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Syntheses and mechanistic studies of some octahedral ruthenium (III) amine complexesIsabirye, David Awubwa. January 1977 (has links)
published_or_final_version / Chemistry / Doctoral / Doctor of Philosophy
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Syntheses and mechanistic studies of some octahedral ruthenium (III) amine complexes.Isabirye, David Awubwa. January 1977 (has links)
Thesis--Ph. D., University of Hong Kong.
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Bis-Picolinamide ruthenium (III) dihalide complexes: dichloride to diiodide exchange generates single trans isomers with high potency and cancer cell selectivityBasri, A.M., Lord, Rianne M., Allison, Simon J., Rodríguez-Bárzano, A., Lucas, S.J., Janeway, F.X., Shepherd, H.J., Pask, C.M., Phillips, Roger M., McGowan, P.C. 22 February 2017 (has links)
Yes / A library of new bis-picolinamide ruthenium(III) dihalide complexes of the type RuX2L2 (X = Cl or I and L = picolinamide) have been synthesised and characterised. They exhibit different picolinamide ligand binding modes, whereby one ligand is bound (N,N) and the other bound (N,O). Structural studies reveal a mixture of cis and trans isomers for the RuCl2L2 complexes but upon a halide exchange reaction to RuI2L2, only single trans isomers are present. High cytotoxic activity against human cancer cell lines was observed, with potencies for some complexes similar to or better than cisplatin. Conversion to RuI2L2 substantially increased activity towards cancer cell lines by >12-fold. The RuI2L2 complexes displayed potent activity against the A2780cis (cisplatin-resistant human ovarian cancer) cell line, with >4-fold higher potency than cisplatin. Equitoxic activity was observed against normoxic and hypoxic cancer cells, indicating the potential to eradicate both the hypoxic and aerobic fractions of solid tumours with similar efficiency. Selected complexes were also tested against non-cancer ARPE-19 cells. The RuI2L2 complexes are more potent than the RuCl2L2 analogues, and also more selective towards cancer cells with a selectivity factor >7-fold.
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Synthesis and redox behaviour of some tetramine complexes of rutheniumIII and iridium III鄧天祐, Tang, Tin-wu. January 1982 (has links)
published_or_final_version / Chemistry / Doctoral / Doctor of Philosophy
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Thermal and photochemical behaviour of some tetramine complexes of ruthenium II and III /Lau, Tai-chu. January 1982 (has links)
Thesis--Ph. D., University of Hong Kong, 1982. / Cover title.
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Synthesis and redox behaviour of some tetramine complexes of ruthenium III and iridium III /Tang, Tin-wu. January 1982 (has links)
Thesis--Ph. D., University of Hong Kong, 1982.
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Thermal and photochemical behaviour of some tetramine complexes of ruthenium II and III劉大鑄, Lau, Tai-chu. January 1982 (has links)
published_or_final_version / Chemistry / Doctoral / Doctor of Philosophy
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Ruthenium(iii) Acetylacetonate / A Homogeneous Catalyst In The Hydrolysis Of Sodium BorohydrideKeceli, Ezgi 01 May 2006 (has links) (PDF)
Ruthenium(III) acetylacetonate was employed for the first time as homogeneous catalyst in the hydrolysis of sodium borohydride. Ruthenium(III) acetylacetonate was not reduced by sodium borohydride under the experimental conditions and remains unchanged after the catalysis, as shown by FT-IR and UV-Vis spectroscopic characterization. Poisoning experiments with mercury, carbon disulfide or trimethylphosphite provide compelling evidence that ruthenium(III) acetylacetonate is indeed a homogenous catalyst in the hydrolysis of sodium borohydride.
Kinetics of the ruthenium(III) acetylacetonate catalyzed hydrolysis of sodium borohydride was studied depending on the catalyst concentration, substrate concentration and temperature. The hydrogen generation was found to be first order with respect to both the substrate concentration and catalyst concentration. The activation parameters of this reaction were also determined from the evaluation of the kinetic data: activation energy / Ea = 25.6 & / #61617 / & / #61472 / 1.3 kJ.mol-1, the enthalpy of activation / & / #8710 / H# = 24.6 ± / 1.2 kJ.mol-1 and the entropy of activation & / #8710 / S# = -170 ± / 5 J& / #61655 / mol-1& / #61655 / K-1. Ruthenium(III) acetylacetonate provides the lowest activation energy ever found for the hydrolysis of sodium borohydride.
