Study of transient luminescence of three kinds of Ru complexes bound to DNA

The transient luminescence of three kinds of ruthenium complexes [Ru(bpy)2(7-CH3-dppz)]2+, [Ru(bpy)2(7-F-dppz)]2+ and [Ru(phen)2(7-F-dppz)]2+ bound to calf thy-mus DNA (ctDNA) has been studied by using the time-resolved spectroscopy. The results show that the luminescence is due to the radiative decay from the charge-transfer states to the ground state. By the interaction with DNA, the radia-tiveless rate of the photoexcited Ru complex molecules decreases, which results in the increase of luminescence lifetime and efficiency. The structure of the Ru com-plex has an important impact on the interaction with DNA. The [Ru(bpy)2(7-CH3-dppz)]2+ shows the longest luminescence lifetime (about 382 ns), while the [Ru(bpy)2(7-F-dppz)]2+ shows the shortest lifetime (about 65 ns). The possible origin of the luminescence dynamics is discussed.

Synthesis of a new iron(Ⅲ) porphyrin acrylate-styrene copolymer and its catalysis for hydroxylation of cyclohexane

A new iron(III)porphyrin acrylate-styrene copo-lymer,P[(PorFe)A-S],was synthesized by the reaction of iron(III)porphyrin acrylate with styrene and characterized by UV-Vis,Infrared spectra(IR),inductively coupled plasma-atomic emission spectrometry(ICP)and molecular weight determination.Its catalytic activity in the hydroxylation of cyclohexane for model cytochrome P450 in the P[(PorFe)A-S]-O_(2)–ascrobate-thiosalicylic acid system has been studied.It was found that the P[(PorFe)A-S]has a higher catalytic activity than non-supported iron(III)porphyrin and its high catalytic activity remained in reuse.The catalytic activity of P[(PorFe)A-S]was discussed in the view of the microenvi-ronment of iron(III)porphyrin.It is proposed that the cata-lytic activity of the P[(PorFe)A-S]may be further enhanced by construction of a homophase catalytic system containing the iron(III)porphyrin acrylate-styrene copolymer.

Photophysical properties of the Corrole photosensitizers

The photophysical properties of a series of hydroxyl Corroles, Corrole-F, Corrole-Cl, Corrole-Br, Corrole-I and Corrole-2I, have been investigated by steady-state and time-resolved transient spectroscopy. The absorption spectra show a strong peak around 420 nm corresponding to B band and several weak Q absorption bands between 450 nm and 650 nm, exhibiting much stronger Q band absorption than that of porphyrin. The absorptions of these Corroles increase with the atom weight and the number of halogen atoms. All samples show similar fluorescence characteristics of an emission peak at 650 nm. The fluorescence intensities significantly decrease with the atom weight and the number of halogen atoms. The fluorescence quantum yield of Corrole-I is 0.947%, which is larger than that of Corrole-2I (0.381%). The fluorescence dynamics of the hydroxyl Corroles shows that both the fluorescence lifetime and the intersystem-crossing transition time of these Corroles decrease sharply with the increase of the atom weight and the number of halogen atoms, which may lead to the increase of the triplet state quantum yield. The heavy-atom effect on active oxygen of PDT has also been discussed by the end of this paper.

DNA Binding Properties and Cytotoxic Activities of Two Trinuclear Ruthenium（Ⅱ） Polypyridyl Complexes

The interactions between two trinuclear Ru（II） complexes and calf thymus DNA（CT DNA） were studied via absorption spectroscopy, reverse salt titrations, binding stoichiometry, DNA melting experiments, as well as viscosity measurement. The results indicate that complexes 1 and 2 bind to DNA via the interaction of the planar π-delocalized system of the complexes with intrinsic binding constants of 4.18 × 10^5 and 3.85 × 10^6 L/tool, respectively, and non-electrostatic binding free energy makes a predominant contribution to the binding free energy. The in vitro cytotoxic activity of complexes 1 and 2 was evaluated by the MTT[3-（4,5-dimethylthiazol-2-yl）-2,5-diphenyl- 2H-tetrazolium bromide] method. Complex I shows higher anticancer potency than complex 2 against four tumor cell lines. Further mechanism study indicates that complexes 1 and 2 can cause cell cycle arrest in the G2/M phase.