Astrocytes Are More Vulnerable than Neurons to Silicon Dioxide Nanoparticle Toxicity in Vitro.
Jorge Humberto Limón-PachecoNatalie Jiménez-BarriosAlejandro Déciga-AlcarazAdriana Martinez-CuazitlMonica Maribel Mata-MirandaGustavo Jesus Vazquez-ZapienPedraza-Chaverri JoséYolanda Irasema ChirinoMarisol Orozco-IbarraPublished in: Toxics (2020)
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.
Keyphrases
- oxide nanoparticles
- spinal cord
- high resolution
- magnetic nanoparticles
- electron microscopy
- cell death
- single cell
- endothelial cells
- high density
- white matter
- spinal cord injury
- magnetic resonance imaging
- blood brain barrier
- optical coherence tomography
- mesenchymal stem cells
- fatty acid
- bone marrow
- signaling pathway
- mass spectrometry
- subarachnoid hemorrhage
- brain injury
- dna binding
- case control