RESUMO
Excessive damage to DNA and lipid membranes by reactive oxygen species reduces the viability of bacteria. In the present study, the proliferation of recAdeficient Escherichia coli strains was revealed to be inhibited by 1% Lhistidine under aerobic conditions. This inhibition of proliferation was not observed under anaerobic conditions, indicating that Lhistidine enhances oxidative DNA damage to E. coli cells. Reverse transcriptionquantitative polymerase chain reaction analysis demonstrated that the expression of recA in E. coli MG1655 increased ~7fold following treatment with 10 mM hydrogen peroxide (H2O2) plus 1% Lhistidine, compared with that following exposure to H2O2 alone. Lhistidine increased the genomic fragmentation of E. coli MG1655 following exposure to H2O2. In addition, Lhistidine increased the generation of intracellular hydroxyl radicals in the presence of H2O2 in E. coli cells. Next, our group investigated the disinfection properties of the H2O2 and Lhistidine combination. The combination of 100 mM H2O2 and 1.0% Lhistidine significantly reduced the number of viable cells of extendedspectrumßlactamaseproducing E. coli and multidrugresistant Pseudomonas aeruginosa, and this treatment was more effective than 100 mM H2O2 alone, but this effect was not observed in methicillinresistant Staphylococcus aureus or vancomycinresistant Enterococcus faecium. The combination of Lhistidine and H2O2 may be a useful strategy to selectively increase the microbicidal activity of oxidative agents against Gramnegative bacteria.