Disturbed mitochondrial quality control involved in hepatocytotoxicity induced by silica nanoparticles

Nanoscale
Yi QiZhiwei Sun

Abstract

The extensive application of silica nanoparticles (SiNPs) brings about inevitable occupational, environmental, and even iatrogenic exposure for human beings. The liver, which is rich in mitochondria, is one of the target organs of SiNPs, but the underlying mechanisms by which these nanoparticles (NPs) interact with liver mitochondria and affect their functions still remain unclear. In the present study, we examined silicon nanoparticle (SiNP)-induced mitochondrial dysfunction, and further revealed its negative effects on mitochondrial quality control (MQC) in the human liver cell line L-02, including mitochondrial dynamics, mitophagy and biogenesis. Consequently, SiNPs induced cellular injury, accompanied by mitochondrial dysfunction, including mitochondrial reactive oxygen generation and mitochondrial membrane potential collapse. In line with the transmission electron microscopy (TEM)-observed abnormalities in the mitochondrial morphology and length distribution, a fission phenotype was manifested in the mitochondria of SiNP-exposed cells, and up-regulated DRP1 and FIS1, and down-regulated MFN1, were detected. Furthermore, the enhanced LC3II level, colocalization of the mitochondria and lysosomes, activated PINK1/Parkin signal...Continue Reading

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Methods Mentioned

BETA
dynamic light scattering
flow cytometry
PCR

Software Mentioned

Image J
Image LabTM
ImageJ

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