C-H...N and C-H...S hydrogen bonds--influence of hybridization on their strength

Simple complexes connected through C-H...S and C-H...N interactions are investigated: CH4...NH3, C2H4...NH3, C2H2...NH3, CH4...SH2, C2H4...SH2, and C2H2...SH2. Ab initio and DFT calculations are performed (SCF, MP2, B3LYP) using different basis sets up to the MP2/aug-cc-pVQZ//MP2/aug-cc-pVDZ level of approximation. The Bader theory is applied since MP2/6-311++G(d,p) wave functions are used to find and to characterize bond critical points in terms of electron densities and their Laplacians. The influence of hybridization on the properties of C-H...S and C-H...N systems is also studied showing that the strength of such interactions increases in the following order: C(sp3)-H...Y, C(sp2)-H...Y, C(sp)-H...Y, where Y = S, N--it is in line with the previous findings on C-H...O hydrogen bonds. The results also show that CH4...SH2 and C2H4...SH2 complexes should be rather classified as van der Waals interactions and not as hydrogen bonds. The frequency associated with the C-H stretch of C(sp3)-H...S is blue-shifted.     

Preparation and characterization of polyvinyl alcohol-capped CdSe nanoparticles at room temperature

Polyvinyl alcohol (PVA)-capped CdSe nanoparticles were successfully prepared by a one-step solution growth technique at room temperature and ambient pressure. X-ray diffraction, transmission electron microscopy, infrared spectra, and X-ray photoelectron spectra were used to characterize the final product. The as-prepared CdSe nanocrystals were well dispersed and uniform in shape and the diameter of the particles was confined within 8 nm. Ultraviolet-visible absorption spectra were used to study the confined growth process of PVA-capped CdSe nanoparticles. Photoluminescence measurement showed the near band-edge luminescence of the final product.     

Conduction in charged PbSe nanocrystal films

Conduction in thin films of PbSe nanocrystals doped by electrochemical gating has been studied. Charging the film, with either electrons or holes, increases the conductance by orders of magnitude. The electrons in the 1S(e) state of nanocrystals in these films have a mobility as high as 5.0 x 10(-3) cm(2) V(-1) s(-1). Electrons in the 1P(e) state were found to have a differential mobility up to 3-5 times greater than the electrons in the 1S(e) state, and a mobility minima was found corresponding to the complete filling of the 1S(e) state. The temperature and electric field dependence of conductance in the film, measured between 4.3 and 135 K, were both well described by a variable range hopping model.     

The cyclic fixation and reduction of molecular nitrogen with [WH4(Ph2PCH2CH2PPh2)2] in γ-irradiated solutions

Yields of NH₃ and N₂H₄ in radiation-catalytic reduction of N₂ by means of a hydride complex of W^IV with dppe in thf solution and in mixtures of thf with other solvents have been estimated. A mechanism proposed earlier of reduction of coordinated N₂ has been confirmed and the role of solvent in reduction of N₂ to NH₃ and amines has been explained.     

Voltammetric studies of the effect of Cisplatin-liposome on Hela cells

In this paper, the voltammetric method was used for the first time to study the effect of Cisplatin-liposome on Hela cells. The results showed the voltammetric behavior of Hela cells was irreversible and the peak current had linear relationship with the cell number. With both Cisplatin-liposome concentration and treating time increasing, the peak current decreased. The peak current decreasing was in accordance with the nuclear damage and loss of mitochondrial membrane potential revealed by two-photon laser scanning microscopy and confocal laser scanning microscopy. This voltammetric method may provide a simple way to study the electron-transfer mechanism in drug-treating cells.     

Kinetics and mechanism of the first aquation stage for the [Cr(pic)3]0 and [Cr(pic)2(OH)]2 0 complexes in HClO4 solutions

