Modeling Lanthanide Complexes: Towards the Theoretical Design of Light Conversion Molecular Devices

Theoretical techniques have been developed and/or improved to predict the molecular structure of lanthanide complexes which were used to calculate their electronic properties, in particular, their electronic spectra and energy levels necessary to calculate the rates of energy transfer from the ligands to the metal ion. The molecular structure has been obtained by the SMLC/AM1 (Sparkle Model for the Calculation of Lanthanide Complexes – Austin Model 1) model where the lanthanide ion is simulated by a sparkle implemented into the AM1 Hamiltonian used to perform a HF-SCF (Hartree-Fock Self-Consistent Field) calculation. The previous implementation of the SMLC/AM1 model (sparkle/1) involving only two parameters has been generalized to be consistent with the AM1 Hamiltonian and the new model (sparkle/2) significantly improved the prediction of molecular structures of Eu(III) complexes. For the electronic spectra and energy level calculations of the lanthanide complexes the model replaces the metal ion by a point charge with the ligands held in their positions as determined by the SMLC/AM1 model, and uses a INDO/S-CI (intermediate neglect of differential overlap/spectroscopic-configuration interaction) model. A preliminary study of the solvent effects on the absorption spectra of the free ligand is also presented. For the ligand-lanthanide ion energy transfer Fermi's golden rule is used with the multipolar and exchange mechanisms being implemented and tested for several complexes. These theoretical techniques have been applied to several complexes yielding very good results when compared to experimental data as well as predictions for the molecular and electronic structures and the relative contributions of the mechanisms for the energy transfer rates. This revised version was published online in June 2006 with corrections to the Cover Date.     

A comparison of measurements of intracellular Ca by Ca electrode and optical indicators

Squid giant axons were injected with aequorin or arsenazo III and impaled with a Ca-sensing electrode. The light output of aequorin or the spectrophotometer output when measuring arsenazo was compared with the voltage output of the electrode when the squid axon was depolarized with high-K solutions, when the seawater was made Na-free, or when the axon was tetanized for several minutes. The results from these treatments were that the optical response rose (as much as 50-fold) with all treatments known to increase Ca entry, while the electrode remained unaffected by these treatments. If axons previously subjected to Ca load are treated with electron-transport poisons such as CN, it is known that [Ca]_i rises after a time necessary to deplete ATP stores. In such axons one expects a rise of [Ca]_i in axoplasm which does not necessarily have to be uniform although the source of such Ca is the mitochondria and these are uniformly distributed in axoplasm. Under conditions of CN application, the optical signals from aequorin or arsenazo and Ca electrode output do rise together when [Ca]_i is high, but there is a region of [Ca]_i concentration where aequorin light output or arsenazo absorbance rises while electrode output does not. Axons not loaded with Ca but injected with apyrase and vanadate have mitochondria that still retain some Ca and this can be released by CN in a truly uniform manner. The results show that such a release (which is small) can be readily measured with aequorin, but again the Ca electrode is insensitive to such [Ca]_i change.     

The role of the nicotinamide and adenine subsites in the negative co-operativity of coenzyme binding to glyceraldehyde-3-phosphate dehydrogenase.

The interaction of 3-aminopyridine-adenine dinucleotide, an NAD ⁺ 2 analogue which is fluorescent at the pyridine end of the molecule, with rabbit muscle glyceraldehyde-3-phosphate dehydrogenase was investigated. The fluorescence properties of the AAD⁺ molecule were used to monitor the nicotinamide subsites ou the GPDHase tetramer, the fluorescent aminopyridine moiety of the molecule serving as an intrinsic probe. Although the binding of AAD⁺ wag found to be negatively co-operative, no conformational changes induced at the nicotinamide subsite upon coenzyme binding were found to be transmitted to neighboring subunits. These findings, in conjunction with our earlier findings and with the observation that different NAD⁺ analogues which differ in the chemistry of the pyridine moiety bind with different extents of co-operativity, enable us to offer specific roles for the nicotinamide and the adenine subsites in generating the negative co-operativity.It is suggested that the structure of the pyridine moiety of the coenzyme controls the mode of binding of the pyridine moiety to the nicotinamide subsite. This, in turn, controls the orientation of the adenine moiety with respect to its subsite, thereby determining the mode of the interactions between the adenine and its binding domain. As the propagation of conformational changes caused by these interactions to neighboring subunits is believed to be the cause of the negative co-operativity exhibited by this enzyme towards coenzyme binding, the structure of the pyridine moiety controls this phenomenon.     

