Thimerosal induces oxidative stress in HeLa S epithelial cells

Area of Science:

• Toxicology
• Cell Biology
• Biochemistry

Background:

• Thimerosal is a widely used preservative in biological products, cosmetics, and contact lens solutions.
• Known to cause epithelial tissue damage like conjunctivitis and contact dermatitis.
• The precise molecular mechanisms of thimerosal's epithelial toxicity remain unclear.

Purpose of the Study:

• To investigate the molecular mechanism of thimerosal-induced cytotoxicity in epithelial cells.
• To determine the role of reactive oxygen species (ROS) in thimerosal toxicity.
• To characterize the cellular and biochemical changes associated with thimerosal exposure.

Main Methods:

• Utilized HeLa S epithelial cells for in vitro studies.
• Assessed cell viability, intracellular glutathione levels, and cell cycle progression via flow cytometry.
• Measured caspase-3 activity, genomic DNA fragmentation, and observed nuclear morphology using Hoechst 33342 staining.
• Investigated the protective effects of N-acetyl-l-cysteine (NAC) as a radical scavenger.

Main Results:

• Thimerosal significantly decreased HeLa S cell viability and reduced intracellular glutathione levels.
• Flow cytometry revealed an increase in hypodiploidic cells, indicative of apoptosis.
• Elevated caspase-3 activity and concentration-dependent DNA fragmentation confirmed apoptotic cell death.
• NAC pretreatment almost completely suppressed thimerosal-induced toxic effects.

Conclusions:

• Reactive oxygen species play a critical role in thimerosal-induced cytotoxicity in epithelial cells.
• Thimerosal triggers apoptosis in epithelial cells via oxidative stress pathways.
• These findings elucidate the molecular mechanism underlying thimerosal's epithelial toxicity.