5 research outputs found
Durability of CaO–CaZrO<sub>3</sub> Sorbents for High-Temperature CO<sub>2</sub> Capture Prepared by a Wet Chemical Method
Powders of CaO sorbent modified with
CaZrO<sub>3</sub> have been
synthesized by a wet chemical route. For carbonation and calcination
conditions relevant to sorbent-enhanced steam reforming applications,
a powder of composition 10 wt % CaZrO<sub>3</sub>/90 wt % CaO showed
an initial rise in CO<sub>2</sub> uptake capacity in the first 10
carbonation–decarbonation cycles, increasing from 0.31 g of
CO<sub>2</sub>/g of sorbent in cycle 1 to 0.37 g of CO<sub>2</sub>/g of sorbent in cycle 10 and stabilizing at this value for the remainder
of the 30 cycles tested, with carbonation at 650 °C in 15% CO<sub>2</sub> and calcination at 800 °C in air. Under more severe
conditions of calcination at 950 °C in 100% CO<sub>2</sub>, following
carbonation at 650 °C in 100% CO<sub>2</sub>, the best overall
performance was for a sorbent with 30 wt % CaZrO<sub>3</sub>/70 wt
% CaO (the highest Zr ratio studied), with an initial uptake of 0.36
g of CO<sub>2</sub>/g of sorbent, decreasing to 0.31 g of CO<sub>2</sub>/g of sorbent at the 30th cycle. Electron microscopy revealed that
CaZrO<sub>3</sub> was present in the form of ≤0.5 μm
cuboid and 20–80 nm particles dispersed within a porous matrix
of CaO/CaCO<sub>3</sub>; the nanoparticles are considered to be the
principal reason for promoting multicycle durability
Ferritin-protein levels in Caco-2 cells following exposure to LM Fe(III) poly oxo-hydroxide (nano Fe), Fe(III) maltol (FeM) or Fe(II) sulphate-ascorbate (FeSO<sub>4</sub> + AA).
<p><b>A</b>, Ferritin-protein regulation in differentiated and undifferentiated cells. ***, <i>p</i>=0.0003. Cells were incubated for 1 h with 200 μM Fe plus a further 23 h in fresh, non-supplemented MEM to allow for ferritin formation. <b>B</b>, Phase distribution of Fe in the BSS uptake medium: i.e. fractional percentage of microparticulate (black bars), nanoparticulate (red bars) and soluble Fe (open bars) for each Fe material. Values are mean ± s.d. of 3 independent experiments. <b>C</b>, Effect of LM Fe(III) poly oxo-hydroxide particle dispersion (in BSS medium, closed bars) or agglomeration (in MEM medium, open bars) on ferritin-protein levels in differentiated cells: the LM Fe(III) poly oxo-hydroxide was dispersed in its nano-form (99 ± 2% nano) using BSS or agglomerated (97 ± 2% microparticulate) using MEM. Data are mean of 3 independent experiments (each experiment with 3 replicate wells). FeM: soluble iron control, Fe(III) maltol. ***, <i>p</i>=0.0002 for the comparison between BSS and MEM. <b>D</b>, TEER changes in differentiated Caco-2 cell monolayer at different time points during incubation with BSS supplemented with LM Fe(III) poly oxo-hydroxide (open circles) or non-supplemented BSS control (closed inverted triangles). Incubations were for 3 h with 200 μM Fe (measurements at 1, 2 & 3 h) plus a further 21 h in fresh, non-supplemented MEM (24-h). Values are expressed as a percentage of the initial measurement and are shown as mean ± s.d. of 3 independent experiments (each experiment with 3 replicate wells). Experimental points are connected with a solid line to aid visualization and not because a linear relationship is assumed between time and TEER measurement. Detailed methodology is available in the Methods Section and in Methods S1.</p
Lysososmal dissolution of LM Fe(III) poly oxo-hydroxide.
