零价铁
大肠杆菌
细胞内
氧化应激
化学
内生
活性氧
生物物理学
突变体
DNA损伤
氧化磷酸化
氧气
生物化学
微生物学
细胞生物学
DNA
生物
有机化学
吸附
基因
作者
Jian Wang,Congcong Liu,Hongwei Sun,Shaohui Wang,Xiaomei Liao,Lizhi Zhang
标识
DOI:10.1016/j.jhazmat.2022.128951
摘要
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.
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