The wide use of ZnO and CuO nanoparticles in research, medicine, industry, and other fields has raised concerns about their biosafety. It is therefore unavoidable to be discharged into the sewage treatment system. Due to the unique physical and chemical properties of ZnO NPs and CuO NPs, it may be toxic to the members of the microbial community and their growth and metabolism, which in turn affects the stable operation of sewage nitrogen removal. This study summarizes the toxicity mechanism of two typical metal oxide nanoparticles (ZnO NPs and CuO NPs) to nitrogen removal microorganisms in sewage treatment systems. Furthermore, the factors affecting the cytotoxicity of metal oxide nanoparticles (MONPs) are summarized. This review aims to provide a theoretical basis and support for the future mitigating and emergent treatment of the adverse effects of nanoparticles on sewage treatment systems.
Wastewater/toxicity* ; Sewage/chemistry* ; Zinc Oxide/chemistry* ; Waste Disposal, Fluid ; Nanoparticles/chemistry* ; Metal Nanoparticles/chemistry* ; Nitrogen/metabolism* ; Water Purification

OBJECTIVE: To comparatively study the toxicity of four metal-containing nanoparticles (MNPs) and their chemical counterparts to the air-blood barrier (ABB) permeability using an in vitro model. METHODS: ABB model, which was developed via the co-culturing of A549 and pulmonary capillary endothelium, was exposed to spherical CuO-NPs (divided into CuO-40, CuO-80, and CuO-100 based on particle size), nano-Al2O3 (sheet and short-rod-shaped), nano-ZnO, nano-PbS, CuSO4, Al2(SO4)3, Zn(CH3COO)2, and Pb(NO3)2 for 60 min. Every 10 min following exposure, the cumulative cleared volume (ΔTCL) of Lucifer yellow by the model was calculated. A clearance curve was established using linear regression analysis of ΔTCL versus time. Permeability coefficient (P) was calculated based on the slope of the curve to represent the degree of change in the ABB permeability. RESULTS: The results found the increased P values of CuO-40, CuO-80, sheet, and short-rod-shaped nano-Al2O3, Al2(SO4)3, and Pb(NO3)2. Among them, small CuO-40 and CuO-80 were stronger than CuO-100 and CuSO4; no difference was observed between Al2(SO4)3 and sheet and short-rod-shaped nano-Al2O3; and nano-PbS was slightly weaker than Pb(NO3)2. So clearly the MNPs possess diverse toxicity. CONCLUSION ABB permeability abnormality means pulmonary toxicity potential. More studies are warranted to understand MNPs toxicity and ultimately control the health hazards.
A549 Cells ; Blood-Air Barrier ; metabolism ; Epithelium ; metabolism ; Humans ; Metal Nanoparticles ; toxicity ; Particle Size ; Permeability

To address the controversial issue of the toxicity of dental alloys and silver nanoparticles in medical applications, an in vivo-like LO2 3-D model was constructed within polyvinylidene fluoride hollow fiber materials to mimic the microenvironment of liver tissue. The use of microscopy methods and the measurement of liver-specific functions optimized the model for best cell performances and also proved the superiority of the 3-D LO2 model when compared with the traditional monolayer model. Toxicity tests were conducted using the newly constructed model, finding that four dental castings coated with silver nanoparticles were toxic to human hepatocytes after cell viability assays. In general, the toxicity of both the castings and the coated silver nanoparticles aggravated as time increased, yet the nanoparticles attenuated the general toxicity by preventing metal ion release, especially at high concentrations.
Cells, Cultured ; Dental Casting Technique ; Hepatocytes/drug effects* ; Humans ; Metal Nanoparticles/toxicity* ; Silver/toxicity* ; Toxicity Tests

OBJECTIVETo investigate the subchronic oral toxicity of silica nanoparticles (NPs) and silica microparticles (MPs) in rats and to compare the difference in toxicity between two particle sizes.

METHODSSprague-Dawley rats were randomly divided into seven groups: the control group; the silica NPs low-, middle-, and high-dose groups; and the silica MPs low-, middle-, and high-dose groups [166.7, 500, and 1,500 mg/(kg•bw•day)]. All rats were gavaged daily for 90 days, and deionized water was administered to the control group. Clinical observations were made daily, and body weights and food consumption were determined weekly. Blood samples were collected on day 91 for measurement of hematology and clinical biochemistry. Animals were euthanized for necropsy, and selected organs were weighed and fixed for histological examination. The tissue distribution of silicon in the blood, liver, kidneys, and testis were determined.

RESULTSThere were no toxicologically significant changes in mortality, clinical signs, body weight, food consumption, necropsy findings, and organ weights. Differences between the silica groups and the control group in some hematological and clinical biochemical values and histopathological findings were not considered treatment related. The tissue distribution of silicon was comparable across all groups.

CONCLUSIONOur study demonstrated that neither silica NPs nor silica MPs induced toxicological effects after subchronic oral exposure in rats.

