Role of oxidative stress in inactivation of Escherichia coli BW25113 by nanoscale zero-valent iron.

An Escherichia coli BW25113 wildtype strain and mutant strains lacking genes that protect against oxidative stress were examined at different growth phases for susceptibility to zero-valent iron (nZVI). Viability of cells was determined by the plate count method. All mutant strains were more susceptible than the wild type strain to nZVI; however, susceptibility differed among the mutant strains. Consistent with the role of rpoS as a global stress regulator, an rpoS gene knockout mutant exhibited the greatest susceptibility to nZVI under the majority of conditions tested (except exponential and declining phases at longer exposure time). Mutants lacking genes encoding the inducible and constitutively expressed cytosolic superoxide dismutases, sodA and sodB, respectively, were more susceptible to nZVI than a mutant lacking the gene encoding sodC, a periplasmic superoxide dismutase. This suggests that nZVI induces oxidative stress inside the cells via superoxide generation. Quantitative polymerase chain reaction was used to examine the expression of katG, a gene encoding the catalase-peroxidase enzyme, in nZVI-treated E. coli at different growth phases. Results showed that nZVI repressed the expression of katG in all but lag phases.

Impact of nanoscale zero valent iron on bacteria is growth phase dependent.

The toxic effect of nanoscale zero valent iron (nZVI) particles on bacteria from different growth phases was studied. Four bacterial strains namely Escherichia coli strains JM109 and BW25113, and Pseudomonas putida strains KT2440 and F1 were experimented. The growth curves of these strains were determined. Bacterial cells were harvested based on the predetermined time points, and exposed to nZVI. Cell viability was determined by the plate count method. Bacterial cells in lag and stationary phases showed higher resistance to nZVI for all four bacterial strains, whereas cells in exponential and decline phases were less resistant to nZVI and were rapidly inactivated when exposed to nZVI. Bacterial inactivation increased with the concentration of nZVI. Furthermore, less than 14% bacterial inactivation was observed when bacterial cells were exposed to the filtrate of nZVI suspension suggesting that the physical interaction between nZVI and cell is necessary for bacterial inactivation.