ArticleEnvironmental science and pollution research international2021
Evidence of a non-apoptotic mode of cell death in microglial BV-2 cells exposed to different concentrations of zinc oxide nanoparticles.
Article in Environmental science and pollution research international, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
3 citing papers in PubMed, 12 citations in OpenAlex.
- Zinc Oxide Nanoparticle-Induced Neurotoxicity: Underlying Molecular Mechanisms and Future Perspectives.Toxics · 2025Review
- Metal nanoparticles in neuroinflammation: impact on microglial dynamics and CNS function.RSC advances · 2025Review
- CysLTBrain sciences · 2022Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Zinc oxide nanoparticles (ZnO NPs) possess huge application potential. However, the toxicity of ZnO NPs is a great cause of concern. Indeed, ZnO NPs have been found to cause neurotoxicity. As microglial dysfunctions have been linked to the neurotoxic potential of NPs, the physico-chemical properties of ZnO NPs were determined and their cytotoxic effects were characterised on murine microglial BV-2 cells. In-house prepared and meticulously characterised ZnO NPs exhibited narrow size distribution with an average size of around 20 nm and a zeta potential at physiological pH around 24 mV. ZnO NPs did not exhibit aggregation in the cell culture medium. When microglial BV-2 cells were exposed for 6 and 24 h to ZnO NPs (5, 10, 20, 40, and 80 μg/mL), several cell damages were observed. Cellular accumulation of NPs in microglial BV-2 cells was associated with cell growth inhibition and cell death induction, measured by the trypan blue exclusion and MTT assays. Mitochondrial dysfunction and lysosomal alteration were associated with increased plasma membrane permeability measured by staining with DiOC
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Registered trials
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