What is it about?
Amorphous silica nanoparticles (SiO2 NPs) have been regarded as relatively benign nanomaterials, however, this widely held opinion has been questioned in recent years by several reports on in vitro and in vivo toxicity. Surface chemistry, more specifically the surface silanol content, has been identified as an important toxicity modulator for SiO2 NPs. Here, quantitative relationships between the silanol content on SiO2 NPs, free radical generation and toxicity have been identified, with the purpose of synthesizing safer-by-design fumed silica nanoparticles.
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Why is it important?
Consistent and statistically significant trends were seen between the total silanol content, cell membrane damage, and cell viability, but not with intracellular reactive oxygen species (ROS), in the macrophages RAW264.7. SiO2 NPs with lower total silanol content exhibited larger adverse cellular effects. The SAEC epithelial cell line did not show any sign of toxicity by any of the nanoparticles. Free radical generation and surface reactivity of these nanoparticles were also influenced by the temperature of combustion and total silanol content.
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This page is a summary of: Safer-by-design flame-sprayed silicon dioxide nanoparticles: the role of silanol content on ROS generation, surface activity and cytotoxicity, Particle and Fibre Toxicology, October 2019, Springer Science + Business Media,
DOI: 10.1186/s12989-019-0325-1.
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Supplementary Information
Additional file 1: Figure S1. TGA temperature-time profile (right ordinate, dashed line), corresponding sample mass (left ordinate) of as-produced (solid lines) and the mass loss normalized to the mass at the end of Step 1. Figure S2. XPS analysis. (a) Si-OH/O-Si-O ratio and total silanol content varying as a function of the combustion enthalpy. (b) Si-OH/O-Si-O ratio as a function of the total silanol. Figure S3. Determining the critical delivered sonication energy of SiO2 NPs. (a) Mean hydrodynamic diameter and (b) polydispersity index as a function of dispersion sonication energy of Wetchem SiO2 NPs, FSP made SiO2 NPs and commercial fumed SiO2 NPs in DI H2O. Figure S4. Fate and transport modeling results for SiO2 NPs. (a) Delivered-to-cell concentration normalized to the administered dose and (b) delivered-to-cell fraction deposited of wet chemistry made silica, FSP made SiO2 NPs and commercial fumed SiO2 NPs in RPMI + 10% (vol/vol) FBS. Solid lines are the fitting curves obtained using eq. 1 and 2. Figure S5. Importance of other modulators in silica NPs effect analyzing RAW264.7 cells. (a, b) short-lived ROS and H2O2 produced by the different SiO2 NPs at a fixed value of silanol content of 150 nmol. (c) Cytotoxicity of different SiO2 NPs at a fixed value of delivered silanol per cell area of 1 × 1014 #/cm2. (d) Viability of different SiO2 NPs at a fixed value of delivered silanol per cell area of 1.5 × 1014 #/cm2. Figure S6. Cytotoxicity (a) and Viability (PrestoBlue assay) (b) measured in SAEC cells. The data represented as function of total silanol delivered per cell area for the three delivered doses used. Data represent an average of three independent experiments performed in triplicate. Figure S7. ROS generation as a measure of oxidative damage (CellROX Green assay) in SAEC cells. After 24-h treatment, ROS generation was measured and data represented as function of total silanol delivered per cell area for the three delivered doses used. Data represent an average of three independent experiments performed in triplicate. Figure S8. Cytotoxicity measured in RAW264.7 cells. The data is represented as function of short life ROS-H2O2 eq. nmol. Data represent an average of three independent experiments performed in triplicate. Table S1. Mean values of the parameters obtained for suspension preparation and colloidal characterization of wet chemistry made silica, FSP made silicas and commercial fumed silica in H2O and RPMI + 10% (vol/vol) FBS. Table S2. The short-lived ROS and H2O2 generated from seven types of silica over the 10–100 μg/mL range. Values have been corrected for sonication and background oxidation of Trolox.
Paper
Surface silanol content plays an important role in cellular toxicity and surface reactivity, although it might not be the sole factor influencing fumed silica NP toxicity. It was demonstrated that synthesis conditions for SiO2 NPs influence the type and quantity of free radicals, oxidative stress, nanoparticle interaction with the biological milieu they come in contact with, and determine the specific mechanisms of toxicity. We demonstrate here that it is possible to produce much less toxic fumed silicas by modulating the synthesis conditions.
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