Humidity-triggered sterilization mechanism of CuCeOx: Hydroxyl radical-mediated protein synthesis inhibition and energy depletion.

Bioaerosols are a major transmission route for respiratory infections. Metal oxide materials sterilize air via contact oxidation and reactive oxygen species (ROS). Bacteria rely on autocatalytic network for survival, where a single node change can impact the entire network. However, the bactericidal efficiency, target sites, and impact on the autocatalytic network of different mechanisms remain unclear. We designed a non-contact experiment to separate two coupling mechanisms in the gas phase and explored ROS migration in air. Combined transcriptomics, proteomics, and metabolomics analysis clarified the molecular biological mechanism. Results showed that CuCeOx achieved 78.80 ± 3.12 % sterilization in non-contact experiments and 98.75 ± 0.49 % in confined environments. Environmental humidity triggered CuCeOx to generate hydroxyl radicals (·OH), which migrated with airflow and further broadened the boundaries of the sterilization system. Multi-omics analysis revealed damage to bacterial ribosomal rRNA and structural proteins, inhibiting translation elongation. Meanwhile, energy metabolism shifted significantly. Oxidative phosphorylation and the TCA cycle were downregulated, while glycolysis and the pentose phosphate pathway were upregulated to reduce endogenous ROS production, generate more NADPH, maintain redox balance, and provide precursors for nucleic acid and protein synthesis. This discovery provided a new pathway for developing efficient air sterilization technologies.