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Interaction of Al2O3 nanoparticles with Escherichia coli and their cell envelope biomolecules

机译:Al2O3纳米粒子与大肠杆菌及其细胞被膜生物分子的相互作用

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Aims The aim of this study is to investigate the antibacterial activity of aluminium oxide nanoparticles (Al2O3 NPs) against multidrug-resistant clinical isolates of Escherichia coli and their interaction with cell envelope biomolecules. Methods and Results Al2O3 NPs were characterized by scanning electron microscope (SEM), high-resolution transmission electron microscope (HR-TEM) and X-ray diffraction (XRD) analyses. Antibacterial activity and interaction of Al2O3 NPs with E.coli and its surface biomolecules were assessed by spectrophotometry, SEM, HR-TEM and attenuated total reflectance/Fourier transform infrared (ATR-FTIR). Of the 80 isolates tested, about 64 (80%) were found to be extended spectrum beta-lactamase (ESBL) positive and 16 (20%) were non-ESBL producers. Al2O3 NPs at 1000 mu gml(-1) significantly inhibited the bacterial growth. SEM and HR-TEM analyses revealed the attachment of NPs to the surface of cell membrane and also their presence inside the cells due to formation of irregular-shaped pits and perforation on the surfaces of bacterial cells. The intracellular Al2O3 NPs might have interacted with cellular biomolecules and caused adverse effects eventually triggering the cell death. ATR-FTIR studies suggested the interaction of lipopolysaccharide (LPS) and L-alpha-Phosphatidyl-ethanolamine (PE) with Al2O3 NPs. Infrared (IR) spectral changes revealed that the LPS could bind to Al2O3 NPs through hydrogen binding and ligand exchange. The Al2O3 NPs-induced structural changes in phospholipids may lead to the loss of amphiphilic properties, destruction of the membrane and cell leaking. Conclusions The penetration and accumulation of NPs inside the bacterial cell cause pit formation, perforation and disorganization and thus drastically disturb its proper function. The cell surface biomolecular changes revealed by ATR-FTIR spectra provide a better understanding of the cytotoxicity of Al2O3 NPs. Significance and Impact of the Study Al2O3 NPs may serve as broad-spectrum bactericidal agents to control the emergent pathogens regardless of their drug-resistance mechanisms.
机译:目的这项研究的目的是研究氧化铝纳米颗粒(Al2O3 NPs)对大肠杆菌多药耐药临床分离株的抗菌活性及其与细胞包膜生物分子的相互作用。方法与结果采用扫描电子显微镜(SEM),高分辨率透射电子显微镜(HR-TEM)和X射线衍射(XRD)分析对Al2O3纳米颗粒进行了表征。通过分光光度法,SEM,HR-TEM和衰减全反射/傅里叶变换红外光谱(ATR-FTIR)评估了Al2O3 NPs与大肠杆菌及其表面生物分子的抗菌活性和相互作用。在测试的80个分离株中,发现约64个(80%)是超光谱β-内酰胺酶(ESBL)阳性,而16个(20%)是非ESBL生产者。 Al2O3 NPs在1000μgml(-1)会明显抑制细菌的生长。 SEM和HR-TEM分析表明,NPs附着在细胞膜表面,并且由于形成不规则形状的凹坑和在细菌细胞表面穿孔而在细胞内存在。细胞内的Al2O3 NP可能已经与细胞生物分子相互作用,并引起了不良反应,最终触发了细胞死亡。 ATR-FTIR研究表明,脂多糖(LPS)和L-α-磷脂酰乙醇胺(PE)与Al2O3 NP相互作用。红外(IR)光谱变化表明,LPS可以通过氢键结合和配体交换与Al2O3 NPs结合。 Al2O3 NPs诱导的磷脂结构变化可能导致两亲性丧失,膜破坏和细胞渗漏。结论NPs在细菌细胞内的渗透和积累会导致核的形成,穿孔和混乱,从而严重破坏其正常功能。 ATR-FTIR光谱揭示的细胞表面生物分子变化提供了对Al2O3 NPs细胞毒性的更好理解。研究的意义和影响Al2O3 NPs可以用作控制新兴病原体的广谱杀菌剂,无论其耐药机制如何。

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