Aims
Lactic acid is a natural antimicrobial in food industry, and also exists in fermented food. It was reported that sublethally injured Escherichia coli could survive in acidic conditions. When conditions become advantageous, injured E. coli can restore physiological function, which is a potential threat in food industry. Recovery is a necessary step for discriminating injured bacteria, but the resuscitation mechanism of injured bacteria is still unknown.
Methods and Results
In our study, sublethal lactic acid treatment (pH 4·2, 60 min) posed oxidative stress on E. coli by decrease of superoxide dismutase (SOD) activity and overproduction of reactive oxygen species (ROS). Zinc with low concentration (1·0 mmol l−1) significantly increased the recovery ratio of injured E.coli induced by lactic acid. The recovery ratios of injured cell in minimal A medium (minA) with 1·0 mmol l−1 zinc reached to that with 3·0 mmol l−1 catalase (CAT). Conversely, the addition of zinc chelator N, N, N′, N′‐tetrakis (2‐pyridylmethyl) decreased the recovery ratio. Zinc accelerated resuscitation of injured E. coli by improving SOD activity, and decreasing ROS production. Deletion of sodC encoding Cu/ZnSOD, katE/katG encoding CAT or regulating gene rpoS significantly decreased the recovery ratio. Among all of the mutants in this study, ΔrpoS and ΔsodC showed the lowest recovery ratio, which means they played significant roles in the process of resuscitation.
Conclusion
We provided direct evidence that zinc mediated resuscitation of lactic acid‐injured E. coli by relieving oxidative stress. Zinc can be used as a low‐cost and effective agent to improve recovery ratio and detection efficiency of injured bacteria.
Significance and Impact of the Study
Antibacterial agents are a challenge for bacteria, but bacteria can survive as a sublethally injured state under stresses. Using injured E. coli induced by lactic acid as a model organism, we validated the significant role of zinc on resuscitation of injured cells.
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