Nickel Oxide Nanoparticles Induced Transcriptomic Alterations in HEPG2 Cells.

Area of Science:

• Toxicology
• Nanotechnology
• Molecular Biology

Background:

• Nickel oxide nanoparticles (NiO-NPs) are widely used, raising concerns about their potential toxicity.
• A comprehensive understanding of NiO-NPs toxicity in human cells is still needed.

Purpose of the Study:

• To elucidate the toxicity mechanisms of NiO-NPs in human hepatocellular carcinoma (HepG2) cells.
• To integrate transcriptomic and genotoxic data for a detailed analysis.

Main Methods:

• Comet assay for DNA damage assessment.
• Flow cytometry for reactive oxygen species (ROS) detection.
• Real-time PCR and qPCR array for gene expression analysis (apoptotic and oxidative stress genes).

Main Results:

• NiO-NPs induced significant DNA damage (26-fold increase in tail moment at 100 μg/ml).
• Concentration-dependent increase in intracellular ROS was observed.
• Upregulation of apoptotic (p53, bax, bcl2) and oxidative stress (SOD1) genes.
• Overexpression of mRNA transcripts related to six cellular pathways.

Conclusions:

• NiO-NPs induce significant oxidative stress and DNA damage in HepG2 cells.
• NiO-NPs trigger apoptosis and alter cellular transcriptome.
• The findings provide unequivocal evidence for NiO-NPs toxicity mechanisms in human liver cells.