Fluorescent determination of trinitrotoluene with bovine serum albumin mediated enhancement of thioglycolic acid capped cadmium selenium quantum dots

Abstract

Here, a spectroscopic investigation of the interaction between bovine serum albumin protein and thioglycolic acid capped cadmium selenide (CdSe) quantum dots is presented. Luminescent water-soluble CdSe quantum dots were synthesized at room temperature by a one-step proctocol. Selenium powder and thioglycolic acid were used as the precursor and stabilizer, respectively. The synthesized thioglycolic acid capped CdSe quantum dots were activated by 1-ethyl-3-(3-dimethylaminopropyl) carbodiimide hydrochloride/N-hydroxysuccinimide treatment and conjugated with bovine serum albumin protein. The fluorescence signal of CdSe quantum dots was enhanced proportionally with the bovine serum albumin concentration from 0.25 to 5?µg/mL. This nano-bioconjugate was employed for the determination of trinitrotoluene with a detection limit of 5.65?ppm trinitrotoluene across a linear range of 4.4?×?10^?6 M to 35.2?×?10^?6 M.     

Fixation for biological ultrastructure. I. A viscometric analysis of the interaction between glutaraldehyde and bovine serum albumin

The increase in viscosity resulting from mixing concentrated solutions of albumin with dilute glutaraldehyde has been investigated. The viscosity changes are slow at first, very sensitive to small changes in glutaraldehyde concentration, and non-linear with time. The cross-linking of the albumin by glutaraldehyde seems to be retarded by the weak mechanical shear forces produced by the viscometer. The significance of these findings to the events in tissue fixation is discussed.     

牛血清蛋白-Au配合物及其复合物制备及表征

以牛血清蛋白(bovine serum albumin,BSA)、氯金酸(HAuCl4)、NaOH等为原料,采用一锅合成法制备了牛血清蛋白-Au配合物(BSA-Au),观察到了样品的宽带红光荧光发射。通过库仑力作用将BSA-Au与表面带有正电荷的金纳米颗粒进行复合,对纳米复合物的吸收光谱及荧光光谱特性进行了研究。实验结果表明,在本实验条件下,金纳米颗粒虽然增强了复合物样品在可见光区域的光吸收,但对BSA-Au红光发光有猝灭作用。     

荧光光谱法研究染料木素与牛血清白蛋白的相互作用

在pH为7.40的Tris-HCl缓冲体系中,采用荧光光谱技术研究了染料木素与牛血清白蛋白（BSA）的相互作用。不同温度（290K、300K、310K、315K）下测得的猝灭常数,证实染料木素对BSA的荧光猝灭为静态猝灭过程。根据热力学参数焓变（ΔH）小于零和熵变（ΔS）小于零（ΔH=-48.905kJ/mol,ΔS=-71.435kJ/mol）,可以判断染料木素与BSA之间主要靠氢键和范德华力相结合。生成自由能变（ΔG）为负值,表明染料木素与BSA的作用过程属自发过程。应用同步荧光光谱技术考察了染料木素对BSA构象的影响。     

荧光光谱法研究葛根素与牛血清白蛋白的相互作用

在不同温度下,采用荧光猝灭光谱法和同步荧光光谱法研究了葛根素与牛血清白蛋白(BSA)相互作用的光谱学行为。根据在292K和311K温度下葛根素对BSA的荧光猝灭作用,利用Stern-Volmer方程及双倒数方程对实验数据进行处理,结果表明葛根素对BSA的荧光猝灭作用属于静态猝灭过程。根据Frster非辐射能量转移理论计算出了葛根素与BSA间的结合距离r=2.84nm,结合常数(Kb)分别为1.334×105mol/L(292K)和4.513×105mol/L(311K)。热力学数据表明,二者主要靠静电引力结合。采用同步荧光光谱法分析了葛根素对BSA构象的影响。     

Fixation for biological ultrastructure. II. Cross-linking of bovine serum albumin by nanosecond pulses of ionizing radiation

Very large doses of ionizing radiation were delivered quickly to concentrated albumin solutions by pulses of 500 keV in air. The electrons penetrated the aluminium foil bottom of the test cell and into the solution. A dose of 4.6 Mrad (4.6 × 10⁴ Gy) produced a gel in the albumin solution comparable to the long-term effect of 0.36% glutaraldehyde in the same albumin solution. The cross-links created by the radiation leading to gel formation are probably irreversible and quite different from those leading to gelation in the glutaraldehyde-albumin reaction. Single large pulses of ionizing radiation may be useful for fast fixation of cells and tissues for microscopy.     

荧光法研究二氧化硫衍生物与牛血清白蛋白的相互作用

目的:研究二氧化硫衍生物与牛血清白蛋白(BSA)的相互作用.方法:用荧光猝灭光谱法和紫外可见吸收光谱法分析BSA及BSA-二氧化硫衍生物相互作用后体系的光谱特征.结果:①在不同温度下,二氧化硫衍生物能使BSA的内源荧光发生有规律的猝灭,猝灭作用可能为静态猝灭.②得出了二氧化硫衍生物和BSA相互作用的热力学常数、结合常数和结合位点数;相互作用力主要为氢键和范德华力,且作用力较弱.③三维荧光光谱表明,二氧化硫衍生物对BSA的构象影响不明显.结论:二氧化硫衍生物与BSA可能的结合方式为二氧化硫衍生物与蛋白质的氨基酸残基发生结合反应,生成不发荧光或者荧光强度较弱的基态复合物,使BSA荧光发生部分猝灭,但对BSA构象影响不明显,具体作用机制还需进一步探讨.     

Exploring the mechanisms of magnolol in the treatment of periodontitis by integrating network pharmacology and molecular docking

Background: Magnolol, a bioactive extract of the Chinese herb Magnolia officinalis has a protective effect against periodontitis. This study is aimed to explore the mechanisms involved in the functioning of magnolol against periodontitis and provide a basis for further research. Methods: Network pharmacology analysis was performed based on the identification of related targets from public databases. The Protein-protein interaction (PPI) network was constructed to visualize the significance between the targets of magnolol and periodontitis. Subsequently, Gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis were performed to predict the functions and the signal regulatory pathways involved in the action of magnolol against periodontitis. The “function-target-pathway” networks were constructed to analyze the core targets and pathways of magnolol against periodontitis. Molecular docking was used to verify the interaction of magnolol and core targets. Results: A total of 58 active targets of magnolol and 644 periodontitis-related targets were collected from public databases. A total of 25 targets of magnolol against periodontitis were identified based on the Venn diagram. GO analysis showed that magnolol has a role in the response to oxidative stress, nicotine, and lipopolysaccharide. KEGG enrichment analysis indicated that the mechanism of magnolol against periodontitis was mainly related to the tumor necrosis factor (TNF), phosphoinositide 3-kinase (PI3K/Akt), and mitogen-activated protein kinase (MAPK) signaling pathways. Combined with PPI network and molecular docking results, the core targets of magnolol against periodontitis included AKT1, MAPK8, MAPK14, TNF, and TP53. Conclusion: To summarize, the anti-periodontitis mechanisms of magnolol are potentially through regulating the TNF, PI3K/Akt, and MAPK signaling pathways.