@article {1010, title = {Complementary inhibition of synoviocyte, smooth muscle cell or mouse lymphoma cell proliferation by a vanadyl curcumin complex compared to curcumin alone}, journal = {Journal of Inorganic Biochemistry}, volume = {98}, number = {12}, year = {2004}, note = {ISI Document Delivery No.: 876VBTimes Cited: 20Cited Reference Count: 62}, month = {Dec}, pages = {2063-2070}, type = {Article}, abstract = {A novel vanadyl curcumin complex (VO(cur)2) has been synthesized and and its physicochemical properties characterized. Biological characterization included in vitro testing for anti-rheumatic activity in synoviocytes, angiogenesis inhibition in smooth muscle cells and anti-cancer potential in mouse lymphoma cells; as well as in vivo testing for hypoglycemic activity by oral gavage in streptozotocin (STZ)-diabetic rats. VO(cur)2 was more effective as an anti-cancer agent, compared to uncomplexed curcumin or vanadyl ion alone, was more than twice as effective as curcumin alone as an anti-arthritic agent, and was more than four times as effective as curcumin alone in inhibiting smooth muscle cell proliferation. In both acute and chronic screening tests, VO(cur)2 was ineffective as an insulin mimetic agent; however, it also proved to be exceptionally non-toxic, with no evidence of negative symptornatology during a month-long treatment period, at doses up to and including 2.0 mmol kg(-1) day(-1). (C) 2004 Elsevier Inc. All rights reserved.}, keywords = {antioxidant, apoptosis, arthritis lymphoma, BIS(MALTOLATO)OXOVANADIUM(IV), CELLS, COMPLEX, COORDINATION, curcurnin, DIABETIC-RATS, DIFERULOYL METHANE CURCUMIN, FREE-RADICALS, INDUCED LIPID-PEROXIDATION, INSULIN MIMICS, LEUKEMIA HL-60, METAL-IONS, OXIDATIVE STRESS, vanadyl ion}, isbn = {0162-0134}, url = {://000225525200010}, author = {Thompson, K. H. and Bohmerle, K. and Polishchuk, E. and Martins, C. and Toleikis, P. and Tse, J. and Yuen, V. and McNeill, J. H. and Orvig, Chris} } @article {465, title = {DNA damage induced by methylated trivalent arsenicals is mediated by reactive oxygen species}, journal = {Chemical Research in Toxicology}, volume = {15}, number = {12}, year = {2002}, note = {ISI Document Delivery No.: 627VUTimes Cited: 104Cited Reference Count: 48}, month = {Dec}, pages = {1627-1634}, type = {Article}, abstract = {Arsenic is a human carcinogen; however, the mechanisms of arsenic{\textquoteright}s induction of carcinogenic effects have not been identified clearly. We have shown previously that monomethylarsonous acid (MMA(III)) and dimethylarsinous acid (DMA(III)) are genotoxic and can damage supercoiled phiX174 DNA and the DNA in peripheral human lymphocytes in culture. These trivalent arsenicals are biomethylated forms of inorganic arsenic and have been detected in the urine of subjects exposed to arsenite and arsenate. We show here by molecular, chemical, and physical methods that reactive oxygen species (ROS) are intermediates in the DNA-damaging activities of MMA(III) and DMA(III). Using the phiX174 DNA nicking assay we found that the ROS inhibitors Tiron, melatonin, and the vitamin E analogue Trolox inhibited the DNA-nicking activities of both MMA(III) and DMA(III) at low micromolar concentrations. The spin trap agent 5,5-dimethyl-1-pyrroline-N-oxide (DMPO) also was effective at preventing the DNA nicking induced by MMA(III) and DMA(III.) ESR spectroscopy studies using DMPO identified a radical as a ROS intermediate in the DNA incubations with DMA(III). This radical adduct was assigned to the DMPO-hydroxyl free radical adduct on the basis of comparison of the observed hyperfine splitting constants and line widths with those reported in the literature. The formation of the DMPO-hydroxyl free radical adduct was dependent on time and the presence of DMA(III) and was completely inhibited by Tiron and Trolox and partially inhibited by DMSO. Using electrospray mass spectrometry, micromolar concentrations of DMA(v) were detected in the DNA incubation mixtures with DMA(III). These data are consistent with the conclusions that the DNA-damaging activity of DMA(III) is an indirect genotoxic effect mediated by ROS-formed concomitantly with the oxidation of DMA(III) to DMA(v).