Administration, Oral ; Animals ; Dose-Response Relationship, Drug ; Female ; Male ; Nanoparticles ; toxicity ; Particle Size ; Rats ; Rats, Sprague-Dawley ; Silicon Dioxide ; toxicity ; Toxicity Tests, Subchronic

OBJECTIVEThis paper aims to elucidate the combined toxicity of magnetite nanoparticles/Chromium [MNPs/Cr(VI)] adducts.

METHODSThe HEK293 cell was exposed to either Cr(VI) or MNPs, or their adducts MNPs/Cr(VI). The cytotoxicity was evaluated by assessing the cell viability, apoptosis, oxidative stress induction, and cellular uptake.

RESULTSThe toxicity of formed adducts is significantly reduced when compared to Cr(VI) anions. We found that the cellular uptake of MNPs/Cr(VI) adduct was rare, only few particles were endocytosed from the extracellular fluid and not accumulated in the cell nucleus. On the other hand, the Cr(VI) anions entered cells, generated oxidative stress, induced cell apoptosis, and caused cytotoxicity.

CONCLUSIONThe results showed minor effects of the nanoadducts on the tested cells and supported that magnetite nanoparticles could be implemented in the wastewater treatment process in which advantageous properties outweigh the risks.

Chromium ; chemistry ; toxicity ; Environmental Restoration and Remediation ; methods ; Ferrosoferric Oxide ; chemistry ; toxicity ; HEK293 Cells ; Humans ; Metal Nanoparticles ; chemistry ; toxicity

OBJECTIVEThe effect of the silica nanoparticles (SNs) on lungs injury in rats was investigated to evaluate the toxicity and possible mechanisms for SNs.

METHODSMale Wistar rats were instilled intratracheally with 1 mL of saline containing 6.25, 12.5, and 25.0 mg of SNs or 25.0 mg of microscale SiO2 particles suspensions for 30 d, were then sacrificed. Histopathological and ultrastructural change in lungs, and chemical components in the urine excretions were investigated by light microscope, TEM and EDS. MDA, NO and hydroxyproline (Hyp) in lung homogenates were quantified by spectrophotometry. Contents of TNF-α, TGF-β1, IL-1β, and MMP-2 in lung tissue were determined by immunohistochemistry staining.

RESULTSThere is massive excretion of Si substance in urine. The SNs lead pulmonary lesions of rise in lung/body coefficients, lung inflammation, damaged alveoli, granuloma nodules formation, and collagen metabolized perturbation, and lung tissue damage is milder than those of microscale SiO2 particles. The SNs also cause increase lipid peroxidation and high expression of cytokines.

CONCLUSIONThe SNs result into pulmonary fibrosis by means of increase lipid peroxidation and high expression of cytokines. Milder effect of the SNs on pulmonary fibrosis comparing to microscale SiO2 particles is contributed to its elimination from urine due to their ultrafine particle size.

Air Pollutants ; toxicity ; Animals ; Dose-Response Relationship, Drug ; Lung ; drug effects ; pathology ; ultrastructure ; Male ; Microscopy, Electron, Transmission ; Nanoparticles ; toxicity ; Pulmonary Fibrosis ; chemically induced ; metabolism ; pathology ; Random Allocation ; Rats ; Rats, Wistar ; Silicon Dioxide ; toxicity ; Specific Pathogen-Free Organisms ; Spectrometry, X-Ray Emission ; Urine ; chemistry

Realgar nanoparticles (NPs) are increasingly used as therapeutic agents for their enhanced anti-proliferation effect and cytotoxicity on cancer cells. However, the alteration of particle size may enhance biological reactivity as well as toxicity. A LC/MS and GC/MS based metabolomics approach was employed to explore the mechanism of realgar NPs-induced hepatotoxicity and identify potential biomarkers. Male Sprague-Dawley rats were administrated intragastrically with realgar or realgar NPs at a dose of 1.0 g·kg·d for 28 days and toxic effects of realgar NPs on liver tissues were examined by biochemical indicator analysis and histopathologic examination. Increased levels of serum enzymes and high hepatic steatosis were discovered in the realgar NPs treated group. Multivariate data analysis revealed that rats with realgar NPs-induced hepatotoxicity could be distinctively differentiated from the animals in the control and realgar treated groups. In addition, 21 and 32 endogenous metabolites were apparently changed in the serum and live extracts, respectively. Realgar NPs might induce free fatty acid and triglyceride accumulation, resulting in hepatotoxicity. In conclusion, the present study represents the first comprehensive LC/MS- and GC/MS-based metabolomics analysis of realgar NPs-induced hepatotoxicity, which may help further research of nanotoxicity.
Animals ; Biomarkers ; blood ; chemistry ; Chromatography, Liquid ; methods ; Fatty Acids ; metabolism ; Gas Chromatography-Mass Spectrometry ; methods ; Liver ; chemistry ; drug effects ; metabolism ; Male ; Mass Spectrometry ; methods ; Metabolomics ; methods ; Nanoparticles ; toxicity ; Rats ; Rats, Sprague-Dawley ; Triglycerides ; metabolism

