Abstract
Atmospheric cold plasma (ACP) treatment can reduce bacterial pathogens in foods. Additional reduction in bacterial cells during storage after ACP treatment was previously reported. The underlying mechanisms of bacterial inactivation during ACP treatment and post-treatment storage need to be understood. This study investigated the changes in the morpho-physiological status of Listeria monocytogenes on ham surfaces after post-ACP-treatment storage of 1 h, 24 h, and 7 days at 4 °C. The membrane integrity, intracellular oxidative stress, and esterase activity of L. monocytogenes were evaluated by flow cytometry. L. monocytogenes cells were under high oxidative stress conditions with slightly permeabilized membranes after 1 h of post-ACP-treatment storage according to the flow cytometry data. During the extended storage of 24 h, the percentage of cells with a slightly permeabilized membrane increased; subsequently, the percentage of cells with intact membranes decreased. The percentage of L. monocytogenes cells with intact membranes decreased to <5% with a treatment time of 10 min and after 7 days of post-treatment storage. In addition, the percentage of L. monocytogenes cells under oxidation stress decreased to <1%, whereas the percentage of cells with completely permeabilized membranes increased to more than 90% for samples treated with ACP for 10 min and 7 days of post-treatment storage. With increased ACP treatment time, for 1 h stored samples, the percentage of cells with active esterase and slightly permeabilized membranes increased. However, during the extended post-treatment storage of 7 days, the percentage of cells with active esterase and slightly permeabilized membranes decreased to below 1%. At the same time, the percentage of cells with permeabilized membrane increased to more than 92% with an increase in ACP treatment time of 10 min. In conclusion, the higher inactivation after 24 h and 7 days post-ACP-treatment storage compared to 1 h stored samples correlated with the loss of esterase activity and membrane integrity of L. monocytogenes cells.
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