Influence of silicon dioxide nanoparticles on dielectric relaxation of triglycine sulfate

Abstract Background Silicon dioxide nanoparticles (SiO2NPs) are widely used as additive in the food industry with controversial health risk. Gut microbiota is a new and hot topic in the field of nanotoxicity. It also contributes a novel and insightful view to understand the potential health risk of food-grade SiO2NPs in children, who are susceptible to the toxic effects of nanoparticles. Methods In current study, the young mice were orally administrated with vehicle or SiO2NPs solution for 28 days. The effects of SiO2NPs on the gut microbiota were detected by 16S ribosomal RNA (rRNA) gene sequencing, and the neurobehavioral functions were evaluated by open field test and Morris water maze. The level of inflammation, tissue integrity of gut and the classical indicators involved in gut–brain, gut–liver and gut–lung axis were all assessed. Results Our results demonstrated that SiO2NPs significantly caused the spatial learning and memory impairments and locomotor inhibition. Although SiO2NPs did not trigger evident intestinal or neuronal inflammation, they remarkably damaged the tissue integrity. The microbial diversity within the gut was unexpectedly enhanced in SiO2NPs-treated mice, mainly manifested by the increased abundances of Firmicutes and Patescibacteria. Intriguingly, we demonstrated for the first time that the neurobehavioral impairments and brain damages induced by SiO2NPs might be distinctively associated with the disruption of gut–brain axis by specific chemical substances originated from gut, such as Vipr1 and Sstr2. Unapparent changes in liver or lung tissues further suggested the absence of gut–liver axis or gut–lung axis regulation upon oral SiO2NPs exposure. Conclusion This study provides a novel idea that the SiO2NPs induced neurotoxic effects may occur through distinctive gut–brain axis, showing no significant impact on either gut–lung axis or gut–liver axis. These findings raise the exciting prospect that maintenance and coordination of gastrointestinal functions may be critical for protection against the neurotoxicity of infant foodborne SiO2NPs.

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Advanced Fiber Metal Laminates Filled with Silicon Dioxide Nanoparticles with Enhanced Mechanical Properties

Fibers and Polymers ◽

10.1007/s12221-021-0192-x ◽

2021 ◽

Author(s):

D. Saber ◽

M. A. Abd El-baky ◽

M. A. Attia

Keyword(s):

Mechanical Properties ◽

Silicon Dioxide ◽

Silicon Dioxide Nanoparticles ◽

Fiber Metal Laminates ◽

Fiber Metal

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Astrocytes Are More Vulnerable than Neurons to Silicon Dioxide Nanoparticle Toxicity in Vitro

Toxics ◽

10.3390/toxics8030051 ◽

2020 ◽

Vol 8 (3) ◽

pp. 51

Author(s):

Jorge Humberto Limón-Pacheco ◽

Natalie Jiménez-Barrios ◽

Alejandro Déciga-Alcaraz ◽

Adriana Martínez-Cuazitl ◽

Mónica Maribel Mata-Miranda ◽

...

Keyword(s):

Nucleic Acids ◽

Silicon Dioxide ◽

Culture Media ◽

Brain Cell ◽

Attenuated Total Reflection ◽

Random Coil ◽

Silicon Dioxide Nanoparticles ◽

Neurotoxic Effects ◽

Α Helix

Some studies have shown that silicon dioxide nanoparticles (SiO2-NPs) can reach different regions of the brain and cause toxicity; however, the consequences of SiO2-NPs exposure on the diverse brain cell lineages is limited. We aimed to investigate the neurotoxic effects of SiO2-NP (0–100 µg/mL) on rat astrocyte-rich cultures or neuron-rich cultures using scanning electron microscopy, Attenuated Total Reflection-Fourier Transform Infrared spectroscopy (ATR-FTIR), FTIR microspectroscopy mapping (IQ mapping), and cell viability tests. SiO2-NPs were amorphous particles and aggregated in saline and culture media. Both astrocytes and neurons treated with SiO2-NPs showed alterations in cell morphology and changes in the IR spectral regions corresponding to nucleic acids, proteins, and lipids. The analysis by the second derivative revealed a significant decrease in the signal of the amide I (α-helix, parallel β-strand, and random coil) at the concentration of 10 µg/mL in astrocytes but not in neurons. IQ mapping confirmed changes in nucleic acids, proteins, and lipids in astrocytes; cell death was higher in astrocytes than in neurons (10–100 µg/mL). We conclude that astrocytes were more vulnerable than neurons to SiO2-NPs toxicity. Therefore, the evaluation of human exposure to SiO2-NPs and possible neurotoxic effects must be followed up.

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