Defect-rich O-doped MoS2 boosted peroxymonosulfate activation for tetracycline removal via nonradical pathways

Peroxymonosulfate (PMS)–based advanced oxidation processes (AOPs) are attractive for abating recalcitrant organics but are hindered by poor selectivity of freely diffusing radicals and the difficulty of steering reactions toward surface-confined, pollutant-selective routes. Molybdenum disulfide (MoS 2 ) has emerged as a promising PMS activator; however, the literature remains divided on the identity of active sites (Mo centers vs. defects) and the dominant pathway (free-radical, 1 O 2 , or interfacial electron transfer pathway(ETP)). Here we resolve these contradictions by decoupling site identity and pathway contributions on a hydrothermally synthesized, oxygen-doped, defect-rich 2H-MoS 2 (Defect-MoS 2 ). Multi-scale characterization reveals the presence of oxygen vacancies and reduced long-range order. A biased non-radical mechanistic protocol, combining quencher assays and electron paramagnetic resonance (EPR) with an explicit correction for non-catalytic direct PMS oxidation showed that the catalytic contribution was governed by an interfacial ETP mediated by surface-bound PMS*, with 1 O 2 as the principal ROS signature and •OH/SO 4 • − playing minor roles. In-situ Raman identified PMS* vibrational features, while chronoamperometry and open-circuit potential tracked PMS* formation/consumption and interfacial electron redistribution in real time. EDTA poisoning and DFT jointly indicated that Mo centers primarily anchored PMS whereas oxygen vacancies (O vac ) activated PMS. The ETP-biased routed robust under neutral–alkaline pH, with common anions, and within membrane nanoconfinement. This study reconciles disparate reports on MoS 2 -mediated PMS activation, establishes a transferable design principle on engineering O vac to activate PMS and supporting surface-confined ETP-PMS* and provides a corrective framework for correcting PMS activation in for PMS-type Fenton systems.