ArticleInternational journal of nanomedicine2013
Multinucleation and cell dysfunction induced by amorphous silica nanoparticles in an L-02 human hepatic cell line.
Article in International journal of nanomedicine, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 33 citations in OpenAlex.
- Fine particulate matter‑induced cardiac developmental toxicity (Review).Experimental and therapeutic medicine · 2025Review
- PARP-1 overexpression does not protect HaCaT cells from DNA damage induced by SiOToxicology research · 2021Article
- Quantitative evaluation of cellular internalization of polymeric nanoparticles within laryngeal cancer cells and immune cells for enhanced drug delivery.Nanoscale research letters · 2021Article
- Multinuclei Occurred Under Cryopreservation and Enhanced the Pathogenicity ofFrontiers in microbiology · 2021Article
- The chronic effect of amorphous silica nanoparticles and benzo[Toxicology research · 2019Article
- Toxicology of silica nanoparticles: an update.Archives of toxicology · 2017Review
- Co-exposure to amorphous silica nanoparticles and benzo[a]pyrene at low level in human bronchial epithelial BEAS-2B cells.Environmental science and pollution research international · 2016Article
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
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Abstract
Silica nanoparticles (SNPs) are one of the most important nanomaterials, and have been widely used in a variety of fields. Therefore, their effects on human health and the environment have been addressed in a number of studies. In this work, the effects of amorphous SNPs were investigated with regard to multinucleation in L-02 human hepatic cells. Our results show that L-02 cells had an abnormally high incidence of multinucleation upon exposure to silica, that increased in a dose-dependent manner. Propidium iodide staining showed that multinucleated cells were arrested in G2/M phase of the cell cycle. Increased multinucleation in L-02 cells was associated with increased generation of cellular reactive oxygen species and mitochondrial damage on flow cytometry and confocal microscopy, which might have led to failure of cytokinesis in these cells. Further, SNPs inhibited cell growth and induced apoptosis in exposed cells. Taken together, our findings demonstrate that multinucleation in L-02 human hepatic cells might be a failure to undergo cytokinesis or cell fusion in response to SNPs, and the increase in cellular reactive oxygen species could be responsible for the apoptosis seen in both mononuclear cells and multinucleated cells.
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