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Aim The aim of the current study is to elucidate the inactivation and molecular response pattern of sublethal Listeria monocytogenes to cold plasma-mediated two-pronged oxidative microenvironments from a high-throughput multi-omics perspective. Methods and results First joint transcriptomics and metabolomics analyses revealed that significantly expressed genes and metabolites were mainly involved in enhanced transmembrane transport and Fe2+/Cu+ efflux, amino acid limitation, cytoplasmic pH homeostasis, reconfiguration of central carbon metabolism flux, and energy conservation strategy, which triggered the surge of intracellular endogenous oxidative stress and finally mediated bacterial ferroptosis and pathogenicity attenuation. Typical antioxidant systems such as the TrxR-Trx system and common antioxidant genes (e.g. sodA, katA, ahpC, trxA, spxA) were inhibited, and the more prominent antioxidant pathways include methionine metabolism, the pentose phosphate pathway, and glutathione metabolism, as well as the DNA repair systems. Conclusions Therefore, our work confirmed from the transcriptional and metabolic as well as physiological levels that cold plasma-mediated intracellular oxidative stress induced big perturbations in pathways as a driving force for the inactivation and pathogenicity attenuation of L. monocytogenes.     Significance and impact of study This study provided new insights for the construction of multi-dimensional mechanisms of bacterial inactivation and pathogenicity attenuation for the precise control and inactivation of microorganisms in plasma non-thermal processing. [ABSTRACT FROM AUTHOR]