Role of humic acid in the stability of Ag nanoparticles in suboxic conditions

Stability and temporal changes in size distributions have been observed for citrate- (cit) and polyvinylpyrrolidone- (PVP) capped silver nanoparticles (AgNPs), in the presence or absence of sulfide and natural organic matter (NOM, as humic acid), while under suboxic conditions. There were substantial differences in the influence of the two capping agents, with PVP–AgNPs showing few or no significant changes in apparent stability or particle size distribution under the conditions examined, while the apparent size distributions of citrate-capped AgNPs changed rapidly. Sulfide and humic acid each individually caused immediate increases in cit–AgNP size distributions, which were then relatively stable over 60–145 days. This may be due to sulfide bridging and cation bridging, respectively. However, in competition, it was the influence of the humic acid that dominated that of the sulfide. These observations have implications for environmental fate and toxicity of AgNP. The increased stability in the presence of even low concentrations of NOM may limit the rapidity of Ag dispersal but may also concentrate the dose received by organisms, which subsequently ingest the stabilized particles

Mechanisms of iron uptake from ferric phosphate nanoparticles in human intestinal Caco-2 cells

Food fortification programs to reduce iron deficiency anemia require bioavailable forms of iron that do not cause adverse organoleptic effects. Rodent studies show that nano-sized ferric phosphate (NP-FePO4) is as bioavailable as ferrous sulfate, but there is controversy over the mechanism of absorption. We undertook in vitro studies to examine this using a Caco-2 cell model and simulated gastrointestinal (GI) digestion. Supernatant iron concentrations increased inversely with pH, and iron uptake into Caco-2 cells was 2–3 fold higher when NP-FePO4 was digested at pH 1 compared to pH 2. The size and distribution of NP-FePO4 particles during GI digestion was examined using transmission electron microscopy. The d50 of the particle distribution was 413 nm. Using disc centrifugal sedimentation, a high degree of agglomeration in NP-FePO4 following simulated GI digestion was observed, with only 20% of the particles ≤1000 nm. In Caco-2 cells, divalent metal transporter-1 (DMT1) and endocytosis inhibitors demonstrated that NP-FePO4 was mainly absorbed via DMT1. Small particles may be absorbed by clathrin-mediated endocytosis and micropinocytosis. These findings should be considered when assessing the potential of iron nanoparticles for food fortificatio

Preparation, characterisation and toxicology of cerium oxide nanoparticles

Ceria nanoparticles have a range of uses, including industrial polishing of silicon wafers and as a diesel fuel additive. A proportion of nanoparticles will be released into the environment. The size of nanoparticles provides the potential for interaction with living cells, as they are similar in size to natural organic matter and biological molecules. Pseudomonas putida are bacteria which live in soil, and this work assessed the toxicity of ceria nanoparticles to these organisms. Suspensions of ceria nanoparticles were prepared and characterised. A batch of nanoparticles was tested for toxicity alongside commercial ceria nanoparticles. Bacteria were cultured in Minimal Davis Media and ceria nanoparticle concentrations between 5mgL-1 and 100mgL-1 were used in toxicity trials. Bacterial growth was monitored over 24 hours, with and without nanoparticles, by the increase in turbidity at 595nm in a well plate reader. Inhibition of bacterial growth due the cerium oxide nanoparticles was evaluated. Commercial ceria inhibited the growth of the P. putida bacteria, but the lower concentrations of ceria were shown to be more toxic than the higher concentrations. Ceria nanoparticles prepared in this laboratory showed no toxicity, and appeared to enhance the growth of the bacteria

Dissolution and bandgap paradigms for predicting the toxicity of metal oxide nanoparticles in the marine environment: an <i>in vivo</i> study with oyster embryos

