Selenide-Driven Reactive Oxygen Species Activation and Fe(II) Regeneration for Enhanced Nanocatalytic Antibacterial Therapeutics.

Abstract

Fenton-based nanocatalytic therapy has attracted widespread attention for its high efficiency and safety. Nevertheless, Fe²⁺ regeneration, as the rate-limiting step of Fenton reaction, hinders the ROS-induced oxidative killing. Herein, a Fe²⁺ auto-regeneration strategy is exemplified by 2D FeSe₂ nanosheets to break the rate limitation of Fenton reaction and subsequently enhances the antibacterial oxidative damage via dual ROS generation pathways. To be specific, the Se species accelerate the Fe³⁺ reduction to maintain high ·OH productivity of Fe²⁺-mediated Fenton reaction, which is accompanied by the production of H₂Se in the presence of H⁺. The H₂Se further converts O₂ into O₂ ^·- and synergistically breaks the oxidative threshold of bacteria, leading to irreversible bacterial death with glutathione depletion, lipid peroxidation, and membrane destruction. In summary, the FeSe₂-mediated Fe²⁺ auto-regeneration and ROS self-production pathways largely elevate its oxidative killing capability, providing a potential ROS enhancement strategy for broad-spectrum nonantibiotic bacterial disinfection.