N-acetylcysteine reverses the decrease of DNA methylation status caused by engineered gold, silicon, and chitosan...

Area of Science:

• Nanomaterials Science
• Epigenetics
• Toxicology

Background:

• Engineered nanoparticles (ENPs) are widely used nanomaterials with potential to induce cellular damage.
• ENPs can cause oxidative stress, leading to changes in DNA methylation, a key epigenetic mechanism.
• The relationship between ENP-induced reactive oxygen species (ROS) and DNA methylation requires further investigation.

Purpose of the Study:

• To investigate the effect of ENP exposure on DNA methylation levels.
• To determine the role of ROS in ENP-induced epigenetic alterations.
• To examine the impact of different ENPs (gold, silicon, chitosan) on DNA methylation in human cells.

Main Methods:

• Human embryonic kidney and HaCaT cells were exposed to gold, silicon (SiNPs), and chitosan (CSNPs) nanoparticles.
• Cytotoxicity, ROS levels, global DNA methylation, and methylation of LINE-1 and Alu elements were assessed.
• Combined bisulfite restriction analysis and HPLC were used to measure DNA methylation.

Main Results:

• SiNPs exposure increased ROS levels in HaCaT cells.
• SiNPs and CSNPs exposure led to global and Alu hypomethylation, with no change in LINE-1.
• Alu demethylation was prevented by antioxidant pretreatment, suggesting indirect ROS involvement.

Conclusions:

• Global DNA methylation changes in ENP-exposed cells are associated with Alu element methylation.
• ENP-induced DNA methylation alterations are specific to ENP type and cell type.
• Changes in DNA methylation are independent of direct ROS effects, occurring indirectly via oxidative defense disruption.