Abstract
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•ZnO nanoparticles (NP) were fabricated using the crustacean immune molecule β-1, 3- glucan binding protein.•Phβ-GBP-ZnO NPs triggered membrane permeability and ROS formation in Staphylococcus aureus and Proteus vulgaris.•CLSM showed a strong impact on biofilm thickness post-treatment with nanoparticles.•Low doses of Phβ-GBP-ZnO NPs inhibit viability of HepG2, leading to key morphological changes.
The effective treatment of cancer and bacterial pathogens are two key challenges in modern nanomedicine. Here, zinc oxide nanoparticles (ZnO NPs) were fabricated using the crustacean immune molecule β-1, 3- glucan binding protein (Phβ-GBP, 100kDa) purified from the heamolymph of Paratelphusa hydrodromus. β-GBP coated zinc oxide nanoparticles (Phβ-GBP-ZnO NPs) were characterized by UV–vis spectroscopy, X-ray diffraction (XRD), Fourier transform infrared spectroscopy (FTIR), and high resolution-transmission electron microscopy (HR-TEM) analyses. Phβ-GBP-ZnO NPs inhibited the growth of Staphylococcus aureus and Proteus vulgaris. Protein and nucleic acid leakage assays showed that Phβ-GBP-ZnO NPs facilitate membrane permeability leading to cell death. The antibacterial activity of Phβ-GBP-ZnO NPs was due to the high level of reactive oxygen species (ROS) release from bacterial cells post-treatment with 75μg/mL of Phβ-GBP-ZnO NPs. Confocal laser scanning microscopy pointed out that biofilm thickness was highly reduced post-treatment with nanoparticles. Cytotoxicity on human liver carcinoma (HepG2) cells highlighted that 75μg/mL of Phβ-GBP-ZnO NPs inhibited viability of HepG2 cells. Phase contrast microscopy showed key morphological changes of HepG2 cells post-treatment with Phβ-GBP-ZnO NPs. Overall, Phβ-GBP-ZnO NPs can be further considered for the development of novel drugs against microbial pathogens and HepG2 cells.