Evaluating mesoporous zinc oxide nanoparticles for dentin pretreatment: Synthesis, characterization, and bond strength performance with a universal adhesive

Background: This study focused on synthesizing and characterizing mesoporous zinc oxide nanoparticles (ZnO NPs) while evaluating their antibacterial effectiveness against Streptococcus mutans. Their antimicrobial properties were compared to conventional ZnO NPs using minimum inhibitory concentration (MIC) and minimum bactericidal concentration (MBC) tests. Methods: Mesoporous ZnO NPs were produced and analyzed for structural properties. Their antibacterial potential was assessed through MIC and MBC determinations, along with inhibition zone measurements. The test groups included calcined and noncalcined mesoporous ZnO NP solutions (10 mg/mL), standard ZnO NP solution (10 mg/mL), normal saline, and chlorhexidine (CHX) solution (2 mg/mL). Results: All ZnO NP solutions exhibited an MIC of 5 mg/mL, with lower concentrations (2.5 mg/mL and below) showing no inhibition against S. mutans. The MIC for CHX (2 mg/mL) was found to be 0.156 mg/mL. MBC values matched MIC results for all NP solutions (5 mg/mL), whereas CHX had an MBC of 0.312 mg/mL. Among the tested solutions, the calcined mesoporous ZnO NP solution produced the largest inhibition zone (19 ± 0.02 mm), followed by the noncalcined version (17.2 ± 0.03 mm). CHX (14.9 ± 0.02 mm) and ZnO NP solution (15.2 ± 0.13 mm) showed similar inhibitory effects. Conclusion: The study suggests that mesoporous ZnO NP solution possesses strong antibacterial properties against S. mutans, offering a promising alternative to CHX, which is widely used in dental disinfection. These findings highlight the potential application of mesoporous ZnO NPs in various dental procedures, including endodontics, restorative treatments, and periodontal therapy.

Nitro-oxidative signalling induced by chemically synthetized zinc oxide nanoparticles (ZnO NPs) in Brassica species

Soil salinization severely restricts the growth and development of crops globally, especially in the northwest Loess Plateau, where apples constitute a pillar industry. Nanomaterials, leveraging their unique properties, can facilitate the transport of nutrients to crops, thereby enhancing plant growth and development under stress conditions. To investigate the effects of nano zinc oxide (ZnO NP) on the growth and physiological characteristics of apple self-rooted rootstock M9-T337 seedlings under saline alkali stress, one-year-old M9-T337 seedlings were used as experimental materials and ZnO NPs were used as donors for pot experiment. Six treatments were set up: CK (normal growth), SA (saline alkali stress,100 mmol/L NaCl + NaHCO3), T1 (saline alkali stress + 50 mg/L ZnO NPs), T2 (saline alkali stress + 100 mg/L ZnO NPs), T3 (saline alkali stress + 150 mg/L ZnO NPs) and T4 (saline alkali stress + 200 mg/L ZnO NPs). The results were found to show that saline alkali stress could significantly inhibit the growth and development of M9-T337 seedlings, reduce photosynthetic characteristics, and cause ion accumulation to trigger osmotic regulation system, endogenous hormone and antioxidant system imbalances. However, the biomass, plant height, stem diameter, total leaf area and leaf perimeter of M9-T337 seedlings were significantly increased after ZnO NP treatment. Specifically speaking, ZnO NPs can improve the photosynthetic capacity of M9-T337 by increasing the content of photosynthetic pigment, regulating photosynthetic intensity and chlorophyll fluorescence parameters. ZnO NPs can balance the osmotic adjustment system by increasing the contents of soluble protein (SP), soluble sugar (SS), proline (Pro) and starch, and can also enhance the activities of enzymatic (SOD, POD, and CAT) and non-enzymatic antioxidant enzymes (APX, AAO, GR, and MDHAR) to enhance the scavenging ability of reactive oxygen species (H2O2, O2•-), ultimately reducing oxidative damage; ZnO NPs promoted the growth of M9-T337 seedlings under saline alkali stress by synergistically responding to auxin (IAA), gibberellin (GA3), zeatin (ZT) and abscisic acid (ABA). Additionally, the Na+/K+ ratio was reduced by upregulating the expression of Na+ transporter genes (MdCAX5, MdCHX15, MdSOS1, and MdALT1) and downregulating the expression of K+ transporter genes (MdSKOR and MdNHX4). After comprehensive analysis of principal components and correlation, T3 (150 mg/L ZnO NPs) treatment possessed the best mitigation effect. In summary, 150 mg/L ZnO NPs(T3) can effectively maintain the hormone balance, osmotic balance and ion balance of plant cells by promoting the photosynthetic capacity of M9-T337 seedlings, and enhance the antioxidant defense mechanism, thereby improving the saline alkaline tolerance of M9-T337 seedlings.