Extraction and analysis of superoxide free radicals (·O−2) from whole mammalian liver

Extraction of whole lobes of normal rat liver with dimethyl sulphoxide (DMSO) under N₂ gives extracts which contain 5—10 μmol/l·O^?₂ (50-100 nmol·O^?₂ per 10 ml extract per 4 g liver; 1.25-2.50 nmol·O^?₂ per millilitre per gram liver). Evidence for ·O^?₂ in the extracts is given by: (1) electron spin resonance signals (ESR), (2) differential pulse polarography (DPP), (3) chemiluminescence (CL), and (4) nitroblue tetrazolium reduction (NBT). All tests yield results identical with those obtained with authentic ·O^?₂. Extraction of ·O^?₂ is enhanced by tetrabutyl ammonium ion, and is maximal at 1-3 min. These results raise the possibility that substantial amounts of ·O^?₂ are normally sequestered in protective membranous sites in vivo.     

Cellular mechanisms of paired electrical stimulation in ferret ventricular myocardium: relationship between myocardial force and stimulus interval change

Summary The subcellular mechanisms of twitch-force potentiation with paired electrical stimulation was studied in ferret ventricular myocardium using the bioluminescent calcium indicator aequorin. It is demonstrated for the first time that interpolation of an extrasystole in a train of conditioned twitches results in a beat-to-beat change in [Ca²⁺]_i and force. Steady-state twitch force and Ca _i ²⁺ were increased with paired stimulation. Increased [Ca²⁺]₀ in the setting of paired stimulation resulted in an increase in the amplitude of the postextrasystole and associated Ca²⁺ transient. Verapamil, a Ca²⁺ channel antagonist, had the opposite effect of increased [Ca²⁺]₀. Postextrasystole potentiation was still present, but diminished in amplitude. These results indicate that postextrasystole potentiation is in part due to a verapamil-depletable store (Ca²⁺). Postextrasystole potentiation is therefore predominantly dependent on sarcoplasmic reticulum (SR) Ca²⁺ loading. Ryanodine, an alkaloid which induces Ca²⁺ leakage from the SR, abolished postextrasystole potentiation; however, in the presence of ryanodine the extrasystole was potentiated. Caffeine, a phosphodiesterase inhibitor which induces SR Ca²⁺ release and impairs uptake, also abolished postextrasystole potentiation. As with ryanodine there was resultant potentiation of the extrasystole. In the case of caffeine the calcium transient consisted of a second slow component associated with extrasystole twitch potentiation. The results are consistent with sarcolemmal Ca²⁺ influx playing a role in potentiation of the extrasystole in the presence of an impaired SR. These data indicate that transsarcolemmal Ca²⁺ influx in the presence of impaired intracellular Ca²⁺ buffering can directly activate the myofilaments in agreement with reports on human myocardium.Abbreviations C conditioned stimulus - ESI extrasystolic interval - L_max active tension - PES postextrasystole - PESI postextrasystolic interval - SR sarcoplasmic reticulum - T test stimulus     

Tunable luminescence of a synthesized furophenanthraquinone derivative: interactions with different solvents