<p>Dissolution and bandgap paradigms have been proposed for predicting the ability of metal oxide nanoparticles (NPs) to induce oxidative stress in different <i>in vitro and in vivo</i> models. Here, we addressed the effectiveness of these paradigms <i>in vivo</i> and under conditions typical of the marine environment, a final sink for many NPs released through aquatic systems. We used ZnO and MnO₂ NPs as models for dissolution and bandgap paradigms, respectively, and CeO₂ NPs to assess reactive oxygen radical (ROS) production via Fenton-like reactions <i>in vivo</i>. Oyster embryos were exposed to 0.5–500 μM of each test NP over 24 h and oxidative stress was determined as a primary toxicity pathway across successive levels of biological complexity, with arrested development as the main pathological outcome. NPs were actively ingested by oyster larvae and entered cells. Dissolution was a viable paradigm for predicting the toxicity of NPs in the marine environment, whereas the surface reactivity based paradigms (i.e. bandgap and ROS generation via Fenton-like reaction) were not supported under seawater conditions. Bio-imaging identified potential cellular storage-disposal sites of solid particles that could ameliorate the toxicological behavior of non-dissolving NPs, whilst abiotic screening of surface reactivity suggested that the adsorption-complexation of surface active sites by seawater ions could provide a valuable hypothesis to explain the quenching of the intrinsic oxidation potential of MnO₂ NPs in seawater.</p

Surfactant protein A (SP-A) inhibits agglomeration and macrophage uptake of toxic amine modified nanoparticles.

The lung provides the main route for nanomaterial exposure. Surfactant protein A (SP-A) is an important respiratory innate immune molecule with the ability to bind or opsonise pathogens to enhance phagocytic removal from the airways. We hypothesised that SP-A, like surfactant protein D, may interact with inhaled nanoparticulates, and that this interaction will be affected by nanoparticle (NP) surface characteristics. In this study, we characterise the interaction of SP-A with unmodified (U-PS) and amine-modified (A-PS) polystyrene particles of varying size and zeta potential using dynamic light scatter analysis. SP-A associated with both 100?nm U-PS and A-PS in a calcium-independent manner. SP-A induced significant calcium-dependent agglomeration of 100?nm U-PS NPs but resulted in calcium-independent inhibition of A-PS self agglomeration. SP-A enhanced uptake of 100?nm U-PS into macrophage-like RAW264.7 cells in a dose-dependent manner but in contrast inhibited A-PS uptake. Reduced association of A-PS particles in RAW264.7 cells following pre-incubation of SP-A was also observed with coherent anti-Stokes Raman spectroscopy. Consistent with these findings, alveolar macrophages (AMs) from SP-A(-/-) mice were more efficient at uptake of 100?nm A-PS compared with wild type C57Bl/6 macrophages. No difference in uptake was observed with 500?nm U-PS or A-PS particles. Pre-incubation with SP-A resulted in a significant decrease in uptake of 100?nm A-PS in macrophages isolated from both groups of mice. In contrast, increased uptake by AMs of U-PS was observed after pre-incubation with SP-A. Thus we have demonstrated that SP-A promotes uptake of non-toxic U-PS particles but inhibits the clearance of potentially toxic A-PS particles by blocking uptake into macrophages

Cerium oxide nanoparticles induce oxidative stress in the sediment-dwelling amphipod <i>Corophium volutator</i>

<p>Cerium oxide nanoparticles (CeO₂ NPs) exhibit fast valence exchange between Ce(IV) and Ce(III) associated with oxygen storage and both pro and antioxidant activities have been reported in laboratory models. The reactivity of CeO₂ NPs once they are released into the aquatic environment is virtually unknown, but this is important to determine for assessing their environmental risk. Here, we show that amphipods (<i>Corophium volutator</i>) grown in marine sediments containing CeO₂ NPs showed a significant increase in oxidative damage compared to those grown in sediments without NPs and those containing large-sized (bulk) CeO₂ particles. There was no exposure effect on survival, but significant increases in single-strand DNA breaks, lipid peroxidation and superoxide dismutase activity were observed after a 10-day exposure to 12.5 mg L⁻¹ CeO₂. Characterisation of the CeO₂ NPs dispersed in deionised or saline exposure waters revealed that more radicals were produced by CeO₂ NPs compared with bulk CeO₂. Electron energy loss spectroscopy (EELS) analysis revealed that both CeO₂ NPs were predominantly Ce(III) in saline waters compared to deionised waters where they were predominantly Ce(IV). In both types of medium, the bulk CeO₂ consisted mainly of Ce(IV). These results support a model whereby redox cycling of CeO₂ NPs between Ce(III) and Ce(IV) is enhanced in saline waters, leading to sublethal oxidative damage to tissues in our test organism.</p