<p><b>A</b>, Solubility in simulated lysosomal conditions at pH 5.0 with 10 mM citric acid and 0.15 M NaCl. Soluble Fe was measured by ICP-OES following 5 min ultrafiltration (3000 Da MWCO) for the LM Fe(III) poly oxo-hydroxide (black) and for un-modified Fe(III) poly oxo-hydroxide (solid blue). Nanoparticulate Fe was obtained from the Fe in the supernatant following centrifugation excluding the soluble (ultrafilterable) Fe, and is shown for LM Fe(III) poly oxo-hydroxide (red) and for un-modified Fe(III) poly oxo-hydroxide (dotted blue). Values are plotted as mean ± s.d. of 3 independent experiments (each experiment with 3 replicates). <b>B</b>, Effect of inhibition of lysosomal acidification using monensin on Fe utilization by differentiated Caco-2 cells. Data are shown as a percentage of the control (without monensin) at 24 h: i.e. 1 h exposure to 200 µM nanoparticulate LM Fe(III) poly oxo-hydroxide (open circles) or Fe(III) maltol (closed squares) ± 5-30 µM monensin followed by 23 h in non-supplemented MEM. Results are means ± s.d. of 3 independent experiments (each experiment with 3 replicate wells). **, <i>p</i><0.005; ***, <i>p</i><0.001 in relation to the soluble Fe control (Fe(III)maltol). <b>C</b>, Change in TEER in the Caco-2 cell monolayer following 1 h exposure to 10 μM monensin (closed squares), 30 μM monensin (open diamonds) or non-supplemented BSS control (closed inverted triangles) and with 23 h further incubation in fresh MEM (24 h in total). Values are expressed as a percentage of the initial measurement at the start of the exposure time (corresponding to 0 h) and are shown as mean ± s.d. of 2 independent experiments (each experiment with 3 replicate wells). Experimental points are connected with a solid line to aid visualization and not because a linear relationship is assumed between time and TEER measurement. ***, <i>p</i>=0.0003; ****, <i>p</i><0.0001 in relation to the non-supplemented BSS control.</p
Characterisation of hydrolysed Fe(III) with simulated digestion and of aquated LM Fe(III) poly oxo-hydroxide.
<p><b>A</b>, Transmission Electron Microscopy (TEM) images collected from a drop of suspension after simulated digestion of 1 mM Fe(III) chloride in the presence of 2 g/L mucin and low molecular weight ligands. The boxed regions are shown magnified below and highlight the presence of fine, poorly crystalline nanoparticles dispersed in an amorphous gel. Crystallinity is indicated by the spots in the inset diffractograms (fast Fourier transforms) in the boxed regions and lattice spacings are discussed in the main text. Scale bar represents 5 nm. <b>B</b>, Whole area EDX analysis of a particle agglomerate similar to those in ‘A’ shows elemental compositions (the specimen support film and grid produce the background C and Cu signals respectively). <b>C</b>, Hydrodynamic size distribution of nanoparticulate 500 µM LM Fe(III) poly oxo-hydroxide in balanced salt solution (BSS) measured by Dynamic Light Scattering (DLS). Values are expressed as mean diameter ± s.d. (3 independent measurements) on a log<sub>10</sub> scale.</p
Systematic Investigation of the Physicochemical Factors That Contribute to the Toxicity of ZnO Nanoparticles
ZnO
nanoparticles (NPs) are prone to dissolution, and uncertainty
remains whether biological/cellular responses to ZnO NPs are solely
due to the release of Zn<sup>2+</sup> or whether the NPs themselves
have additional toxic effects. We address this by establishing ZnO
NP solubility in dispersion media (Dulbecco’s modified Eagle’s
medium, DMEM) held under conditions identical to those employed for
cell culture (37 °C, 5% CO<sub>2</sub>, and pH 7.68) and by systematic
comparison of cell–NP interaction for three different ZnO NP
preparations. For NPs at concentrations up to 5.5 μg ZnO/mL,
dissolution is complete (with the majority of the soluble zinc complexed
to dissolved ligands in the medium), taking ca. 1 h for uncoated and
ca. 6 h for polymer coated ones. Above 5.5 μg/mL, the results
are consistent with the formation of zinc carbonate, keeping the solubilized
zinc fixed to 67 μM of which only 0.45 μM is as free Zn<sup>2+</sup>, i.e., not complexed to dissolved ligands. At these relatively
high concentrations, NPs with an aliphatic polyether-coating show
slower dissolution (i.e., slower free Zn<sup>2+</sup> release) and
reprecipitation kinetics compared to those of uncoated NPs, requiring
more than 48 h to reach thermodynamic equilibrium. Cytotoxicity (MTT)
and DNA damage (Comet) assay dose–response curves for three
epithelial cell lines suggest that dissolution and reprecipitation
dominate for uncoated ZnO NPs. Transmission electron microscopy combined
with the monitoring of intracellular Zn<sup>2+</sup> concentrations
and ZnO–NP interactions with model lipid membranes indicate
that an aliphatic polyether coat on ZnO NPs increases cellular uptake,
enhancing toxicity by enabling intracellular dissolution and release
of Zn<sup>2+</sup>. Similarly, we demonstrate that needle-like NP
morphologies enhance toxicity by apparently frustrating cellular uptake.
To limit toxicity, ZnO NPs with nonacicular morphologies and coatings
that only weakly interact with cellular membranes are recommended