Inhibition mechanism of high voltage prick electrostatic field (HVPEF) on Staphylococcus aureus through ROS-mediated oxidative stress

In our previous research, high voltage prick electrostatic field (HVPEF) was found to have good antibacterial effects against Staphylococcus aureus (S. aureus) on solid surface through destructing cell membranes. In the current study, the mechanism of HVPEF against S. aureus from the aspect of ROS-mediated oxidative stress was investigated. The ROS levels increased remarkably under HVPEF stress, and the addition of ROS scavengers significantly decreased ROS levels and mortality rates of S. aureus, indicating that ROS was a vital mediator in the antibacterial role of HVPEF. HVPEF treatment decreased the superoxide dismutase (SOD) activity and glutathione levels, and induced bacterial peroxidation. Gas chromatography-mass spectrometry (GC-MS) results indicated HVPEF treatment changed the fatty acid composition of the bacterial membranes. Sodium dodecyl sulphate polyacrylamide gel electrophoresis (SDS-PAGE), circular dichroism (CD) spectra and flow cytometry results showed that HVPEF treatment induced DNA oxidative damage, destroyed the structure of DNA and proteins, changed the expression of genes related to oxidative stress (sodA, katE, ahpC, G6PD, fabG and fabF) and led to bacteria apoptosis. This study further investigated oxidative stress of S. aureus under HVPEF based on our previous study, aiming to provide a better understanding of the antibacterial mechanism of the electric field.