Investigation of the electronic ground states for a reduced pyridine(diimine) uranium series: evidence for a ligand tetraanion stabilized by a uranium dimer.

The electronic structures of a series of highly reduced uranium complexes bearing the redox-active pyridine(diimine) ligand, (Mes)PDI(Me) ((Mes)PDI(Me) = 2,6-(2,4,6-Me3-C6H2-N═CMe)2C5H3N) have been investigated. The complexes, ((Mes)PDI(Me))UI3(THF) (1), ((Mes)PDI(Me))UI2(THF)2 (2), [((Mes)PDI(Me))UI]2 (3), and [((Mes)PDI(Me))U(THF)]2 (4), were examined using electronic and X-ray absorption spectroscopies, magnetometry, and computational analyses. Taken together, these studies suggest that all members of the series contain uranium(IV) centers with 5f (2) configurations and reduced ligand frameworks, specifically [(Mes)PDI(Me)](•/-), [(Mes)PDI(Me)](2-), [(Mes)PDI(Me)](3-) and [(Mes)PDI(Me)](4-), respectively. In the cases of 2, 3, and 4 no unpaired spin density was found on the ligands, indicating a singlet diradical ligand in monomeric 2 and ligand electron spin-pairing through dimerization in 3 and 4. Interaction energies, representing enthalpies of dimerization, of -116.0 and -144.4 kcal mol(-1) were calculated using DFT for the monomers of 3 and 4, respectively, showing there is a large stabilization gained by dimerization through uranium-arene bonds. Highlighted in these studies is compound 4, bearing a previously unobserved pyridine(diimine) tetraanion, that was uniquely stabilized by backbonding between uranium cations and the η(5)-pyridyl ring.

Synthesis, characterization, and multielectron reduction chemistry of uranium supported by redox-active α-diimine ligands.

Uranium compounds supported by redox-active α-diimine ligands, which have methyl groups on the ligand backbone and bulky mesityl substituents on the nitrogen atoms {(Mes)DAB(Me) = [ArN═C(Me)C(Me)═NAr], where Ar = 2,4,6-trimethylphenyl (Mes)}, are reported. The addition of 2 equiv of (Mes)DAB(Me), 3 equiv of KC(8), and 1 equiv of UI(3)(THF)(4) produced the bis(ligand) species ((Mes)DAB(Me))(2)U(THF) (1). The metallocene derivative, Cp(2)U((Mes)DAB(Me)) (2), was generated by the addition of an equimolar ratio of (Mes)DAB(Me) and KC(8) to Cp(3)U. The bond lengths in the molecular structure of both species confirm that the α-diimine ligands have been doubly reduced to form ene-diamide ligands. Characterization by electronic absorption spectroscopy shows weak, sharp transitions in the near-IR region of the spectrum and, in combination with the crystallographic data, is consistent with the formulation that tetravalent uranium ions are present and supported by ene-diamide ligands. This interpretation was verified by U L(III)-edge X-ray absorption near-edge structure (XANES) spectroscopy and by variable-temperature magnetic measurements. The magnetic data are consistent with singlet ground states at low temperature and variable-temperature dependencies that would be expected for uranium(IV) species. However, both complexes exhibit low magnetic moments at room temperature, with values of 1.91 and 1.79 µ(B) for 1 and 2, respectively. Iodomethane was used to test the reactivity of 1 and 2 for multielectron transfer. While 2 showed no reactivity with CH(3)I, the addition of 2 equiv of iodomethane to 1 resulted in the formation of a uranium(IV) monoiodide species, ((Mes)DAB(Me))((Mes)DAB(Me2))UI {3; (Mes)DAB(Me2) = [ArN═C(Me)C(Me(2))NAr]}, which was characterized by single-crystal X-ray diffraction and U M(4)- and M(5)-edge XANES. Confirmation of the structure was also attained by deuterium labeling studies, which showed that a methyl group was added to the ene-diamide ligand carbon backbone.

Single dose of glutamine enhances myocardial tissue metabolism, glutathione content, and improves myocardial function after ischemia-reperfusion injury.

BACKGROUND: Myocardial ischemia and reperfusion (I/R) injury causes significant morbidity and mortality. Protection against I/R injury may occur via preservation of tissue metabolism and ATP content, preservation of reduced glutathione, and stimulation of heat shock protein (HSP) synthesis. Supplementation with glutamine (GLN) has been reported to have beneficial effects on all of these protective pathways. Thus, we hypothesized that GLN pretreatment given to the rat in vivo would protect the myocardium against I/R-induced dysfunction. METHODS: GLN (0.52 g/kg, intraperitoneally, given as alanine-glutamine dipeptide), alanine alone (0.23 g/kg), or a Ringer's lactate solution (control) was administered to Sprague-Dawley rats 18 hours before heart excision, perfusion, exposure to global ischemia (15 minutes) and reperfusion (1 hour). Tissue metabolites were analyzed via magnetic resonance spectroscopy. RESULTS: In control and alanine-treated animals, I/R injury resulted in cardiac dysfunction, indicated by a decrease in cardiac output. Administration of GLN 18 hours before I/R injury preserved cardiac output after reperfusion. Metabolic analysis of the myocardial tissue revealed that [/R injury led to significant diminution of myocardial tissue glutamate, ATP content, accumulation of myocardial lactate, and a reduction in reduced glutathione content in control animals. GLN significantly reduced the deleterious changes in myocardial metabolism and improved reduced glutathione content. No changes in pre- or post-I/R injury HSP expression were observed after GLN administration. CONCLUSIONS: These observations demonstrate that remote in vivo administration of GLN before cardiac I/R injury can improve post-I/R cardiac function. This effect may be mediated via improved myocardial metabolism and enhanced reduced glutathione content.