Steering CO2 electroreduction toward ethanol production by a surface-bound Ru polypyridyl carbene catalyst on N-doped porous carbon.

Electrochemical reduction of CO2 to multicarbon products is a significant challenge, especially for molecular complexes. We report here CO2 reduction to multicarbon products based on a Ru(II) polypyridyl carbene complex that is immobilized on an N-doped porous carbon (RuPC/NPC) electrode. The catalyst utilizes the synergistic effects of the Ru(II) polypyridyl carbene complex and the NPC interface to steer CO2 reduction toward C2 production at low overpotentials. In 0.5 M KHCO3/CO2 aqueous solutions, Faradaic efficiencies of 31.0 to 38.4% have been obtained for C2 production at -0.87 to -1.07 V (vs. normal hydrogen electrode) with 21.0 to 27.5% for ethanol and 7.1 to 12.5% for acetate. Syngas is also produced with adjustable H2/CO mole ratios of 2.0 to 2.9. The RuPC/NPC electrocatalyst maintains its activity during 3-h CO2-reduction periods.

A Novel Ruthenium(II) Polypyridyl Complex Bearing 1,8-Naphthyridine as a High Selectivity and Sensitivity Fluorescent Chemosensor for Cu2+ and Fe3+ Ions.

A novel ruthenium(II) polypyridyl complex bearing 1,8-naphthyridine was successfully designed and synthesized. This complex was fully characterized by EI-HRMS, NMR, and elemental analyses. The recognition properties of the complex for various metal ions were investigated. The results suggested that the complex displayed high selectivity and sensitivity for Cu2+ and Fe3+ ions with good anti-interference in the CH3CN/H2O (1:1, v/v) solution. The fluorescent chemosensor showed obvious fluorescence quenching when the Cu2+ and Fe3+ ions were added. The detection limits of Cu2+ and Fe3+ were 39.9 nmol/L and 6.68 nmol/L, respectively. This study suggested that this Ru(II) polypyridyl complex can be used as a high selectivity and sensitivity fluorescent chemosensor for Cu2+ and Fe3+ ions.

A naked-eye colorimetric molecular "light switch" based on ruthenium(II) polypyridyl complex [Ru(phen)2ttbd]2+ as binder and stabilizer for RNA duplex and triplex.

Binding of [Ru(phen)2ttbd]2+ (phen = 1,10-phenanthroline, ttbd = 4-(6-propenylpyrido-[3,2-a]- phenzain-10-yl-benzene-1,2-diamine) to the RNA triplex poly(U-A*U) (herein "-" and "*" refer to the Watson-Crick and Hoogsteen binding, respectively) and the duplex poly(A-U) have been investigated by spectral technology and viscosity method. Analysis of spectral titrations and viscosity experiments as well as melting measurements suggest that [Ru(phen)2ttbd]2+ binds to the studied RNA triplex and duplex through intercalation, while its binding constant toward the triplex is greater than the duplex. Luminescent titrations indicate that [Ru(phen)2ttbd]2+ can act as a molecular "light switch" for the two RNAs and the switch effect can be detected by the naked-eye. Moreover, the "light switch" can be repeatedly cycled off and on by adjusting the pH of the solution, whereas color change in the case of the triplex is more significant compared with the duplex. To our knowledge, [Ru(phen)2ttbd]2+ is the first small molecule capable of serving as a pH-controlled reversible visual molecular "light switch" for both the RNA triplex poly(U-A*U) and duplex poly(A-U). Thermal denaturation experiments suggest that [Ru(phen)2ttbd]2+ can obviously increase the triplex stabilization, while it stabilizing third-strand is more marked in comparison with the template duplex of the triplex, indicating this complex preferentially binds to third-strand. The obtained results may be useful for understanding the binding of Ru(II) polypyridyl complexes to RNAs.

The cell-impermeable Ru(II) polypyridyl complex as a potent intracellular photosensitizer under visible light irradiation via ion-pairing with suitable lipophilic counter-anions.

