The preparation of a new series of Ir(III) tetrazolato complexes with the general formula [Ir(C^N)2(N^N)]0/+, where the ancillary ligand (N^N) is represented in turn by 2-pyridyltetrazolato (P Show more
The preparation of a new series of Ir(III) tetrazolato complexes with the general formula [Ir(C^N)2(N^N)]0/+, where the ancillary ligand (N^N) is represented in turn by 2-pyridyltetrazolato (PTZâ), 2-pyrazinyltetrazolato (PYZâ) or 2-pyridyl 5-trifluoromethyl tetrazolato (PTZ-CF3â), is described herein. The design of the cyclometalated (C^N) ligands, namely 2-phenylisonicotinonitrile (ppyCN) and 2-(2,4-difluorophenyl)isonicotinonitrile (F2ppy-CN), features the well-known ppy- or F2ppy core, with the introduction of one electron-withdrawing cyano (âCN) group at the para position of the pyridyl ring. The photophysical and electrochemical properties of the new Ir(III) cyclometalated complexes have been investigated and the resulting data suggest how the (C^N) ligands significantly rule the luminescence behavior of the new complexes. Further blue or red shifting of the emission profiles of the neutral complexes was observed upon their conversion into cationic species through the regioselective addition of a methyl moiety to the coordinated tetrazolato ring. Lastly, neutral [Ir(F2ppy-CN)2(PTZ)] was used as an emissive phosphor for the fabrication of an OLED-type device.
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Herein, we describe a new family of tris chelate homoleptic Ru (II) complexes, [Ru(N^N)3]2+, where the role of the diimineâtype ligands (N^N) was fulfilled by 2âpyridyl (PTZ) or 2âquinolyl tetrazole ( Show more
Herein, we describe a new family of tris chelate homoleptic Ru (II) complexes, [Ru(N^N)3]2+, where the role of the diimineâtype ligands (N^N) was fulfilled by 2âpyridyl (PTZ) or 2âquinolyl tetrazole (QTZ) derivatives decorated with various alkyl substituents at the Nâ2 position of the tetrazole ring. The new Ru (II) complexes with general formula [Ru (PTZâR)3]2+ and [Ru (QTZâR)3]2+, were obtained as mixtures of facial (fac) and meridional (mer) isomers, as suggested by NMR (1H, 13C) experiments, and confirmed in the case of merâ[Ru (QTZâMe)3]2+, by Xâray crystallography. The photophysical behavior of the tetrazoleâbased [Ru(N^N)3]2+ type species was investigated by UVâvis absorption spectroscopy, providing trends typical of polypyridyl Ru (II) complexes. The new homoleptic complexes fac/merâ[Ru (PTZâR)3]2+ and fac/merâ[Ru (QTZâR)3]2+ have been assessed for any eventual antimicrobial activity towards two different bacteria such as Gramânegative Escherichia coli and Gramâpositive Deinococcus radiodurans. Whereas being inactive toward E. coli, the response of agar disks diffusion tests suggested that some of the new fac/mer Ru (II) complexes could inhibit the growth of D. radiodurans. This effect was further investigated by determining the growth kinetics in liquid medium of D. radiodurans exposed to the fac/merâ[Ru (PTZâR)3]2+ and fac/merâ[Ru (QTZâR)3]2+ complexes at different concentrations. The outcome of these experiments highlighted that the turnâon of the growth inhibitory effect took place as the linear hexyl chain was appended to the PTZ or QTZ scaffold, suggesting also how the inhibitory activity appeared more pronouncedly exerted by the facial isomers facâ[Ru (PTZâHex)3]2+ and facâ[Ru (QTZâHex)3]2+ (MIC = ca. 3.0 ÎŒg/ml) with respect to the corresponding meridional isomers (MIC = ca. 6.0 ÎŒg/ml). Show less
Abstract Significance: Mitochondria are the energetic, metabolic, redox, and information signaling centers of the cell. Substrate pressure, mitochondrial network dynamics, and cristae morphology Show more
Abstract Significance: Mitochondria are the energetic, metabolic, redox, and information signaling centers of the cell. Substrate pressure, mitochondrial network dynamics, and cristae morphology state are integrated by the protonmotive force Î p or its potential component, ΠΚ , which are attenuated by proton backflux into the matrix, termed uncoupling. The mitochondrial uncoupling proteins (UCP1â5) play an eminent role in the regulation of each of the mentioned aspects, being involved in numerous physiological events including redox signaling. Recent Advances: UCP2 structure, including purine nucleotide and fatty acid (FA) binding sites, strongly support the FA cycling mechanism: UCP2 expels FA anions, whereas uncoupling is achieved by the membrane backflux of protonated FA. Nascent FAs, cleaved by phospholipases, are preferential. The resulting Î p dissipation decreases superoxide formation dependent on Î p . UCP-mediated antioxidant protection and its impairment are expected to play a major role in cell physiology and pathology. Moreover, UCP2-mediated aspartate, oxaloacetate, and malate antiport with phosphate is expected to alter metabolism of cancer cells. Critical Issues: A wide range of UCP antioxidant effects and participations in redox signaling have been reported; however, mechanisms of UCP activation are still debated. Switching off/on the UCP2 protonophoretic function might serve as redox signaling either by employing/releasing the extra capacity of cell antioxidant systems or by directly increasing/decreasing mitochondrial superoxide sources. Rapid UCP2 degradation, FA levels, elevation of purine nucleotides, decreased Mg 2+ , or increased pyruvate accumulation may initiate UCP-mediated redox signaling. Future Directions: Issues such as UCP2 participation in glucose sensing, neuronal (synaptic) function, and immune cell activation should be elucidated. Antioxid. Redox Signal. 29, 667â714. Show less