The synthesis is described of a luminescent furophenanthraquinone derivative, 9‐methoxyphenanthro[4,3‐b]furan‐4,5‐dione (MPFD). The biological importance of tetracyclic furophenanthraquinones was considered and the tunable luminescence of MPFD in different solvents was studied to explore the nature of the specific interactions between MPFD and solvents. Observation of dual emission bands and identical nature of the fluorescence excitation spectra of MPFD monitored at the emission wavelength in polar solvents indicated the formation of two different types of species in the excited state, probably due to proton transfer from the solvent to MPFD. Luminescence intensity due to anionic species was found to be increased and the corresponding peak was red shifted with increase in the proton‐donating ability of the solvents, acting as an acid with respect to MPFD. Availability of more acidic protons in the solvent facilitated this phenomenon occurring in the excited state. MPFD also interacted with halogen‐containing solvents by forming electron donor–acceptor charge transfer (CT) complexes. This CT complex formation was dependent on the number of chlorine atoms; the position of the corresponding luminescence band varied with the polarity of the solvent. Extent of the CT increased with increase in the number of chlorine atoms in the dichloro, trichloro and tetrachloro solvents, whereas the luminescence peak due to the CT complex was found to be blue shifted with decrease in solvent polarity. Interaction of the synthesized bioactive MPFD with different solvents deserves biological importance as proton transfer and CT play pivotal roles in biology.     

铽(Ⅲ)离子及其复合物:从发光特性到传感应用

稀土元素也称镧系元素,因其独特的发光性质和配位性质,其发光复合物被广泛研究于生物技术领域。其中稀土铽(Ⅲ)离子复合物因具有优异的光谱特性,关于其研究呈现出快速的发展趋势。主要从其发光特性的角度出发,探讨了其发光机理,并对铽(Ⅲ)离子与不同有机化合物结合形成的发光铽配合物以及铽(Ⅲ)离子及其配合物与不同纳米材料形成的复合物进行了分类综述。此外,还详细地阐述了铽离子及其复合物在荧光探针、生物传感器、药物递送、细胞成像、癌症治疗等相关领域的应用。最后,对其今后发展趋势和潜在的研究价值进行了展望。     

Gaussia分泌型萤光素酶的研究进展及其应用

Gaussia分泌型萤光素酶是近年发现的一种来源于海洋桡脚类动物Gaussia princeps的新型分泌型萤光素酶,是目前已知的可自然分泌的最小萤光素酶,因其分子小、灵敏度高、半衰期短和可高效分泌,而成为一种理想的报告基因,广泛应用于体内外研究。我们就Gaussia分泌型萤光素酶的发光原理、荧光特性及其应用等进行简要综述。     

Energy transfer between Ce3+ → Gd3+ or Tb3+ in KNaSO4 microphosphor

KNaSO₄ microphosphor doped with Ce,Gd and Ce,Tb and prepared by a wet chemical method was studied using X‐ray diffraction (XRD), scanning electron microscopy (SEM) and photoluminescence (PL) characterization. KNaSO₄ has a 5‐µm particle size detected by SEM. KNaSO₄:Ce³⁺,Tb³⁺ showed blue and green emission (at 494 nm, 557 nm, 590 nm) of Tb³⁺ due to ⁵D₄ → ⁷F_J (J = 4, 5, 6) transitions. KNaSO₄:Ce³⁺,Gd³⁺ showed luminescence in the ultraviolet (UV) light region at 314 nm for an excitation at 271 nm wavelength. It was observed that efficient energy transfer took place from Ce³⁺ → Gd³⁺ and Ce³⁺ → Tb³⁺ sublattices indicating that Ce³⁺ could effectively sensitize Gd³⁺ or Tb³⁺ (green emission). Ce³⁺ emission weakened and Gd³⁺ or Tb³⁺ enhanced the emission significantly in KNaSO₄. This paper discusses the development and understanding of photoluminescence and the effect of Tb³⁺ and Gd³⁺ on KNaSO₄:Ce³⁺. Copyright © 2015 John Wiley & Sons, Ltd.     

Synthesis of highly fluorescent nitrogen and phosphorus doped carbon dots for the detection of Fe3+ ions in cancer cells

Highly fluorescent nitrogen and phosphorus‐doped carbon dots with a quantum yield 59% have been successfully synthesized from citric acid and di‐ammonium hydrogen phosphate by single step hydrothermal method. The synthesized carbon dots have high solubility as well as stability in aqueous medium. The as‐obtained carbon dots are well monodispersed with particle sizes 1.5–4 nm. Owing to a good tunable fluorescence property and biocompatibility, the carbon dots were applied for intercellular sensing of Fe³⁺ ions as well as cancer cell imaging. Copyright © 2015 John Wiley & Sons, Ltd.