摘要

       本研究合成了一种新型 Au-氧化石墨烯 (GO)-Co3O4 空心球 (Au/GO-Co3O4)，并研究了其与抗生素抗性基因 (ARG) 结合并抑制其复制的潜力。选择具有两个扩增子长度的四环素抗性基因 (tetA) 作为模型 ARG，因为它在环境中被高度检测到。 Au/GO-Co3O4 复合材料是使用四正丁基溴化铵 (TBAB) 作为中介合成的。我们发现，与纯 Co3O4 和 GO-Co3O4 杂交体相比，它可以与 tetA 结合，从而在更大程度上抑制其复制。此外，与长片段 (L-tetA) 相比，Au-GO-Co3O4 复合物与 tetA-ARG 的短片段 (S-tetA) 的结合效率更高。使用光谱方法（FTIR、拉曼、UV-Vis 和荧光光谱）、分离滤液测定和凝胶电泳系统地分析了复合材料和 tetA 之间的相互作用机制。发现 GO 和金纳米粒子对 tetA 的吸附以及氧化钴/钴离子的裂解作用在 tetA 的捕获和损伤中起着关键作用。此外，我们发现 Co3O4 和 GO-Co3O4 与 tetA 的相互作用主要通过嵌入机制，而 Au/GO-Co3O4 与 tetA 的相互作用主要通过凹槽结合机制。本研究的这些发现揭示了净化 ARGs 污染水和通过新型抑制剂消除 ARGs 的抗生素耐药性的新方法。

       A novel Au-graphene oxide (GO)-Co3O4 hollow sphere (Au/GO-Co3O4) was synthesized and its potential in binding with antibiotic resistance genes (ARGs) and inhibiting their replication was examined in this study. Tetracycline-resistant genes (tetA) with two amplicon lengths were selected as the model ARGs due to its highly detected in the environment. The Au/GO-Co3O4 composite was synthesized using tetra-n-butylammonium bromide (TBAB) as a mediating proxy. We found that it could bind with tetA and consequently inhibit its replication to a greater extent compared with pure Co3O4 and GO-Co3O4 hybrid. Furthermore, the Au-GO-Co3O4 composite was more efficient in binding with short fragments of tetA-ARGs (S-tetA) than long fragments (L-tetA). The interaction mechanism between the composite and tetA was systematically analyzed using spectra methods (FTIR, Raman, UV–Vis, and fluorimetric spectra), isolated filtrate assays, and gel electrophoresis. It is found that the adsorption of both GO and gold nanoparticles for tetA as well as cleavage effect of cobalt oxide/cobalt ions played a critical role in the capture and damage of tetA. Furthermore, we found that the interaction of both Co3O4 and GO-Co3O4 with tetA was mainly through intercalation mechanism, however, that of Au/GO-Co3O4 with tetA was mainly through groove binding mechanism. These findings in this study throw light on the new approaches for purification of ARGs contaminated water and elimination of antibiotic resistance of ARGs by novel inhibitor.

https://www.sciencedirect.com/science/article/abs/pii/S1385894718304662