Developing the cell-impermeable Ru(II) polypyridyl cationic complexes as effective photosensitizers (PS) which have high cellular uptake and photo-toxicity, but low dark toxicity, is quite challenging. Here we found that the highly reactive singlet oxygen (1O2) can be generated by the irradiation of a typical Ru(II) polypyridyl complex Ru(II)tris(tetramethylphenanthroline) ([Ru(TMP)3]2+) under visible light irradiation by ESR with TEMPO (2,2,6,6-tetramethyl-4-piperidone-N-oxyl) as 1O2 probe. Effective cellular and nuclear delivery of cationic [Ru(TMP)3]2+ was achieved through our recently developed ion-pairing method, and 2,3,4,5-tetrachlorophenol (2,3,4,5-TeCP) was found to be the most effective among all chlorophenols tested. The accelerated cellular, especially nuclear uptake of [Ru(TMP)3]2+ results in the formation of 8-oxo-7,8-dihydro-2'-deoxyguanosine (8-oxodG) and DNA strand breaks, caspase 3/7 activation and cell apoptosis in HeLa cells upon light irradiation. More importantly, compared with other traditional photosensitizers, [Ru(TMP)3]2+ showed significant photo-toxicity but low dark toxicity. Similar effects were observed when 2,3,4,5-TeCP was substituted by the currently clinically used anti-inflammatory drug flufenamic acid. This represents the first report that the cell-impermeable Ru(II) polypyridyl complex ion-paired with suitable lipophilic counter-anions functions as potent intracellular photosensitizer under visible light irradiation mainly via a 1O2-mediated mechanism. These findings should provide new perspectives for future investigations on other metal complexes with similar characteristics as promising photosensitizers for potential photodynamic therapy.

A phenolic hydroxyl in the ortho- and meta-positions on the main ligands effect on the interactions of [Ru(phen)2(o-HPIP)]2+ and [Ru(phen)2(m-HPIP)]2+ with the poly(U)·poly(A)*poly(U) triplex.

The association of two ruthenium(II) complexes [Ru(phen)2(o-HPIP)]2+ (Ru1; phen = 1,10-phenanthroline, o-HPIP = 2-(2-hydroxyphenyl)-imidazo[4,5-f][1,10] phenanthroline) and [Ru(phen)2(m-HPIP)]2+ (Ru2; m-HPIP = 2-(3-hydroxyphenyl)-imidazo[4,5-f][1,10]phenan- throline) with the RNA poly(U)·poly(A)⁎poly(U) triplex has been investigated by spectrophotometric titrations and melting experiments in this work. All experimental data reveal an intercalative triplex-binding mode of the two complexes, whereas the binding constant for Ru1 is significantly higher than that for Ru2. Circular dichroism spectroscopic investigations show that the two complexes could bind to the chiral environment of the triplex, but the triplex perturbation effects induced by Ru1 are more marked. Thermal denaturation experiments demonstrate that both Ru1 and Ru2 display a large binding preference and stabilizing effect for the third strand over the Watson-Crick base-paired duplex of the triplex. However, the third-strand stabilizing effect of Ru1 is much more effective than that of Ru2. The obtained results suggest that positions of the phenolic group on the main ligands have significant effect on the binding of the two complexes with poly(U)·poly(A)⁎poly(U) triplex.

New ruthenium polypyridyl complexes functionalized with fluorine atom or furan: Synthesis, DNA-binding, cytotoxicity and antitumor mechanism studies.

Two novel ruthenium(II) polypyridyl complexes, namely, [Ru(dmp)2(CAPIP)](ClO4)2 (Ru(II)-1) and [Ru(dmp)2(CFPIP)](ClO4)2 (Ru(II)-2), which respectively contain (E)-2-(2-(furan-2-yl)vinyl)-1H-imidazo[4,5-f][1,10]phen-anthroline (CAPIP) and (E)-2-(4-fluorostyryl)-1H-imidazo[4,5-f][1,10]phenanthroline. (CFPIP), were first designed and characterized (dmp = 2,9-dimethyl-1,10-phenanthroline). DNA binding experiments indicated that Ru(II) complexes interact with CT DNA through intercalative mode. In addition, the complexes Ru(II)-1 and Ru(II)-2, showed remarkable cell cytotoxicity, giving the respective IC50 values of 4.1 ±â€¯1.4 µM and 6.1 ±â€¯1.4 µM on the A549 cancer cells. These values indicated higher activity than CAPIP, CFPIP, cisplatin (8.2 ±â€¯1.4 µM) and other corresponding Ru(II) polypyridyl complexes. Furthermore, the Ru(II) complexes could arrive the cytoplasm through the cell membrane and accumulate in the mitochondria. Significantly, complexes Ru(II)-1 and Ru(II)-2 induced A549 cells apoptosis was mediated by increase of ROS levels and dysfunction of mitochondria, and resulted in cell cycle arrest and increased anti-migration activity on A549 cells. Overall, these results indicated that complexes Ru(II)-1 and Ru(II)-2 could be suitable candidates for further investigation as a chemotherapeutic agent in the treatment of tumors.