Ruthenium(III) acetylacetonate was found to be highly active catalyst providing 1183 total turnovers in the hydrolysis of sodium borohydride over 180 min before they are deactivated. The recorded turnover frequency (TOF) is 6.55 min-1.
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Avaliação do Potencial Citotóxico, Genotóxico e Antitumoral do Ditionato de cis-Tetraamino(oxalato)rutênio(III) em Diferentes Linhagens Celulares / Assessment of the Potential genotoxic and the Antitumor Ditionato Tetraamino cis-(oxalate) ruthenium (III) in Different Cell linesPEREIRA, Flávia de Castro 22 January 2010 (has links)
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Previous issue date: 2010-01-22 / Despite the resounding success of cisplatin and closely related platinum antitumor agents, the movement of other transition-metal antitumor agents toward the clinic has been exceptionally slow. Non-Platinum chemotherapeutic metallopharmaceuticals hold much promise for the future, and needs to be actively explored in a large variety of tumor types in combination therapies. The preparations of metallocomplexes with potential antitumor activity has been one of the main targets of transition metal chemistry since Rosenberg s discovery of cisplatin cisdiamminedichloridoplatinum (II), cis-[Pt(NH3)2Cl2]} cytotoxic activity in the 1960s. In 1978, cisplatin was approved as the first platinumbased drug for the oncology
treatment, although several negative side-effects (nephrotoxicity, neurotoxicity, nausea, etc.) had been induced on treated patients. Nevertheless, cisplatin was
followed by carboplatin {cis-diammine-1,1´ - yclobutanedicarboxylateplatinum(II), [Pt(NH3)2(cbdc)], approved in 1985} and oxaliplatin 1R,2Rdiamminocyclohexaneoxalatoplatinum(II), [Pt(dach)(ox)], approved in 1996}, which met requirements of improving antitumor activity and reducing disadvantages of
cisplatin, carboplatin and oxaliplatin represent the second, and third platinum-based drug generations, respectively. Nowadays, not only platinum-bearing complexes are
extensively studied with the aim to broaden a spectrum of transition metal-based complexes which could be used in the treatment of cancer. Ruthenium complexes
have shown potential utility in chemotherapy and photodynamic therapy. Ruthenium complexes generally have lower toxicities compared to cisplatin attributed to their
specific accumulation in cancer tissues. In vitro and in vivo studies show high anticancer activity of Ruthenium complexes and some of them are currently undergoing clinical trials. In the present work we studied the antitumor activity of the
Ruthenium(III) compound cis-Tetraammine(oxalato)Ruthenium(III) Dithionate {cis- [Ru(C2O4)(NH3)4]2(S2O6)} against different tumor and normal cells lineages, analising cell viabilities, cell cycle distribution, apoptosis induction mecanistics and genome DNA damage. Correlation tests were performed to determine the effects of the time of exposure and concentration of Ruthenium complex on mitotic index (MI) and mitotic aberration index on Allium cepa root cells. A comparison of MI results of cis- [Ru(C2O4)(NH3)4]2(S2O6) to those of lead nitrate reveals that the Ruthenium complex
demonstrates an average mitotic inhibition eightfold higher than lead, with the frequency of cellular abnormalities almost fourfold lower and mitotic aberration threefold lower. A. cepa root cells exposed to a range of Ruthenium complex
concentrations did not display significant clastogenic effects. The cis- Tetraammine(oxalato)Ruthenium(III) Dithionate therefore exhibits a remarkable capacity to inhibit mitosis, perhaps by inhibiting DNA synthesis or blocking the cell
cycle in the G2 phase. Results showed that Ruthenium(III) causes a significant reduction of proliferation of A549 cells with viabilities ranging from 55.5% to 24.6% when treated with 40 μM for 24 and 48h; and 32% to 18.2% when treated with 150 μM for 24 and 48h. The Ruthenium(III) compound induced a moderate (31.9% and 39.6% for concentrations 10 and 40 μM, respectively) to high degree (74% for concentration 32 μM) of cytotoxic activity against A549 cells (IC50= 33.72 μM). On the other hand, the normal lung fibroblast MRC-5 did not show significant reduction