Aquation of [Cr(pic)₃]⁰ and [Cr(pic)₂(OH)]₂ ⁰ in aqueous HClO₄ solutions leads to formation of the common product – [Cr(pic)₂(H₂O)₂]⁺. The first, reversible stage, the ring opening via Cr—N bond breaking in [Cr(pic)₃]⁰ is followed by the second, rate-determining step – one-end bonded pic ligand liberation. In the case of the [Cr(pic)₂(OH)]₂ ⁰ complex, the first faster stage produces the singly bridged dimer, which undergoes cleavage into the parent monomers in the second, much slower step. The subsequent aquation of [Cr(pic)₂(H₂O)₂]⁺ is extremely slow and leads to [Cr(pic)(H₂O)₄]²⁺ formation, which practically does not undergo further ligand substitution under the conditions applied. Kinetics of the first aquation stage for [Cr(pic)₃]⁰ and of the second step for [Cr(pic)₂(OH)]₂ ⁰ were studied spectrophotometrically in the 0.1–1.0 M HClO₄ range at I = 1.0 M. The observed pseudo-first order rate constant for [Cr(pic)₃]⁰ decreases with [H⁺] increase according to the rate law: k _obs = k ₁ + k _–1 Q ₁/[H⁺], where k ₁ and k _–1 are the rate constants of the forward and the reverse processes in the unprotonated substrate and Q ₁ is the protonation constant of the pyridine nitrogen atom. In the case of the [Cr(pic)₂(OH)]₂ ⁰ complex, the rate for the singly bridged dimer cleavage does not depend on [H⁺]. The activation parameters for the chelate-ring opening in [Cr(pic)₃]⁰ and for the singly bridged dimer cleavage have been determined and discussed. Some kinetic data of the slow, second aquation stage for the [Cr(pic)₃]⁰ complex and of the fast, first aquation stage for the doubly bridged dimer have been studied; for both reactions the rate increases linearly with the increase in [H⁺].     

Phototransformations of 5-aminolevulinic acid-induced protoporphyrin IX in vitro: a spectroscopic study

Human adenocarcinoma cells of the line WiDr were incubated with 5-aminolevulinic acid to induce protoporphyrin IX (PpIX) and then exposed to laser light of wavelength 635 nm. The PpIX fluorescence decreased with increasing exposure. The decay rate was slightly dependent on the initial PpIX concentration. The PpIX fluorescence was halved by a fluence of about 40 J/cm2. Several fluorescing photoproducts were formed. The main one, supposedly the chlorine-type photoprotoporphyrin (Ppp), had a fluorescence excitation spectrum stretching out to about 680 nm with a maximum at around 668 nm. The formation kinetics of this product was dependent on the initial PpIX concentration. Moreover, it was selectively bleached by exposure to light at 670 nm. A photoproduct with an emission maximum at 652 nm, different from Ppp, remained after this exposure. Traces of a photoproduct(s) with fluorescence emission slightly blue-shifted compared with that of PpIX, supposedly water-soluble porphyrins, were also detected after light exposure.     

三角波交流示波极谱的研究(Ⅰ)——示波极谱图的性质

用三角波电流代替正弦波电流,进行交流示波极谱滴定,所得示波极谱图与正弦波结果相似。对一些离子的滴定表明,两法所得结果均在定量分析允许误差范围以内。报道了三角波交流示波极谱图的一些性质。     

Interaction between sodium tanshinone IIA sulfonate and the adriamycin semiquinone free radical: A possible mechanism for antagonizing adriamycin-induced cardiotoxity

Adriamycin (ADR) is a powerful and widely used antitumor drug, but its dose dependent cardiotoxicity limits its application. This side effect is believed to be caused by the adriamycin semiquinone free radical (ASFR). The primary focus of this work is to test effects of sodium tanshinone IIA sulfonate (STS) on ASFR and adriamycin–induced lipid peroxidation. It was found that ADR, whether in the system of heart homogenate, heart mitochondria or heart submitochondria, with NADH as the substrate or in xanthine/xanthine oxidase under anaerobic conditions, all produced ASFR rapidly. STS was shown to effectively scavenge ASFR in all these systems and postpone the appearance of ASFR. The delayed time was proportional to the amount of STS. Under aerobic conditions, ASFR could be oxidized to generate oxygen free radicals. STS could not scavenge these oxygen free radicals, but it could effectively scavenge lipid free radicals generated from membrane lipid peroxidation of heart mitochondria. STS could significantly reduce mitochondrial swelling and lipid peroxidation induced by ADR. Animal experiments show that treatment of STS could inhibit endogenous lipid peroxidation caused by ADR. Here, a protective mechanism of STS is suggested that STS can rapidly and univalently oxidize ASFR, causing the cycle of adriamycin between its quinone form and semiquinone form and inhibiting the accumulation of ASFR. Under aerobic condition, STS can protect heart mitochondria by scavenging lipid free radicals generated from adriamycin-induced mitochondrial lipid peroxidation. This investigation shows that STS may be a physiological drug to antagonize the cardiotoxicity of ADR.