Zinc oxide nanoparticles disrupt the mammary epithelial barrier via Z-DNA binding protein 1-triggered PANoptosis

Zinc oxide nanoparticles induce lipoxygenase-mediated apoptosis and necrosis in human neuroblastoma SH-SY5Y cells

This study aimed to investigate the characterization of zinc oxide nanoparticles (ZnONPs) produced from Cucurbita pepo L. (pumpkin seeds) and their selective cytotoxic effectiveness on human colon cancer cells (HCT 116) and African Green Monkey Kidney, Vero cells. The study also investigated the antioxidant activity of ZnONPs. The study also examined ZnONPs' antioxidant properties. This was motivated by the limited research on the comparative cytotoxic effects of ZnO NPs on normal and HCT116 cells. The ZnO NPs were characterized using Fourier-transform infrared spectroscopy (FTIR), Thermogravimetric Analysis (TGA), Transmission Electron Microscope/Selected Area Electron Diffraction (TEM/SAED), and Scanning Electron Microscope-Energy Dispersive X-ray (SEM-EDX) for determination of chemical fingerprinting, heat stability, size, and morphology of the elements, respectively. Based on the results, ZnO NPs from pumpkins were found to be less than 5 μm and agglomerates in nature. Furthermore, the ZnO NPs fingerprinting and SEM-EDX element analysis were similar to previous literature, suggesting the sample was proven as ZnO NPs. The ZnO NPs also stable at a temperature of 380°C indicating that the green material is quite robust at 60-400°C. The cell viability of Vero cells and HCT 116 cell line were measured at two different time points (24 and 48 h) to assess the cytotoxicity effects of ZnO NP on these cells using AlamarBlue assay. Cytotoxic results have shown that ZnO NPs did not inhibit Vero cells but were slightly toxic to cancer cells, with a dose-response curve IC50 = ~409.7 μg/mL. This green synthesis of ZnO NPs was found to be non-toxic to normal cells but has a slight cytotoxicity effect on HCT 116 cells. A theoretical study used molecular docking to investigate nanoparticle interaction with cyclin-dependent kinase 2 (CDK2), exploring its mechanism in inhibiting CDK2's role in cancer. Further study should be carried out to determine suitable concentrations for cytotoxicity studies. Additionally, DPPH has a significant antioxidant capacity, with an IC50 of 142.857 μg/mL. RESEARCH HIGHLIGHTS: Pumpkin seed extracts facilitated a rapid, high-yielding, and environmentally friendly synthesis of ZnO nanoparticles. Spectrophotometric analysis was used to investigate the optical properties, scalability, size, shape, dispersity, and stability of ZnO NPs. The cytotoxicity of ZnO NPs on Vero and HCT 116 cells was assessed, showing no inhibition of Vero cells and cytotoxicity of cancer cells. The DPPH assay was also used to investigate the antioxidant potential of biogenic nanoparticles. A molecular docking study was performed to investigate the interaction of ZnO NPs with CDK2 and to explore the mechanism by which they inhibit CDK2's role in cancer.

