Mapping the Reactions in a Single Zero-Valent Iron Nanoparticle

Nanoscale zerovalent iron (nZVI) possesses unique functionalities for metal–metalloid removal and sequestration. So far, direct evidence on the heavy metal–nZVI reactions in the solid phase is still limited due to low concentration of heavy metals and small size of nanoparticles. In this work, angstrom-resolution spectral mappings on the reactions of nZVI with chromate, arsenate, nickel, silver, cesium, and zinc ions are presented. This work was achieved with spherical aberration-corrected scanning transmission electron microscopy integrated with high-sensitivity X-ray energy-dispersive spectroscopy-scanning transmission electron microscopy (XEDS-STEM). Results confirm that iron nanoparticles have a core–shell structure. In addition, the removal mechanism significantly depends on the standard potential <i>E</i>⁰ (<i>E</i>⁰ is standard potential w.r.t. standard hydrogen electrode at 25 °C when free ion activity is 1.). For strong oxidizing agents, such as Cr­(VI), the removal mechanism is diffusion and encapsulation in the core area of the nZVI particle. For moderate oxidizers, such as As­(V) with E⁰ more positive than that of iron, the removal mechanism is adsorption at the surface, followed by diffusion and encapsulation into the particle between the core and the shell. For metal cations with an E⁰ close to or more negative than that of iron, such as Cs­(I) and Zn­(II), the removal mechanism is sorption or surface-complex formation. For metal cations with <i>E</i>⁰ much more positive than that of iron, such as Ag­(I), the removal mechanism is rapid reduction on the surface of nZVI. Meanwhile, metals with <i>E</i>⁰ slightly more positive than that of iron, such as Ni­(II), can be immobilized at the nanoparticle surface via sorption and reduction. The synergetic effects of sorption, reduction, and encapsulation mechanisms of nZVI lead to rapid reactions and high efficiency for treatment and immobilization of many toxic heavy metals. Results also demonstrate that the XEDS-STEM technique is a powerful tool for studying reactions in individual nanoparticles and is particularly valuable for mapping trace-level elements in environmental media

Histopathologic examinations by H&E (1 and 2) and PAS (3) in co-infection group.

<p>A1, B1 and C1 showed different lever of suppurative granulomatous inflammation in the dermis tissue at the 2^nd, 3^rd and 5^th weeks(×100); A2, B2 and C2 showed most of the inflammatory cells were histocytes and epithelioid cells around necrosis center (×400); A3, B3 and C3 showed <i>S. schenckii</i> cells (arrow) at the 2^nd, 3^rd and 5^th weeks (×400).</p

Morphology of <i>Taenia taeniaeformis</i>.

<p>(A) Taenia cyst covered the entire liver; (B) <i>Taenia taeniaeformis</i> larva with large scolex, long neck and pseudo segmentation of entire body length with terminal bulged portion. (C) Histology of a <i>Taenia</i> cyst revealed armed rostellum characterized by 2 rows of hooks and four suckers.</p

Cytokines IFN-γ, IL-10 and IL-17 released during <i>S. schenckii</i> infection and co-infection with <i>Taenia taeniaeformis</i> (A, B and C).

<p>IFN-γ and IL-10 (A and B) productions occurred in large amounts in the 1^st, 2^nd and 3^rd weeks after <i>S. schenckii</i> infection in fungus-infected group, and reached the peak in the 2^nd week PI. IL-17 productions (C) of the co-infected group. There was a significant difference between the two groups for IL-17 levels (P<0.05).</p

Histopathologic examinations by H&E (1 and 2) and PAS (3) in fungus-infection group.

<p>A1, B1 and C1 showed different level of suppurative granulomatous inflammation in the dermis tissue at the 2^nd, 3^rd and 5^th weeks(×100); A2, B2 and C2 showed multinucleated giant cells (arrow) were formed except histocytes and epithelioid cells around necrosis center (×400); A3 and B3 showed <i>S. schenckii</i> cells (arrow) in multinucleated giant cells at the 2^nd, 3^rd, and no <i>S. schenckii</i> cell was observed in C3 at the 5^th weeks PI (×400).</p

Dectin-1 immunohistochemical staining of skin lesions from the co-infected group (A) and fungus-infected group (B).

<p>A1–A2 showed a lot of positive cells in the lesion and mainly gathered in the tuberculosis-like layer. B1–B2 showed no positive cells.</p

Lesions of the co-infected group (A) and fungus-infected group (B): 1–3 showed the 2^nd, 3^rd and 5^th weeks post-inoculation (PI).

<p>Lesions of the co-infected group (A) and fungus-infected group (B): 1–3 showed the 2^nd, 3^rd and 5^th weeks post-inoculation (PI).</p

Expression of EGFR protein in lung SCC cells, lung ADC cells and the control of non-cancerous lung tissue were detected by IHC using specific antibody as described in the section of materials and methods.

<p>Strong positive staining of EGFR protein was found in cell membranes and cytoplasm of lung SCC and lung ADC cells (Fig 2A and 2B, 20×, IHC, DAB staining). Negative staining of EGFR was showed in non-cancerous lung tissue (Fig 2C, 20×, IHC, DAB staining). Negative control showed no EGFR staining in the lung SCC cells (Fig 2D, 20×, IHC, DAB staining).</p

Expression of Flot-2 and EGFR proteins in lung SCC and lung ADC compared to the control of non-cancerous lung tissues.

<p>Results showed that there were significant differences between the groups which were statistically evaluated by chi-square test.</p

Expression of Flot-2 protein in lung SCC cells, lung ADC cells and control of non-cancerous lung tissues were detected by IHC using specific antibody as described in the section of materials and methods.

<p>Strong positive staining of Flot-2 protein was found on cell membranes of lung SCC and lung ADC cells (Fig 1A and 1B, 20×, IHC, DAB staining). Negative staining of Flot-2 was showed in non-cancerous lung tissue (Fig 1C, 20×, IHC, DAB staining). Negative control showed no Flot-2 staining in lung ADC cells (Fig 1D, 20×, IHC, DAB staining).</p