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Cerium dioxide nanoparticles induce apoptosis and autophagy in human peripheral blood monocytes

Salik Hussain1, Faris Al-Nsour, Annette B Rice

  • 1Clinical Research Unit, National Institute of Environmental Health Sciences/National Institute of Health, Research Triangle Park 27709, North Carolina, United States. salik.hussain@nih.gov

ACS Nano
|June 22, 2012
PubMed

Insights

Cerium dioxide nanoparticles (CeO(2) NPs) show toxicity in human monocytes by inducing apoptosis and autophagy. These nanoparticles damage mitochondria, leading to cell death even at low doses.

Area of Science:

  • Nanomedicine
  • Toxicology
  • Cell Biology

Background:

  • Cerium dioxide nanoparticles (CeO(2) NPs) have broad industrial applications and emerging therapeutic potential.
  • Limited mechanistic data exists on CeO(2) NP effects on primary human cells.
  • Understanding CeO(2) NP cytotoxicity in human monocytes is crucial for safety assessment.

Purpose of the Study:

  • To characterize the cytotoxic effects of CeO(2) NPs in primary human peripheral blood monocytes.
  • To elucidate the mechanisms underlying CeO(2) NP-induced cellular injury.
  • To investigate the roles of apoptosis, autophagy, and mitochondrial damage in CeO(2) NP toxicity.

Main Methods:

  • Characterization of CeO(2) NPs using TEM, dynamic light scattering, and zeta potential analysis.
  • Isolation of CD14+ monocytes from healthy human volunteers.
  • Exposure of monocytes to varying concentrations of CeO(2) NPs (0.5-10 microg/mL) for 20-40 hours.
  • Assessment of cell viability, apoptosis markers (Bax, mitochondrial membrane potential, DNA fragmentation), autophagy, and p53 activity.

Main Results:

  • TEM confirmed internalization of CeO(2) NPs into monocytes.
  • CeO(2) NP exposure significantly decreased cell viability and induced apoptosis via mitochondrial damage and apoptosis-inducing factor (AIF) overexpression.
  • Toxicity was independent of caspase activation and reactive oxygen species (ROS) production.
  • CeO(2) NPs triggered autophagy, which was enhanced by p53 inhibition and partially reversed cell death upon inhibition.

Conclusions:

  • CeO(2) NPs exhibit significant toxicity towards primary human monocytes at low doses.
  • Mitochondrial damage and AIF-mediated apoptosis are key mechanisms of CeO(2) NP toxicity.
  • Autophagy plays a protective role against CeO(2) NP-induced cell death in monocytes.

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