Effect of the Addition of a Fused Donor-Acceptor Ligand on a Ru(II) Complex: Synthesis, Characterization, and Photoinduced Electron Transfer Reactions of Ru(TTF-dppz)(2)(Aqphen) (2+)

The synthesis and the photophysical properties of the complex [Ru(TTF-dppz)(2)(Aqphen)](2+) (TTF = tetrathiafulvalene, dppz = dipyrido-[3,2-a:2',3'-c]phenazine, Aqphen = anthraquinone fused to phenanthroline via a pyrazine bridge) are described. In this molecular triad excitation into the metal ligand charge transfer bands results in the creation of a long-lived charge separated state with TTF acting as electron donor and anthraquinone as terminal acceptor. The lifetime of the charge-separated state is 400 ns in dichloromethane at room temperature. A mechanism for the charge separation involving an intermediate charge-separated state is proposed based on transient absorption spectroscopy.

RhoH/TTF negatively regulates leukotriene production in neutrophils

Leukotriene B(4) (LTB(4)) is an important proinflammatory lipid mediator generated by neutrophils upon activation. GM-CSF stimulation is known to enhance agonist-mediated LTB(4) production of neutrophils within minutes, a process called "priming". In this study, we demonstrate that GM-CSF also limits the production of LTB(4) by neutrophils via a transcriptional mechanism at later time points. We identified hemopoietic-specific Ras homologous (RhoH)/translocation three four (TTF), which was induced following GM-CSF stimulation in neutrophils, as a key regulator in this process. Neutrophils derived from RhoH/TTF-deficient (Rhoh(-/-)) mice demonstrated increased LTB(4) production upon activation compared with normal mouse neutrophils. Moreover, neutrophils from cystic fibrosis patients expressed enhanced levels of RhoH/TTF and generated less LTB(4) upon activation compared with normal human neutrophils. Taken together, these data suggest that RhoH/TTF represents an inducible feedback inhibitor in neutrophils that is involved in the limitation of innate immune responses.