}, keywords = {DIMETHYLARSINIC ACID, DRINKING-WATER, ENZYMATIC METHYLATION, FREE-RADICALS, HEPATOCYTES, HUMAN, HUMAN URINE, MALE F344 RATS, MONOMETHYLARSONOUS ACID MMA(III), ORAL-EXPOSURE, RAT-LIVER CYTOSOL}, isbn = {0893-228X}, url = {://000179957500017}, author = {Nesnow, S. and Roop, B. C. and Lambert, G. and Kadiiska, M. and Mason, R. P. and Cullen, W. R. and Mass, M. J.} } @article {4717, title = {Arsenic species that cause release of iron from ferritin and generation of activated oxygen}, journal = {Archives of Biochemistry and Biophysics}, volume = {382}, number = {2}, year = {2000}, note = {ISI Document Delivery No.: 367PNTimes Cited: 90Cited Reference Count: 61}, month = {Oct}, pages = {195-202}, type = {Article}, abstract = {The in vitro effects of four different species of arsenic (arsenate, arsenite, monomethylarsonic acid, and dimethylarsinic acid) in mobilizing iron from horse spleen ferritin under aerobic and anaerobic conditions were investigated. Dimethylarsinic acid (DMA((V))) and dimethylarsinous acid (DMA((III))) significantly released iron from horse spleen ferritin either with or without the presence of ascorbic acid, a strong synergistic agent. Ascorbic acid-mediated iron release was time-dependent as well as both (DMA((III))) and ferritin concentration-dependent. Iron release from ferritin by DMA((III)) alone or with ascorbic acid was not significantly inhibited by superoxide dismutase (150 or 300 units/ml). However, the iron release was greater under anaerobic conditions (nitrogen gas), which indicates direct chemical reduction of iron from ferritin by DMA((III)), with or without ascorbic acid. Both DMA((V)) and DMA((III)) released iron from both horse spleen and human liver ferritin. Further, the release of ferritin-iron by DMA((III)) with ascorbic acid catalyzed bleomycin-dependent degradation of calf thymus DNA. These results indicate that exogenous methylated arsenic species and endogenous ascorbic acid can cause (a) the release of iron from ferritin, (b) the iron-dependent formation of reactive oxygen species, and (c) DNA damage. This reactive oxygen species pathway could be a mechanism of action of arsenic carcinogenesis in man. (C) 2000 Academic Press.}, keywords = {arsenic, ascorbic acid, BIOCHEMICAL PARAMETERS, DAMAGE, DIMETHYLARSINIC ACID, DNA-DAMAGE, ferritin, FREE-RADICALS, INORGANIC ARSENICS, iron, LIPID-PEROXIDATION, MAIN METABOLITE, OXIDATIVE, oxygen species, REACTIVE, reactive oxygen, VITAMIN-C}, isbn = {0003-9861}, url = {://000090070800005}, author = {Ahmad, S. and Kitchin, K. T. and Cullen, W. R.} } @article {3600, title = {The near infrared electronic spectrum of tungsten methylidyne, WCH}, journal = {Journal of Chemical Physics}, volume = {105}, number = {15}, year = {1996}, note = {ISI Document Delivery No.: VM554Times Cited: 19Cited Reference Count: 29}, month = {Oct}, pages = {6168-6182}, type = {Article}, abstract = {The laser excitation spectrum of tungsten methylidyne, WCH, has been recorded in the 12 000-15 400 cm(-1) region. A total of 14 vibronic bands of WCH and 16 bands of WCD have been observed in this region. Rotational analysis shows that the ground state is (X) over tilde 3/2((2) Delta), with the substitution structure r(0)(W=C)=1.7366(5) Angstrom and r(0)(C-H)=1.076(5) Angstrom. The excited vibronic levels have been assigned, on the basis of their WCH/WCD isotope shifts and their wavelength resolved fluorescence patterns, to three electronic states, (A) over tilde 3/2((2) Delta), (B) over tilde 1/2((2) Pi), and (C) over tilde 5/2(2 Phi), at 12 090, 13 392, and 14 110 cm(-1), respectively. The wavelength resolved fluorescence spectra have also established the low-lying vibrational levels of the ground state. The ground state bending fundamental lies at 660 cm(-1), while the W-C stretching frequency is 1006 cm(-1); the corresponding frequencies in WCD are 501 cm(-1) and 953 cm(-1), respectively. No evidence for the C-H stretching frequency has been