Active and molecular biological mechanisms of Escherichia coli death caused by CuCeO_x: Synergy of ROS-mediated oxidative stress and cuproptosis-associated metabolic collapse

To mitigate the health risks posed by pathogenic microorganisms in bioaerosols and aquatic environments, a non-noble metal antibacterial material, copper–ceria oxide (CuCeO_x), was synthesized. Its multistage synergistic inactivation mechanism against Escherichia coli （ E. coli ） was systematically elucidated. Results demonstrated that CuCeO_x exhibited excellent stability (sterilization efficiency >70 % after ten cycles) and strong antibacterial activity. Comprehensive characterizations revealed that the abundant oxygen vacancy defects and ion-mediated redox cycling in CuCeO_x synergistically enhanced the generation of reactive oxygen species (ROS). In the gas-phase system, hydroxyl radicals (·OH) were identified as the dominant bactericidal ROS, whereas in the liquid-phase system, lipophilic alkoxy radicals (RO·) induced lipid peroxidation, leading to cell membrane disruption and subsequent radical quenching. At the cellular level, CuCeO_x caused severe structural damage to E. coli , resulting in leakage of intracellular contents and irreversible cell death. Multi-omics analyses further confirmed the bactericidal mechanism: Gene Ontology (GO) enrichment in proteomics indicated disruption of cell wall and membrane-related pathways; combined metabolomics and transcriptomics analyses revealed that perturbations in sulfur metabolism, arginine and proline metabolism reflected oxidative stress induced by ROS accumulation. The tricarboxylic acid (TCA) cycle and lipoic acid metabolism were implicated in a cuproptosis-like pathway, wherein Cu⁺ targeted key TCA cycle proteins, triggering proteotoxic stress. These interconnected mechanisms ultimately led to the apoptosis of E. coli .