Vanadium compounds induce stronger growth suppression in PTEN-deficient prostate cancer cells by ROS-mediated mechanism

In the present study, we investigated the antiproliferative effect and the underlying mechanism of three antidiabetic vanadium compounds, metavanadate, VO（acac）2 and VO（ma）2, in human prostate cancer cells （PC-3 and DU-145）. The results showed that vanadium compounds caused cell cycle arrest at G2/M phase evidenced by the elevation ofphosphorylated Cdc2 at tyr-15. Moreover, the results revealed that vanadium compounds induced reactive oxygen species （ROS） elevation in the two cell lines. The decreased level of Cdc25C could be rescued by the antioxidant, N-acetylcysteine, indicating that vanadium compounds-induced G2/M arrest was mediated by ROS. Additionally, the three vanadium compounds exerted more potent growth inhibitory effect on PC-3 cells which are PTEN-deficient and with higher level of basal ROS. It suggested that PTEN protein might serve as a biomarker for the selectivity of antitumor therapy using ROS-generating agents. Since the studied vanadium compounds have been shown the antidiabetic activities in the previous studies, there may be additional benefits in the potential application of vanadium compounds to suppress the growth of prostate cancer cells.

Optical transmission in thin films of vanadium compounds

Thin films of five vanadium compounds/composite： （1） VO2（3-fl） （3-fl = 3-Hydroxyflavone）, （2） VO（pbd）： （pbd = 1-Phenyl-l, 3-butadione）, （3） VO（dbm）2 （dbm = Dibenzoylmethane）, （4） VPc （Vanadyl Phthalocyanine） and （5） V2O5-PEPC （V2O5- poly-N-epoxypropylcarbazole composite）, were deposited by the dropcasting method from the solution in benzene. The transmittance-irradiance relationships were investigated and the transmission in the visible spectrum and optical images were obtained as well. It was found that the transmittance of the VO2（3-fl）, VO（pbd）2, VO（dbm）2 and VPc, was practically independent of the irradiance; whereas the transmittance of V2O5-PEPC decreased by 4% for thin and 9% for thick films with an increase of the irradiance.

Study on stabilities and electrochemical behavior of V(V) electrolyte with acid additives for vanadium redox flow battery

Several acid compounds have been employed as additives of the V(V) electrolyte for vanadium redox flow battery(VRB) to improve its stability and electrochemical activity. Stability of the V(V) electrolyte with and without additives was investigated with ex-situ heating/cooling treatment at a wide temperature range of-5 ?C to 60 ?C. It was observed that methanesulfonic acid, boric acid, hydrochloric acid, trifluoroacetic acid,polyacrylic acid, oxalic acid, methacrylic acid and phosphotungstic acid could improve the stability of the V(V) electrolyte at a certain range of temperature. Their electrochemical behaviors in the V(V) electrolyte were further studied by cyclic voltammetry(CV), steady state polarization and electrochemical impedance spectroscopy(EIS). The results showed that the electrochemical activity, including the reversibility of electrode reaction, the diffusivity of V(V) species, the polarization resistance and the flexibility of charge transfer for the V(V) electrolyte with these additives were all improved compared with the pristine solution.

Prediction of the Gibbs Free Energies of Formation of Intermediate Compounds in a Binary System

A method for predicting the Gibbs free energies of intermediate compounds in a binary system has been presented, based upon the regulations of the Gibbs free energies of formation of intermediate compounds in the system. The application of this procedure to the V-O system demonstrates that this method is feasible.

The IR Spectra Analysis and Crystal Structure of V_3(μ_3-O)(μ_2-O_2CEt)_6(O)_2(THF)·2CHCl_3

The title compound (C_ 24H_ 40Cl_6O_ 16V_3, M_r = 950.08) was synthesized from the reaction of VCl_3 and NaO_2CEt in CHCl_3 and THF. The crystal structure has been determined by X-ray single-crystal diffraction analysis. It crystallizes in monoclinic space group C2/c with a = 12.5768(4), b= 16.5601(4), c = 19.3574(7) , β = 99.879(1)°, V = 3971.3(2)3, D_c = 1.589 g/cm3, μ= 1.157 mm -1, F(000)=1932, Z=4, R = 0.055, wR = 0.1539 (I2σ(I)). This compound has an unusual coplanar V_3O core with a C_2 axis passing through O(1), V(1), O(10): one V-μ_3O is short (1.628 ), the other two are longer (2.381 ). It was characterized by IR, 1H NMR, and EPR spectra. It was unstable and the decomposition process of this compound was studied using IR spectroscopy.

Nanostructure and thermal-optical properties of vanadium dioxide thin films

A novel nanopolycrystalline structure of vanadium dioxide thin films is deposited on silicon or fused silica substrates by reactive ion sputtering and followed by an annealing. The characteristic analysis＇shows that the films have a columnar nanostructure with an average grain of 8 nm. The resistivities as a function of ambient temperatures tested by four-point probes for as-deposited films present that the transition temperature for nanostructure of vanadium dioxide films is near 35 ℃ which lowers about 33 ℃ in comparison with the transition temperature at 68 ℃ in its microstructure.

Amavadin induced PTP opening not through the promotion of ROS generation in rat kidney mitochondria

Amavadin is a natural vanadium compound that accumulates to high level in poisonous Amanita mushrooms. Recently, amavadin was found to have potential therapeutic effect in cancer treatment. However, its toxicity and the possible mechanism of actions are still not clear. In this study, we investigated the toxic effects of amavadin on rat kidney mitochondria and the possible mechanism. We found that amavadin induced significantly permeability transition pore （PTP） opening in the mitochondria. Amavadin y inhibited the generation of reactive oxygen species （ROS） in succinate buffer, and at high concentration of 200 gM it increased the ROS generation in malate buffer. With the addition of rotenone, the ROS generation in malate buffer was strongly enhanced than that induced by amavadin alone, but remained unchanged in succinate buffer. Results from the present study suggest that amavadin act upon electron transport chain downstream of rotenone, and the ubiquinone binding site in complex I is the most possible binding site.