Perfluorooctane Sulfonate (PFOS) Disrupts Mitochondrial Activity and Cell Adhesion in Liver Cells

Area of Science:

• Environmental Toxicology
• Molecular Toxicology
• Hepatology

Background:

• Perfluorooctane sulfonate (PFOS) is a persistent environmental pollutant with known health risks.
• The precise mechanisms of PFOS-induced liver toxicity are not fully elucidated.
• Understanding PFOS toxicology is crucial due to its widespread environmental distribution.

Purpose of the Study:

• To investigate the toxicological effects of PFOS on human liver cells.
• To explore the molecular mechanisms underlying PFOS-induced hepatotoxicity.
• To assess the impact of PFOS on cell viability, stress, and death pathways.

Main Methods:

• Utilized HepG2 and THLE-2 human hepatic cell models.
• Assessed cell viability, oxidative stress (ROS), and apoptosis.
• Performed transcriptomic analysis via cDNA sequencing and rt-qPCR.
• Determined inhibitory concentration (IC50) values.

Main Results:

• PFOS exposure caused a dose-dependent decrease in cell viability, with an IC50 around 100 micromolar.
• Observed morphological changes, elevated reactive oxygen species (ROS), and induced early apoptosis after 6 hours.
• Transcriptomic analysis revealed downregulation of mitochondrial oxidative phosphorylation genes (e.g., COX, ND, ATP synthase) and alterations in cell adhesion molecules (CAMs).

Conclusions:

• PFOS inhibits liver cell growth, induces oxidative stress, and increases apoptosis.
• These effects are mediated by transcriptomic alterations affecting mitochondrial activity and cell adhesion.
• The study provides insights into the molecular mechanisms of PFOS hepatotoxicity.