Journal
ACS APPLIED MATERIALS & INTERFACES
Volume 12, Issue 5, Pages 5557-5568Publisher
AMER CHEMICAL SOC
DOI: 10.1021/acsami.9b20193
Keywords
silver nanoparticle; cell envelope; peptidoglycan; lipopolysaccharide; lipoteichoic acid; phospholipid; reactive oxygen radicals; toxicity
Funding
- Australian Research Council [DP180100474]
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The work describes the interactions of nanosilver (NAg) with bacterial cell envelope components at a molecular level and how this associates with the reactive oxygen species (ROS)-mediated toxicity of the nanoparticle. Major structural changes were detected in cell envelope biomolecules as a result of damages in functional moieties, such as the saccharides, amides, and phosphodiesters. NAg exposure disintegrates the glycan backbone in the major cell wall component peptidoglycan, causes complete breakdown of lipoteichoic acid, and disrupts the phosphate-amine and fatty acid groups in phosphatidylethanolamine, a membrane phospholipid. Consistent with the oxidative attacks, we propose that the observed cell envelope damages are inflicted, at least in part, by the reactive oxygen radicals being generated by the nanoparticle during its leaching process, abiotically, without cells. The cell envelope targeting, especially those on the inner membrane phospholipid, is likely to then trigger the rapid generation of lethal levels of cellular superoxide (O-2(center dot-)) and hydroxyl (OH center dot) radicals herein seen with a model bacterium. The present study provides a better understanding of the antibacterial mechanisms of NAg, whereby ROS generation could be both the cause and consequence of the toxicity, associated with the initial cell envelope targeting by the nanoparticle.
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