ZnO nanoparticles induce cell wall remodeling and modify ROS/ RNS signalling in roots of Brassica seedlings

Zinc oxide nanoparticles (ZnO NPs) exhibit diverse applications, including antimicrobial, UV-blocking, and catalytic properties, due to their unique structure and properties. This study focused on the characterization of zinc oxide nanoparticles (ZnO NPs) synthesized from Juglans regia leaves and their application in mitigating the impact of simultaneous infection by Meloidogyne arenaria (root-knot nematode) and Macrophomina phaseolina (root-rot fungus) in cowpea plants. The characterization of ZnO NPs was carried out through various analytical techniques, including UV-visible spectrophotometry, Powder-XRD analysis, FT-IR spectroscopy, and SEM-EDX analysis. The study confirmed the successful synthesis of ZnO NPs with a hexagonal wurtzite structure and exceptional purity. Under in vitro conditions, ZnO NPs exhibited significant nematicidal and antifungal activities. The mortality of M. arenaria juveniles increased with rising ZnO NP concentrations, and a similar trend was observed in the inhibition of M. phaseolina mycelial growth. SEM studies revealed physical damage to nematodes and structural distortions in fungal hyphae due to ZnO NP treatment. In infected cowpea plants, ZnO NPs significantly improved plant growth parameters, including plant length, fresh mass, and dry mass, especially at higher concentrations. Leghemoglobin content and the number of root nodules also increased after ZnO NP treatment. Additionally, ZnO NPs reduced gall formation and egg mass production by M. arenaria nematodes and effectively inhibited the growth of M. phaseolina in the roots. Furthermore, histochemical analyses demonstrated a reduction in oxidative stress, as indicated by decreased levels of reactive oxygen species (ROS) and lipid peroxidation in ZnO NP-treated plants. These findings highlight the potential of green-synthesized ZnO NPs as an eco-friendly and effective solution to manage disease complex in cowpea caused by simultaneous nematode and fungal infections.

The advent of nanotechnology has revolutionized many commercial and industrial fields. Mass production of these materials warrants concerns of incidental exposure to environmental and human health alike. Zinc oxide nanoparticles (ZnO NPs) are one of the most highly produced nanoparticles and have been determined to be toxic to many cell types in vitro. The mechanism responsible for the cell death they induce and their effect on functional immunity however is largely unknown. Our preliminary findings show that ZnO NPs have a cytotoxic effect on immune cells in in vitro cultures, implicating immunotoxic potential. In this thesis, we determine the effect, and extent of the immunocompromising effect through a systematic approach. We formulate consistent ZnO NPs and characterize their capacity for inducing toxicity and elucidating the mechanism. Using a modified FluoZin-3 assay, we determine that high concentrations of zinc ions release from the surface of ZnO NPs and Zn²⁺ can directly induce cell death and this is Reactive Oxygen Species (ROS) dependent. We find that EDTA and Ca ions effectively prevent ZnO NPs from inducing death of the immune cells while glutathione (GSH) protects the cell downstream. Finally, the autophagy inhibitor 3-MA eliminates ZnO NP death at the level of cell signaling. The mode of cell death induced by ZnO NPs was found to be autophagy-related and not apoptosis, necrosis, pyroptosis, or necroptosis. Importantly, ROS were required for ZnO NP induction of autophagy. Our in vivo studies indicate ZnO NPs cause morbidity and deplete immune cell populations in the spleens of mice. Chronic exposure on the other hand, allows the mice to develop ZnO NP tolerance. Mice exhibited normal viral clearance, however distinct changes in the immune response were observed. We conclude that zinc ion release is the primary mediators of ZnO NP induced death of immune cells, initiating excessive ROS production which in turn induce autophagic death. The effect of this in vivo exposure is a much more complex, and appears to be finely balanced between detrimental and possibly beneficial to immunity due to increased inflammation.

