Flower-like ZnO micro/nanostructures were successfully fabricated via a surfactant-free co-precipitation method. The as-synthesized product was characterized using X-ray diffraction (XRD), field emission scanning electron microscopy (FESEM), energy dispersive X-ray (EDX), transmission electron microscopy (TEM), fourier transform infrared spectroscopy (FTIR), UV-vis diffuse reflectance spectroscopy (UV-vis DRS) and photoluminescence (PL) analyses. In the presence of visible light irradiation, the as-synthesized flower-like ZnO showed higher antibacterial activities against Enterococcus faecalis (E. faecalis) and Micrococcus luteus (M. luteus) than that of commercial ZnO. The excellent antibacterial performance of synthesized flower-like ZnO was also observed via the bacterial morphological change, K+ ions leakage and protein leakage in extracellular suspension. In addition, the FTIR investigation on both treated bacteria further confirmed the bacterial membrane damage via cellular substance alteration. The enhancement of the antibacterial activity of synthesized ZnO can be attributed to the unique flower-like morphology which can increase the surface OH- groups and the quantity of photogenerated electron-hole pair available to participate in the photocatalytic reaction. The reactive oxidizing species (ROS) scavengers experiments showed that H2O2 played a main role in the photocatalytic antibacterial process. Our study showed that the synthesized flower-like ZnO micro/nanostructures can act as efficient antibacterial agents in the photocatalytic antibacterial process under visible light irradiation.
Salivaricin B is a 25 amino acid polycyclic peptide belonging to the type AII lantibiotics and first shown to be produced by Streptococcus salivarius. In this study we describe the bactericidal mode of action of salivaricin B against susceptible Gram-positive bacteria. The killing action of salivaricin B required micro-molar concentrations of lantibiotic whereas the prototype lantibiotic nisin A was shown to be potent at nano-molar levels. Unlike nisin A, salivaricin B did not induce pore formation or dissipate the membrane potential in susceptible cells. This was established by measuring the fluorescence of the tryptophan residue at position 17 when salivaricin B interacted with bacterial membrane vesicles. The absence of a fluorescence blue shift indicates a failure of salivaricin B to penetrate the membranes. On the other hand, salivaricin B interfered with cell wall biosynthesis, as shown by the accumulation of the final soluble cell wall precursor UDP-MurNAc-pentapeptide which is the backbone of the bacterial peptidoglycan. Transmission electron microscopy of salivaricin B-treated cells showed a reduction in cell wall thickness together with signs of aberrant septum formation in the absence of visible changes to cytoplasmic membrane integrity.