Mechanisms of Multi‐Target Damage Induced by Excimer Far‐ UV Light (222 nm) in Pseudomonas aeruginosa : From Membrane Lipid Peroxidation to Ribosomal Damage

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Abstract
This study systematically compares the inactivation mechanisms of 222 nm far‐UVC (UV222) and conventional 254 nm UV (UV254) against Pseudomonas aeruginosa . Unlike UV254, which primarily targets DNA by inducing cyclobutane pyrimidine dimers, UV222 operates through a multi‐target synergistic pathway involving membrane lipid peroxidation, ribosomal damage, and reactive oxygen species (ROS) accumulation. Specifically, UV222 exposure increased cell membrane permeability, induced a 2.3‐fold rise in malondialdehyde (MDA) levels, and caused 37.6% of treated cells to exhibit elevated intracellular ROS, as detected by DCFH‐DA flow cytometry. Transcriptomic analysis revealed 669 differentially expressed genes (DEGs) under UV222, enriched in ribosome biogenesis and carbon metabolism, while UV254 triggered 1185 DEGs linked to DNA repair and stress responses. RT‐qPCR confirmed upregulation of ribosomal protein genes exclusively after UV222 treatment. The Weibull model best described inactivation kinetics for both wavelengths, with UV222 showing multi‐mechanism synergy. These findings establish UV222 as a promising mechanism‐driven alternative to UV254 for sustainable disinfection in food processing and healthcare settings.
Funding Information
  • National Key Research and Development Program of China (2023YFC2605801)

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