Cobalt or chromium alloys are the most common clinical materials of prosthesis and there have been some investigators at home and abroad have done related researches about the genotoxic effects of cobalt and chromium ions and nanoparticles. People have certain understanding about the mechanism of production of ions as well as their influence on cells. However, chromium or cobalt nanoparticles genotoxicity related research is still in its preliminary stage. In each stage, the mechanisms, from creating of the particles, through entering cells, until finally causing genotoxic, are still contained many problems to be solved. This article reviews the research progress in mechanisms of production and genotoxic effects of cobalt, chromium ions and nanoparticles.
Chromium ; toxicity ; Cobalt ; toxicity ; DNA Damage ; Humans ; Ions ; Nanoparticles ; toxicity ; Prostheses and Implants

OBJECTIVETo explore the protein expression of heme oxygenase-1 (HO-1) and platelet endothelial cell adhesion molecules-1 (PECAM-1) in human coronary artery endothelial cells induced with Zinc Oxide Nanoparticle (ZnO-NPs).

METHODSMTT assay was used to determine the cell viability of ZnO-NPs. Levels of HO-1 and PECAM-1 protein in culture supernatants were measured using ELISA after human coronary artery endothelial cells were treated with different concentrations (0, 10, 20, 40µg/ml) of ZnO-NPs for 24 h.

RESULTSThe cell viability of human coronary artery endothelial cells in each group was 89.76%, 83.61%, 63.10%, 53.20%, 48.11%, 42.35%, 38.06%, 25.44% respectively when treated with different concentrations of ZnO-NPs (12.5, 25, 50, 70, 80, 90, 100, 200µg/ml). Protein levels of HO-1 (ng/L) in each group were 0.041±0.011, 0.512±0.076, 0.906±0.059, 1.062±0.089 respectively after the stimulation of different concentrations of ZnO-NPs (0, 10, 20, 40µg/ml). Comparisons in each group were statistically significant (P < 0.05). Protein levels of PECAM-1 (µg/L) in each group were 7.966 ± 0.046, 7.993 ± 0.036, 8.629 ± 0.052, 8.811 ± 0.039 respectively after the stimulation of different concentrations of ZnO-NPs (0, 10, 20, 40 µg/ml). Compared with the control group, protein levels of PECAM-1 increased (P < 0.05) when the concentration of ZnO-NPs was 20µg/ml or 40 µg/ml.

CONCLUSIONZnO-NPs stimulation could inhibit the viability of human coronary artery endothelial cells and upregulate the protein expression of HO-1 and PECAM-1.

Blood Platelets ; Cell Survival ; Coronary Vessels ; Endothelial Cells ; drug effects ; Heme Oxygenase-1 ; metabolism ; Humans ; Nanoparticles ; toxicity ; Platelet Endothelial Cell Adhesion Molecule-1 ; metabolism ; Zinc Oxide ; toxicity

OBJECTIVES: With recent advances in nanoparticle manufacturing and applications, potential exposure to nanoparticles in various settings is becoming increasing likely. No investigation has yet been performed to assess whether respiratory tract exposure to cerium oxide (CeO2) nanoparticles is associated with alterations in protein signaling, inflammation, and apoptosis in rat lungs. METHODS: Specific-pathogen-free male Sprague-Dawley rats were instilled with either vehicle (saline) or CeO2 nanoparticles at a dosage of 7.0 mg/kg and euthanized 1, 3, 14, 28, 56, or 90 days after exposure. Lung tissues were collected and evaluated for the expression of proteins associated with inflammation and cellular apoptosis. RESULTS: No change in lung weight was detected over the course of the study; however, cerium accumulation in the lungs, gross histological changes, an increased Bax to Bcl-2 ratio, elevated cleaved caspase-3 protein levels, increased phosphorylation of p38 MAPK, and diminished phosphorylation of ERK-1/2-MAPK were detected after CeO2 instillation (p<0.05). CONCLUSIONS: Taken together, these data suggest that high-dose respiratory exposure to CeO2 nanoparticles is associated with lung inflammation, the activation of signaling protein kinases, and cellular apoptosis, which may be indicative of a long-term localized inflammatory response.
Animals ; Apoptosis/*drug effects ; Caspase 3/metabolism ; Cerium/chemistry ; Inflammation ; Lung/*drug effects/metabolism/pathology ; Male ; Metal Nanoparticles/chemistry/*toxicity ; Mitogen-Activated Protein Kinase 1/metabolism ; Mitogen-Activated Protein Kinase 3/metabolism ; Mitogen-Activated Protein Kinases/*metabolism ; Phosphorylation/drug effects ; Proto-Oncogene Proteins c-bcl-2/metabolism ; Rats ; Rats, Sprague-Dawley ; Signal Transduction/*drug effects ; bcl-2-Associated X Protein/metabolism ; p38 Mitogen-Activated Protein Kinases/metabolism