ABSTRACT
Four new terbium(III) ternary complexes, [Tb(fod)3 (indazole)] (1), [Tb(fod)3 (tptz)] (2), [Tb(fod)3 (impy)] (3) and [Tb(fod)3 (tppo)2 ] (4) with 6,6,7,7,8,8,8-heptafluoro-2,2-dimethyl-3,5-octanedione, (Hfod) and N and O donors are synthesized and structurally characterized. The photoluminescence of the complexes are studied in solid, chloroform solution and thin PMMA hybrid films (PMMA is a poly(methyl methacrylate)). The ligand-based emission is dominant in solution of 3 and 4. The effect of ancillary ligands on the photoluminescence of terbium(III) ion is investigated. The mechanism of energy transfer is discussed and correlates the luminescence of acceptor terbium ion with the triplet state energy level of donor ligands. Among the four complexes studied, the luminescence from 1 is most intense followed by 2, 4 and 3. The Commission International de I'Eclairage (CIE) color coordinates of these complexes are calculated and presented. The complexes 3 and 4 show intraphase color tuning when excited under different UV wavelengths. The emission color of [Tb(fod)3 (tppo)2 ] (4) changes from pure blue to turquoise green via almost pure white under 360, 328 and 280 nm UV excitation wavelengths respectively. The [Tb(fod)3 (impy)] (3) show similar results. The complex [Tb(fod)3 (tptz)] (2) displays interphase color tuning from yellow (solution) to turquoise green (solid) and fascinatingly incorporation of complex in PMMA polymer generates white light under same excitation wavelength (360 nm).
ABSTRACT
Connexin 43 (Cx43) is a gap junction protein expressed in various tissues and organs of vertebrates. Besides functioning as a gap junction, Cx43 also regulates diverse cellular processes like cell growth and differentiation, cell migration, cell survival, etc. Cx43 is critical for normal cardiac functioning and is therefore abundantly expressed in cardiomyocytes. On the other hand, ATP-sensitive potassium (KATP) channels are metabolic sensors converting metabolic changes into electrical activity. These channels are important in maintaining the neurotransmitter release, smooth muscle relaxation, cardiac action potential repolarization, normal physiology of cellular repolarization, insulin secretion and immune function. Cx43 and KATP channels are part of the same signaling pathway, regulating cell survival during stress conditions and ischemia/hypoxia preconditioning. However, the underlying molecular mechanism for their combined role in ischemia/hypoxia preconditioning is largely unknown. The current review focuses on understanding the molecular mechanism responsible for the coordinated role of Cx43 and KATP channel protein in protecting cardiomyocytes against ischemia/hypoxia stress.
