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Silver nanoparticles modulate mitochondrial dynamics and biogenesis in HepG2 cells.

Jiangyan Li1, Bangyong Zhang1, Xiaoru Chang1

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Silver nanoparticles (AgNPs) disrupt mitochondrial function and structure in HepG2 cells. This damage impacts mitochondrial dynamics and biogenesis, highlighting mitochondria as a key target for AgNP toxicity.

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Area of Science:

  • Cell Biology
  • Nanotoxicology
  • Biochemistry

Background:

  • Silver nanoparticles (AgNPs) are widely used, raising concerns about their environmental release and toxicity.
  • Previous research links AgNP exposure in HepG2 cells to mitochondrial damage, including ROS increase, membrane potential collapse, and apoptosis.

Purpose of the Study:

  • To investigate the effects of AgNPs on mitochondrial dynamics and biogenesis in HepG2 cells.
  • To elucidate the molecular mechanisms underlying AgNP-induced mitochondrial dysfunction.

Main Methods:

  • Exposure of HepG2 cells to AgNPs.
  • Analysis of mitochondrial morphology and structure.
  • Western blot analysis of key proteins involved in mitochondrial fission/fusion (Drp1, Fis1, OPA1, Mff, Mfn1, Mfn2), mitochondrial biogenesis (PGC-1α), and autophagy (LC3B, p62).

Main Results:

  • AgNPs induced significant alterations in mitochondrial morphology and structure.
  • AgNPs altered the expression of proteins regulating mitochondrial dynamics, notably up-regulating p-Drp1 (Ser616) and reducing PGC-1α.
  • Increased expression of autophagy markers (LC3B, p62) was observed in AgNP-treated cells.

Conclusions:

  • AgNPs trigger cytotoxicity by targeting mitochondria, disrupting their function, structure, and dynamics.
  • Mitochondrial biogenesis and dynamics are impaired by AgNP exposure.
  • Mitochondria serve as a critical target for AgNP toxicity and their functions can be used to assess AgNP cytotoxicity.