of starch–myristic acid complex (SMC) derivatives. The study attempts to prepare a SMC by frying. By liquid–liquid extraction, starch–myristic acid complex nanostructured materials are isolated. X-ray diffractometry and transmission electron microscopy are used to determine the morphology and crystallization of the extract. The study performs various assays to assess the toxicological profile of starch–myristic acid complex-derived nanostructured materials (SMC-NMs), including cellular viability tests, cellular and nuclear morphological examinations, mitochondrial membrane potential (MMP), and intracellular reactive oxygen species (ROS) measurements. Transmission electron microscopy (TEM) images reveal nanoscale particles between 30 and 90 nm in water fraction-based SMC-NMs (WSMC-NMs) and 160 and 250 nm in methanol fraction-based SMC-NMs (MSMC-NMs). The WSMC-NMs and MSMC-NMs decrease the cell viability by 77% and 91% at 250 µg mL⁻¹, respectively. The SMC-NMs enhance necrotic cell death by increasing the level of ROS in human mesenchymal stem cells (hMSCs). The SMC-NMs alter gene expression within 24 h. Gene expression of GSTM3 and GSR has explicitly upregulated in a dose-dependent manner in WSMC-NMs and MSMC-NMs exposed cells. The study finds that nanoscale particles may develop during cooking, increasing the risk of diabetes, cardiovascular diseases, and obesity.     

Biogenic silica–metal phosphate (metal = Ca,Fe or Zn) nanocomposites: fabrication from rice husk and their biomedical applications

In this investigation, we fabricated biogenic silica–metal phosphate nanocomposites (BSMPNs) using rice husk from agricultural waste as a silica source. The morphologies and dimensions of the synthesized nanocomposites were analyzed using transmission electron microscopy (TEM). Fourier-transform infrared spectroscopy results confirmed that metal phosphate crystals were formed with the biogenic silica. The X-ray diffraction patterns of the BSMPNs showed the presence of hexagonal calcium and iron phosphate and orthorhombic zinc phosphate nanoparticles embedded in the matrix of biogenic silica. The TEM images suggested that spherical and irregularly shaped tiny particles with dimensions between 50 and 100 nm were dispersed in the biogenic silica. The in vitro biological properties of the nanocomposites were studied by a cell viability assay and through the analysis of microscopy images. The cytocompatibility studies proved that the material was nontoxic and had excellent biocompatibility with human mesenchymal stem cells. The synthetic route for these nanocomposites is interesting and may be helpful in the fabrication of various novel silica-based composites and in the exploitation of eco-friendly agricultural biomass. Our results revealed that these nanocomposites can be used in bone tissue engineering.     

Identification of Nanoscale Ingredients in Commercial Food Products and their Induction of Mitochondrially Mediated Cytotoxic Effects on Human Mesenchymal Stem Cells

Titanium dioxide (E171) and silicon dioxide (E551) are common additives found in food products, personal‐care products, and many other consumer products used in daily life. Recent studies have reported that these food additives (manufactured E171 and E551) contain nanosized particles of less than 100 nm. However, the particle size distribution and morphology of added TiO₂ and SiO₂ particles are not typically stated on the package label. Furthermore, there is an increasing debate regarding health and safety concerns related to the use of synthetic food additives containing nanosized ingredients in consumer products. In this study, we identified the size and morphology of TiO₂ and SiO₂ particles in commercially available food products by using transmission electron microscope (TEM). In addition, the in vitro toxicological effects of E171 and E551 on human mesenchymal stem cells (hMSCs), an adult stem cell‐based model, were assessed using the MTT assay and a flow cytometry‐based JC‐1 assay. Our TEM results confirmed the presence of nanoscale ingredients in food products, and the in vitro toxicology results indicated that the nanoscale E171 and E551 ingredients induced dose‐dependent cytotoxicity, changes in cellular morphology, and the loss of mitochondrial trans‐membrane potential in hMSCs. These preliminary results clearly demonstrated that the nanoscale E171 and E551 particles had adverse effects on hMSCs by inducing oxidative stress‐mediated cell death. Accordingly, further studies are needed to identify the specific pathway involved, with an emphasis on differential gene expression in hMSCs.     

Ononitol Monohydrate—A Glycoside Potentially Inhibit HT-115 Human Colorectal Cancer Cell Proliferation through COX-2/PGE-2 Inflammatory Axis Regulations

We aimed to inhibit HT-115 human colorectal cancer cell proliferation using ononitol monohydrate (OMH), a bioactive principle isolated from Cassia tora (L.). The cytotoxicity of OMH has been assayed using MTT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide), cell and nuclear morphology, and apoptosis mechanisms have been analyzed using real-time PCR. Higher doses of OMH potentially inhibit 84% of HT-115 cell viability; we observed that the IC₅₀ level was 3.2 µM in 24 h and 1.5 µM in 48 h. The treatment with 3.2 µM of OMH for 48 h characteristically showed 64% apoptotic cells and 3% necrotic cells, confirmed by propidium iodide and acridine orange/ethidium bromide (AO/ErBr) staining. We found the overexpression of cyclooxygenase-2 (COX-2) and prostaglandin E2 (PGE-2) in the control HT-115 cells, which was directly associated with colorectal tumorigenesis. However, 3.2 µM of OMH treatment to HT-115 cells for 48 h significantly reduced inflammatory genes, such as TNF-α/IL-1β and COX-2/PGE-2. The downregulation of COX-2 and PGE-2 was more significant with the 3.2 µM dose when compared to the 1.5 µM dose of OMH. Additionally, the protein levels of COX-2 and PGE-2 were decreased in the 3.2 µM OMH-treated cells compared to the control. We found significantly (p ≤ 0.01) increased mRNA expression levels of tumor-suppressor genes, such as pRb2, Cdkn1a, p53, and caspase-3, and decreased Bcl-2, mdm2, and PCNA after 48 h was confirmed with apoptotic stimulation. In conclusion, the antiproliferative effect of OMH via the early suppression of protumorigenic inflammatory agents TNF-α/IL-1β, COX-2/PGE-2 expression, and the increased expression levels of tumor-suppressor genes Cdkn1a and pRb2, which enhanced the activation of Bax and p53.     

Unraveling the physicochemical and toxicological properties of food product isolated E341/E171

Nanostructured materials have been extensively exploited in the food sector for nutrient delivery, sensing, packaging, and food additives. It has exhibited size, shape, chemical nature, and surface area-dependent physicochemical and biological properties. Currently, nanoscale ingredients are identified in approved food additives. Still, food-grade nanostructured material's impact on biological systems is unexplored well. Thus, in this study, we have identified and analyzed the physicochemical properties of nanoscale ingredients in commercial food product isolate E341 and E171 combinations. Also, we have evaluated the E341/E171 combination cytotoxic potential on human mesenchymal stem cells. The food isolated E341/E171 exhibits spherical nature with a 60–200 nm diameter. The E341 and E171 combination exposure increased the cell viability loss to ~36% at a high dose in human mesenchymal stem cells (hMSCs). The E341/E171 treatment-induced cellular and nuclear damage at a moderate dose. The mitochondrial membrane potential loss and ROS generation were observed in E341/E171 treated cells. The E341/E171 alters the gene expression pattern in hMSCs dose-dependently. The GSR and POR gene expression is upregulated significantly in E341/E171 treatment. Our study results revealed that E341/E171 induced toxicity in hMSCs at high concentrations. Thus, E341/E171 potential impact on the biological system should be reexamined for food industrial implications.