proliferation in the presence of Ruthenium(III) compound. Even when treated with higher concentrations of cis-Tetraammine(oxalato)Ruthenium(III) Dithionate for 48
hours, MRC-5 cells showed viabilities ranging from 85% to 78,4% for 40 μM and 150 μM, respectively. The antiproliferative and cytotoxic activity revealed that K562 cells
cultured with concentrations 40 and 150 μg mL-1 of Ruthenium(III) compound showed significant reduction of proliferation after 72h of exposition, with viabilities ranging from 88.2% to 55.6% when treated with 40 μM for 24 and 72h; and 76.2% to 26.7% when treated with 150 μM for 24 and 72h. The Ruthenium(III) compound induced low [22.4% (24h) to 28.2% (48h) and 29.8% (24h) to 35.7% (48h) for concentrations 10
and 40 μM, respectively] to moderate [44% (24h) and 53% (48h) for concentration 150 μM] of cytotoxic activity against K562. After incubation for 48 h, the IC50 value was 18.28 μM. Compared to the cell cycle profiles of untreated cells, flow cytometric analysis indicated a sub-G1 arresting effect of Ruthenium compound on K562 cells, inducing a 1.7-fold, 2.2-fold and 2.4-fold increase in the number of sub-G1 cells for
24, 48 and 72 h, respectively, when compared to control. The compound also caused a significant increase in tailed cells in any of the concentrations tested compared with negative control that can be associated cytotoxicity with direct effect on K562 cells DNA. / Apesar do sucesso da cisplatina e dos medicamentos à base de platina, o mercado de fármacos ainda é acessível para novas drogas á base de metal que oferecem uma melhor viabilidade, tais como a administração oral, o que pode ajudar
a diminuir os efeitos colaterais graves e custos clínicos. Além disso, novos estudos concentram-se na investigação de novas drogas com maior eficácia, ou seja, drogas que interajam de forma diferente com o DNA, o que pode levar à superação da resistência inata ou adquirida de certos tipos de tumores. Dentre os vários complexos a base de metais desenvolvidos, os complexos de rutênio (III) representam uma nova família de promissores agentes anticâncer. No presente
estudo foi investigado in vitro o efeito do composto Ditionato de cis- Tetraamino(oxalato)rutênio(III) sobre a viabilidade celular, distribuição das fases do ciclo celular, mecanismos de indução de apoptose e danos a molécula de DNA. Os
resultados provenientes da análise do teste Allium cepa mostraram um efeito tempo dose-dependente. A avaliação mostrou que a concentração de rutênio teve um impacto maior do que o tempo de exposição. O efeito também se mostrou cumulativo, com uma quase completa inibição da mitose em uma concentração de rutênio de 0,1 mg mL-1 ou superior por períodos superiores a 24 h. Por outro lado, os
resultados não revelaram efeitos clastogênicos significativos nas células meristemáticas expostas ao complexo de rutênio (III). A comparação entre os valores dos Índice Mitótico de células meristemáticas de cebolas tratadas com o complexo de rutênio em relação às células tratadas com nitrato de chumbo também mostrou que o complexo de rutênio induziu uma inibição mitótica média oito vezes maior do que o chumbo. Notadamente, as freqüências de anomalias e aberrações celulares mitóticas foram quase quatro vezes e três vezes menores, respectivamente. Os resultados mostram que o composto estudado causa significativa redução da proliferação das células A549 com viabilidades entre 55,5%
para 24,6% quando tratados com 40 μM por 24 e 48h; e 32% para 18,2% quando tratados com 150 μM por 24 e 48h. O composto de rutênio(III) induz moderada (31,9% e 39,6% para concentrações 10 e 40 μM, respectivamente) para alta