BackgroundZinc oxide nanoparticles (ZnO NPs) are used in an increasing number of products, including rubber manufacture, cosmetics, pigments, food additives, medicine, chemical fibers and electronics. However, the molecular mechanisms underlying ZnO NP nephrotoxicity remain unclear. In this study, we evaluated the potential toxicity of ZnO NPs in kidney cells in vitro and in vivo.ResultsWe found that ZnO NPs were apparently engulfed by the HEK-293 human embryonic kidney cells and then induced reactive oxygen species (ROS) generation. Furthermore, exposure to ZnO NPs led to a reduction in cell viability and induction of apoptosis and autophagy. Interestingly, the ROS-induced hypoxia-inducible factor-1α (HIF-1α) signaling pathway was significantly increased following ZnO NPs exposure. Additionally, connective tissue growth factor (CTGF) and plasminogen activator inhibitor-1 (PAI-1), which are directly regulated by HIF-1 and are involved in the pathogenesis of kidney diseases, displayed significantly increased levels following ZnO NPs exposure in HEK-293 cells. HIF-1α knockdown resulted in significantly decreased levels of autophagy and increased cytotoxicity. Therefore, our results suggest that HIF-1α may have a protective role in adaptation to the toxicity of ZnO NPs in kidney cells. In an animal study, fluorescent ZnO NPs were clearly observed in the liver, lungs, kidneys, spleen and heart. ZnO NPs caused histopathological lesions in the kidney and increase in serum creatinine and blood urea nitrogen (BUN) which indicate possible renal possible damage. Moreover, ZnO NPs enhanced the HIF-1α signaling pathway, apoptosis and autophagy in mouse kidney tissues.ConclusionsZnO NPs may cause nephrotoxicity, and the results demonstrate the importance of considering the toxicological hazards of ZnO NP production and application, especially for medicinal use.Electronic supplementary materialThe online version of this article (doi:10.1186/s12989-016-0163-3) contains supplementary material, which is available to authorized users.

Zinc oxide nanoparticles (ZnO NPs) are being rapidly developed for use in consumer products, wastewater treatment, and chemotherapy providing several possible routes for ZnO NP exposure to humans and aquatic organisms. Recent studies have shown that ZnO NPs undergo rapid dissolution to Zn(2+), but the relative contribution of Zn(2+) to ZnO NP bioavailability and toxicity is not clear. We show that a fraction of the ZnO NPs in suspension dissolves, and this fraction cannot account for the toxicity of the ZnO NP suspensions to Daphnia magna. Gene expression profiling of D. magna exposed to ZnO NPs or ZnSO(4) at sublethal concentrations revealed distinct modes of toxicity. There was also little overlap in gene expression between ZnO NPs and SiO(x) NPs, suggesting specificity for the ZnO NP expression profile. ZnO NPs effected expression of genes involved in cytoskeletal transport, cellular respiration, and reproduction. A specific pattern of differential expression of three biomarker genes including a multicystatin, ferritin, and C1q containing gene were confirmed for ZnO NP exposure and provide a suite of biomarkers for identifying environmental exposure to ZnO NPs and differentiating between NP and ionic exposure.

Zinc oxide nanoparticles (ZnO NPs) are being utilized in an increasing number of fields and commercial applications. While their general toxicity and associated oxidative stress have been extensively studied, the toxicological pathways that they induce in developmental stages are still largely unknown. In this study, the developmental toxicity of ZnO NPs to embryonic/larval zebrafish was investigated. The transcriptional expression profiles induced by ZnO NPs were also investigated to ascertain novel genomic responses related to their specific toxicity pathway. Zebrafish embryos were exposed to 0.01, 0.1, 1, and 10 mg/L ZnO NPs for 96 h post-fertilization. The toxicity of ZnO NPs, based on their Zn concentration, was quite similar to that in embryonic/larval zebrafish exposed to corresponding ZnSO4 concentrations. Pericardial edema and yolk-sac edema were the principal malformations induced by ZnO NPs. Gene-expression profiling using microarrays demonstrated 689 genes that were differentially regulated (fold change >1.5) following exposure to ZnO NPs (498 upregulated, 191 downregulated). Several genes that were differentially regulated following ZnO NP exposure shared similar biological pathways with those observed with ZnSO4 exposure, but six genes (aicda, cyb5d1, edar, intl2, ogfrl2 and tnfsf13b) associated with inflammation and the immune system responded specifically to ZnO NPs (either in the opposite direction or were unchanged in ZnSO4 exposure). Real-time reverse-transcription quantitative polymerase chain reaction confirmed that the responses of these genes to ZnO NPs were significantly different from their response to ZnSO4 exposure. ZnO NPs may affect genes related to inflammation and the immune system, resulting in yolk-sac edema and pericardia edema in embryonic/larval developmental stages. These results will assist in elucidating the mechanisms of toxicity of ZnO NPs during development of zebrafish.