Anticancer activity studies of a ruthenium(II) polypyridyl complex against human hepatocellular (BEL-7402) cells.

A Ru(II) polypyridyl complex [Ru(bpy)2(HMSPIP)](ClO4)2 (1) (bpy=2,2'-bipyridine, HMSPIP=2-(4-methylsulfonyl)phenyl-1H-imidazo[4,5-f][1,10] phenanthroline) was synthesized. The IC50 value of the complex against human hepatocellular cell BEL-7402 is 21.6±2.7 µM. The complex shows no cytotoxic activity toward human lung adenocarcinoma cell A549, human osteosarcoma cell MG-63 and human breast cancer cell SK-BR-3 cells. It is easily for complex 1 to be taken up by BEL-7402 cells. The complex can enhance the reactive oxygen species (ROS) levels and induce the decrease in the mitochondrial membrane potential. The complex inhibits the cell growth in BEL-7402 cells at G2/M phase. Complex 1 can regulate the expression of Bcl-2 family proteins. The results show that the complex induces apoptosis of BEL-7402 cells through a ROS-mediated mitochondrial dysfunction pathway.

Ruthenium(II) complexes: DNA-binding, cytotoxicity, apoptosis, cellular localization, cell cycle arrest, reactive oxygen species, mitochondrial membrane potential and western blot analysis.

The aim of our study was to investigate DNA-binding and cytotoxic activity of the four new Ru(II) polypyridyl complexes [Ru(dmb)2(HMHPIP)](ClO4)2 (1), [Ru(bpy)2(HMHPIP)](ClO4)2 (2), [Ru(phen)2(HMHPIP)](ClO4)2 (3) and [Ru(dmp)2(HMHPIP)](ClO4)2 (4). The complexes interact with DNA through intercalative mode and show relatively high cytotoxic activity against A549 cells, no cytotoxicity toward MG-63 cells. Complexes 1-4 can enhance the levels of ROS in A549 cells and induce the decrease of the mitochondrial membrane potential. These complexes inhibit the cell growth in A549 cells at G0/G1 or S phase. Complex 3 activated caspase 7, and down-regulated the expression of the anti-apoptotic protein Bcl-2. Complexes 1-4 induce apoptosis in A549 cells through ROS-mediated mitochondrial dysfunction pathway.

Synthesis, characterization, DNA interaction, antioxidant and anticancer activity studies of ruthenium(II) polypyridyl complexes.

Two new Ru(II) polypyridyl complexes [Ru(phen)2(adppz)](ClO4)2 (1) and [Ru(dip)2(adppz)](ClO4)2 (2) have been synthesized and characterized. The DNA-binding constants were determined to be 6.54 ± 0.42 × 10(5) and 7.65 ± 0.20 × 10(5)M(-1) for complexes 1 and 2. DNA binding experiments indicated that complexes 1 and 2 interact with DNA through intercalative mode. Antioxidant activity shows that the complexes have significant hydroxyl radical scavenging activity. Cytotoxic activities suggest that the complex 2 exhibits higher cytotoxic activity against BEL-7402, MG-63 and SKBR-3 cells than complex 1 under identical conditions. Complexes 1 and 2 can induce apoptosis of BEl-7402 cells. We have identified several cellular mechanisms induced by 1 and 2 in BEL-7402 cells, including the level detection of ROS, activation of procaspase 3, caspase 7, the expression of antiapoptotic proteins Bcl-x, Bcl-2, proapoptotic proteins Bad, Bax, Bid and cell cycle arrest. Thus, complexes 1 and 2 inhibit growth of BEL-7402 cells through induction of apoptotic cell death, enhancement of ROS levels and S-phase and G0/G1 cell cycle arrest. Further investigations have shown that complex 2 induces apoptosis by regulating the expression of Bcl-2 family proteins.