degradação (74% para a concentração 150 μM) para avaliação da atividade citotóxica das células A549 (IC50= 33,72 μM). Quanto à linhagem de fibroblasto de pulmão humano normal MRC-5, não mostrou redução significativa na proliferação celular na presença do composto. Quando tratadas com altas concentrações do Ditionato cis-Tetraamino(oxalato)rutênio(III) por 48 horas, celulas MRC-5 mostraram
viabilidades altas de 85% e 78,4% para 40 μM e 150 μM, respectivamente. A atividade citotóxica e antiproliferativa revelou que a cultura de células K562 nas concentrações de 40 e 150 μg mL-1 do composto de Rutênio(III) mostrou redução significativa na proliferação 72h de exposição, com viabilidades de 88,2% para 55,6% quando tratadas com 40 μM por 24 e 72h; e 76,2% para 26,7% quando tratadas com 150 μM por 24 e 72h. O composto de Rutênio(III) induziu baixa [22,4% (24h) para 28,2% (48h) e 29,8% (24h) para 35,7% (48h) para concentrações de 10 e 40 μM, respectivamente] para moderada [44% (24h) e 53% (48h) para concentrações de 150 μM] atividade citotóxica em células K562. Após a incubação de 48 h, o valor da IC50 foi de 18,28 μM. Quando comparado o ciclo celular de células não tratadas, a análise indica que as células foram arrastadas para sub-G1
apresentando um aumento de 1,7 para 2,2 e 2.4% no número de células em sub-G1 por 24, 48 e 72 h, respectivamente, quando comparado com o grupo controle. O composto também causou um significativo aumento em danos celulares nas concentrações testadas quando comparado com o controle negativo, o que pode estar associado com efeitos citotóxicos diretamente no DNA celular.
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Testing The Ruthenium(iii) Acetylacetonate And 1,2-bis(diphenylphosphino)ethane System As Homogeneous Catalyst In The Hydrolysis Of Sodium BorohydrideDemiralp, Tulin 01 June 2008 (has links) (PDF)
Recent studies have shown that ruthenium(III) acetylacetonate is acting as homogeneous catalyst in the hydrolysis of sodium borohydride. Although trimethlyphosphite is found to be a poison for the catalytic hydrolysis of sodium borohydride, a longer observation of the reaction in the presence of ruthenium(III) acetylacetonate and 2 equivalent trimethylphosphite shows an unexpected enhancement in the catalytic activity after an induction period. The same rate enhancement is observed when 2 equivalent triphenylphosphine is added into the reaction solution. Addition of 1 equivalent 1,2-bis(diphenylphosphino)ethane, dppe, into the solution shows similarly a rate enhancement in the hydrolysis of sodium borohydride catalyzed by ruthenium(III) acetylacetonate. The effect of 1,2-bis(diphenylphosphino)ethane on the catalytic activity of ruthenium(III) acetylacetonate in the hydrolysis of sodium borohydride was studied by varying mole ratio of dppe / Ru(acac)3, ruthenium concentration, substrate concentration and temperature. The highest enhancement in the rate of hydrolysis was obtained when 1 equivalent dppe was used and therefore, this mole ratio of dppe / Ru(acac)3 was used in the further studies. The rate of the reaction was found to be first order in catalyst concentration and zero order in substrate concentration. From the evaluation of rate constant versus temperature data, the activation parameters for the hydrolysis of sodium borohydride catalyzed by ruthenium(III) acetylacetonate plus 1 equivalent dppe were found to be Ea= 59 ± / 2 kJ/mol, & / #8710 / H& / #8800 / = 60 ± / 1 kJ.mol-1 and & / #8710 / S& / #8800 / = -50 ± / 3 J.(mol.K)-1. A series of control experiments were performed to characterize the active catalyst. However, the only useful information could be obtained by comparison of the UV-vis electronic absorption spectra taken from the solution during the catalytic reaction, is that, ruthenium(III) is reduced to ruthenium(II) in the course of reaction. It was concluded that a ruthenium(II) species is formed as a transient and may be the active catalyst in the reaction. After the reaction, the only ruthenium species isolated from the solution was the ruthenium(III) acetylacetonate.
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