Membrane disruption boosts iron overload and endogenous oxidative stress to inactivate Escherichia coli by nanoscale zero-valent iron

The inactivation of microorganisms by nanoscale zero-valent iron (nZVI) was extensively reported, but what happens inside the cells is rarely explored. Herein, we revealed that nZVI caused the drastic increase of intracellular iron concentrations, which subsequently catalyzed the Haber-Weiss reaction to produce high levels of endogenous reactive oxygen species (ROSs) and inactivated E. coli cells by oxidative damage of DNA, evidenced by the significantly higher inactivation efficiencies of E. coli mutant strains deficient in iron uptake regulation and DNA repair than the parental strain. The intracellular iron levels, endogenous ROSs levels and the inactivation efficiencies of E. coli were positively correlated. The permeabilized cytomembrane due to the close contact between nZVI and E. coli was responsible for the iron overload. This work demonstrates experimentally for the first time that nZVI causes iron overload and endogenous oxidative stress to inactivate E. coli, thus deepening our knowledge of the nZVI antimicrobial mechanism.

Automated summary

The study reveals that nanoscale zero-valent iron (nZVI) causes an increase in intracellular iron concentrations, leading to the production of high levels of endogenous reactive oxygen species (ROSs) and the oxidative damage of DNA, resulting in the inactivation of E. coli cells. The close contact between nZVI and E. coli leads to increased permeabilization of the cytomembrane and iron overload, which enhances the efficiency of E. coli inactivation.