Toxicity Mechanism Of ZnO Nanoparticles To Escherichia Coli And The Influence Of Biofilms

With the rapid development of nanotechnology, diverse nanomaterials and nanoproducts are emerging. However, numerous consumer nanoproducts are discharged into the environment as waste, the potential risks to the environment and human health has caused widespread concern. As many other pollutants, nanomaterials will enter into the water eventually, they will not only affect aquatic ecosystems, but also enters the human body through the food chain be dangerous to human health.In this study, we explored the mechanism of ZnO NP toxicity to Escherichia coli which was still controversial. By using an oxidative stress mutant (△oxyR mutant) and a biofilm-forming deficient mutant (△luxS mutant), the role of its extracellular substances was also investigated. Antibacterial tests revealed that, in LB medium, the toxicity of ZnO NPs came from the dissolved zinc; but in ultrapure water, generation of ROS by ZnO NPs in bacterial cells lead to the oxidation of membrane lipids, damages of DNA and proteins, resulting in cellular death. Lipid peroxidation subsequently leads to the internalization of ZnO NPs and Zn2+. Intracellular Zn2+ may competitively inhibit the redox reactions (e.g. Fenton reaction), and protect the bacteria cells, while the high concentration of Zn2+ lead cell damage.Furthermore, the more biofilms were formed the less sensitive Escherichia coli strain was to ZnO NPs. Despite the fact that more Zn2+ was adsorbed to the extracellular polymeric substances, these substances, more importantly, act as a barrier, protecting the cell against Zn ingress and preventing intracellular damage.