期刊
NANOMATERIALS
卷 13, 期 10, 页码 -出版社
MDPI
DOI: 10.3390/nano13101652
关键词
ZnO; antibacterial; S. aureus; phosphates; antimicrobial; surface photovoltage
Nano- and microscale zinc oxide (ZnO) shows promise as an antibacterial agent in biomedical applications, but the mechanisms behind its antimicrobial action are unclear. This study investigates the effects of interactions with phosphate-rich environments and bacteria on ZnO particles. The results demonstrate significant changes in surface photovoltage and sub-bandgap surface electronic structure after exposure to phosphate-rich environments, suggesting adsorption of phosphates at zinc deficiency defects on the ZnO surface. However, the presence of Staphylococcus aureus bacteria suppresses this effect, supporting the competitive nature of interactions between S. aureus, aqueous phosphates, and the free surface of ZnO.
Nano- and microscale zinc oxide (ZnO) exhibits significant potential as a novel antibacterial agent in biomedical applications. However, the uncertainty regarding the underlying mechanisms of the observed antimicrobial action inhibits the realization of this potential. Particularly, the nature of interactions at the free crystalline surface and the influence of the local bacterial environment remains unclear. In this investigation, we utilize ZnO particles synthesized via tunable hydrothermal growth method as a platform to elucidate the effects of interactions with phosphate-rich environments and differentiate them from those with bacteria. This is achieved using the time- and energy-dependent surface photovoltage (SPV) to monitor modifications of the surface electronic structure and surface charge dynamics of the ZnO particles due to these interactions. It is found that there exists a dramatic change in the SPV transients after exposure to phosphate-rich environments. It also presents differences in the sub-bandgap surface electronic structure after these exposures. It can be suggested that these phenomena are a consequence of phosphate adsorption at surface traps corresponding to zinc deficiency defects. This effect is shown to be suppressed in the presence of Staphylococcus aureus bacteria. Our results support the previously proposed model of the competitive nature of interactions between S. aureus and aqueous phosphates with the free surface of ZnO and bring greater clarity to the effects of phosphate-rich environments on bacterial growth inhibition of ZnO.
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