The embryotoxicity of ZnO nanoparticles to marine medaka, Oryzias melastigma

BackgroundZinc oxide nanoparticle (ZnO NP) is one of the metal nanomaterials with extensive use in many fields such as feed additive and textile, which is an emerging threat to human health due to widely distributed in the environment. Thus, there is an urgent need to understand the toxic effects associated with ZnO NPs. Although previous studies have found accumulation of ZnO NPs in testis, the molecular mechanism of ZnO NPs dominated a decline in male fertility have not been elucidated.ResultsWe reported that ZnO NPs exposure caused testicular dysfunction and identified spermatocytes as the primary damaged site induced by ZnO NPs. ZnO NPs led to the dysfunction of spermatocytes, including impaired cell proliferation and mitochondrial damage. In addition, we found that ZnO NPs induced ferroptosis of spermatocytes through the increase of intracellular chelatable iron content and lipid peroxidation level. Moreover, the transcriptome analysis of testis indicated that ZnO NPs weakened the expression of miR-342-5p, which can target Erc1 to block the NF-κB pathway. Eventually, ferroptosis of spermatocytes was ameliorated by suppressing the expression of Erc1.ConclusionsThe present study reveals a novel mechanism in that miR-342-5p targeted Erc1 to activate NF-κB signaling pathway is required for ZnO NPs-induced ferroptosis, and provide potential targets for further research on the prevention and treatment of male reproductive disorders related to ZnO NPs.Graphical

Zinc oxide nanoparticles (ZnO NPs) have anticancer, antidiabetic, antibacterial, and anti-inflammatory properties in the biotechnology field. Cafestol, which is the one of the diterpene in coffee, has antimicrobial and anticancer activities. This study aimed to synthesize the cafestol–chitosan–ZnO NP system to evaluate its antibacterial activity. ZnO NPs were produced by the chemical precipitation method. Optimization studies were performed to obtain the desired size of the ZnO NPs. The type of zinc salt [ZnCl2, Zn(SO4)], salt concentration (0.1; 0.2; 0.5 M), base type (NH3, NaOH), reaction time (6, 12, 18, 24 h), mixing speed (300, 400, 500 rpm), and calcination time (1, 2, 3 h) parameters in the method were investigated to yield the targeted size. The optimum experimental conditions required to synthesize in the 45–60 nm size range were determined as a 0.2 M Zn(SO4) salt type and concentration, NaOH base type, 18 h reaction time, at 400 rpm mixing speed and 2 h calcination time. After synthesizing the ZnO NPs coated with chitosan (CS), the cafestol was ligated to the CS–ZnO NP. It was proved by Fourier-transform infrared, differential scanning calorimeter/thermogravimetry analysis/diamond thermogravimetry analysis and scanning electron microscope analyses that cafestol–CS–ZnO NPs were successfully synthesized. The antibacterial effects of cafestol, CS, ZnO NPs, CS–ZnO NPs and cafestol–CS–ZnO NPs were evaluated on human pathogenic Gram-positive strains Staphylococcus aureus ATCC 25923 and Bacillus cereus ATCC 11778 and Gram-negative strains Pseudomonas aeruginosa PA01and Escherichia coli ATCC 25922. The ZnO NPs, CS–ZnO NP, and cafestol–CS–ZnO NP (varying between 20 and 1000 μg/mL) completely inhibited bacterial growth for S. aureus, B. cereus, and E. coli. The incorporation of CS and CS–cafestol improved the antibacterial activity of the ZnO NPs samples against P. aeruginosa PA01 with a 75–87.5% inhibition. The obtained data shows that CS–ZnO and cafestol–CS–ZnO NPs have great potential for biological and pharmaceutical applications.