found. Emission has also been observed to a low-lying electronic state, 813 cm(-1) above the (X) over tilde 3/2 state. The pattern of rotationally resolved emission to this state clearly indicates that it is a (4) Sigma(1/2) state. Its bending frequency is 612 cm(-1), and its W-C stretching frequency is 971 cm(-1), indicating a slightly longer bond length than in the (X) over tilde 3/2 state. High resolution cw laser spectra of the (0,0) bands of the two lowest excited electronic states [(A) over tilde 3/2((2) Delta) and (B) over tilde 1/2((2) Pi)] reveal a small splitting of the four principal tungsten isotopes (W-182, W-183, W-184, and W-186) which serves to confirm the presence of tungsten in the carrier. Hyperfine splitting associated with the W-183 nucleus (I = 1/2) has been observed for the (0,0) band of the (A) over tilde 3/2- (X) over tilde 3/2 system, allowing the electron configuration of the ground state to be elucidated. (C) 1996 American Institute of Physics.}, keywords = {COMPLEXES, FREE-RADICALS, GAS-PHASE, HYPERFINE-STRUCTURE, LASER-INDUCED FLUORESCENCE, SPECTROSCOPY, STATES, SYSTEM, TRANSITION, ZNCH3}, isbn = {0021-9606}, url = {://A1996VM55400009}, author = {Barnes, M. and Gillett, D. A. and Merer, A. J. and Metha, G. F.} } @article {3837, title = {Theory of muon spin relaxation of gaseous C(2)H(4)Mu}, journal = {Physical Review A}, volume = {54}, number = {6}, year = {1996}, note = {ISI Document Delivery No.: VX714Times Cited: 5Cited Reference Count: 32}, month = {Dec}, pages = {4815-4829}, type = {Article}, abstract = {A theoretical study of the muon spin relaxation of the gaseous muonated ethyl radical C(2)H(4)Mu is expanded in this paper to include both longitudinal and transverse signals. This study is based upon an operator expansion of the spin-density operator for the radical with its time dependence described by the linearized quantum Boltzmann equation. Relaxation is due to collisions which reorient the radical{\textquoteright}s rotational angular momentum while effects on the muon{\textquoteright}s spin are due to couplings between the muon{\textquoteright}s spin, the radical{\textquoteright}s free-electron spin, and the radical{\textquoteright}s rotational angular momentum. The coefficients of the radical{\textquoteright}s spin Hamiltonian and the collisional lifetimes (cross sections) are used as fitting parameters to describe the transverse signals. A fit to the transverse data by itself and a global fit to both the transverse and longitudinal data are obtained with good accuracy.}, keywords = {CHARGE-EXCHANGE, CONSTANTS, FREE-RADICALS, GAS-PHASE, IRREDUCIBLE CARTESIAN TENSORS, KINETIC-EQUATIONS, PRESSURE-DEPENDENCE, RESONANCE}, isbn = {1050-2947}, url = {://A1996VX71400033}, author = {Turner, R. E. and Snider, R. F.} } @article {7151, title = {EVIDENCE FOR NUCLEOPHILIC-ADDITION BY MUONIUM TO PYRAZINE IN WATER - CONTRAST WITH ORDINARY HYDROGEN}, journal = {Journal of the American Chemical Society}, volume = {113}, number = {24}, year = {1991}, note = {ISI Document Delivery No.: GQ931Times Cited: 15Cited Reference Count: 24}, month = {Nov}, pages = {9096-9099}, type = {Article}, abstract = {The presence of heterocyclic N atoms in an aromatic solute enhance its rate of reaction toward muonium, and the free radicals formed are seen to have muonium attached to a C atom of the ring. This contrasts the behavior of H-1 in water, where addition to N-heterocyclic rings occurs an order of magnitude slower and with H attaching to N, at least in acid solution. Muonium evidently shows nucleophilic character while ordinary hydrogen atoms are electrophilic. Pyrazine (1,4-diazine) was used for this comparison with benzene because it has the advantage over pyridine of forming only two possible radicals.}, keywords = {1-HYDROPYRIDINYL RADICALS, ATOMS, ELECTRON-SPIN RESONANCE, FREE-RADICALS, LEVEL-CROSSING-RESONANCE, LIQUIDS, ORGANIC, ROTATION, SPECTROSCOPY}, isbn = {0002-7863}, url = {://A1991GQ93100010}, author = {Wu, Z. and Barnabas, M. V. and Stadlbauer, J. M. and Venkateswaran, K. and Porter, G. B. and Walker, D. C.} }