Nanoscale FeSe₂ particle mediated mitigation of oxidative lesions: Impact on DNA, protein, and cellular integrity in in-vitro models

Excessive copper accumulation poses a significant threat to organisms due to its potential to catalyze the generation of harmful reactive oxygen species (ROS), leading to oxidative stress and damage to vital biomolecules. In the present study, we synthesized as well as characterized FeSe₂ nanoparticles (FeSe₂ NPs) and explored their efficacy in safeguarding DNA, protein, and lipids against copper-induced oxidative damage. Transmission electron microscopy (TEM) analysis recorded the hexagonal morphology of the FeSe₂ NPs with an average diameter ranging from 100 to 250 nm, while Energy Dispersive X-ray analysis (EDX) confirmed the weight percentages of iron and selenide found to be 34.222 and 65.744. Power X-ray diffraction (XRD) confirmed their high purity and crystalline nature, respectively. Remarkably, the FeSe₂ NPs exhibited concentration-dependent protection against protein oxidation, and 30 ng/µL of FeSe₂ NPs was reduced by around 88.17 % protein carbonyl formation. Similarly, 90 % of DPPH and ABTS^[rad]+ radicals were neutralized by FeSe₂ NPs at 20 ng/µL and 10 ng/µL concentration, respectively. At the highest concentration tested (30 ng/µL), the FeSe₂ NPs effectively prevented DNA cleavage, preserving its structural integrity. Furthermore, in cellular studies, FeSe₂ NPs displayed the ability to shield HepG2 cells from oxidative damage induced by hydrogen peroxide, as demonstrated by MTT viability assays and ROS assessments. Collectively, our findings highlight the potential of FeSe₂ NPs as a protective agent against copper-induced oxidative stress and heavy metal toxicity. These nanoparticles offer a promising avenue for mitigating the adverse effects of copper exposure in living systems and hold great potential for future applications in biomedical and environmental contexts.