Mo(SO)2 porous nanoparticles achieve effective antibacterial through electron attack on the respiratory chain

Manipulating the “bacterial current” by targeting the electron transport chain (ETC) presents a transformative antibacterial strategy, yet achieving precise targeting and elucidating the molecular mechanism remain challenging. Here, we break through the synthetic bottleneck to engineer a robust, electron-donating nanomaterial for targeted bacterial ETC disruption. A novel in-situ sulfur-doping and vacancy-engineering strategy was employed to fabricate porous Mo(SO)₂ from MoS₂, which features abundant oxygen vacancies and expanded interlayer spacing. These vacancies serve as electron-deficient centers that facilitate a rapid and strong electron donation. By functionalizing with 4-mercaptophenylboronic acid (4-MPBA) for targeting, the electrons are specifically transferred to the bacterial ETC. We systematically unveil the molecular mechanism: the donated electrons suppress the expression of ubiC , a key chorismate lyase for ubiquinone synthesis, via interaction with the guanidyl group of Arg63. This disruption halts proton pumping and ATP synthesis, leading to bacterial death via energy depletion.