Possible Cobalt-Cobalt Bridging by a Hemiacetal in the Dinuclear Cobalt Complex Bearing the Ligand Bis(3-(2-pyridylmethyleneamino)phenyl) Sulfone

A dinuclear cobalt complex bearing the ligand bis(3-(2-pyridylmethyleneamino)phenyl) sulfone (BPMAPS) was prepared. It is proposed that the structure of this is [Coz(BPMAPS)(m-0AcMhemi-Et)]PF6 wherein the cobalt centers are bridged by two carboxylato groups in m-fashion and a hemiacetal with an ethoxy group (hemi-Et). This proposal is based on the similarity of the FT-IR, UV-Vis, and FAB-MS results with the crystallographically characterized dinuclear manganese complex [Mn2(BPMAPS)(m-OAcMhemi-Me)]PF6, and elemental analysis results

Syntheses and characterization of homodinuclear manganese and cobalt complexes bridged by a hemiacetal or by an acetato group in a μ-(η2:η1) bridging mode

The complex [Mn2(BPMAPS)(μ-OAc)2(hemi)]PF6 (1), where hemi is the hemiacetal group, methoxy(2-pyridyl)methoxo, was prepared from bis[3-(2-pyridylmethyleneamino)phenyl] sulfone (BPMAPS), 2-pyridinecarbaldehyde, and manganese(II) acetate in methanol. The complexes Mn2(BPMAPS)(μ-OAc)2(μ-1,1-OAc)(η1-OAc) (2) and Co2(BPMAPS)(μ-OAc)2-[μ-(η2:η1)OAc](η1-OAc) (3) were prepared from manganese(II) acetate and cobalt(II) acetate, respectively, with BPMAPS in methanol. All three complexes were characterized by elemental analysis, FT-IR, MS, UV–Vis spectroscopy, and X-ray crystallography. The manganese ions of complex 1 are bridged by a hemiacetal through the oxygen atom of the alkoxo with the nitrogen atom of the pyridine group coordinating to one of the manganese atoms. The metal ions of complexes 2 and 3 are bridged by acetato groups in μ-1,1 or μ-η2:η1 modes, respectively

Electronic effects in oxidation reactions utilizing dinuclear copper complexes with the Bis[3-[2-hydroxybenzylldeneamino)phenyll sulfone ligand

Copper acetate and the ligands bis[3-(3-tert-butyl-2-hydroxy-5-methoxybenzylidene-amino)phenyl] sulfone and bis[3-(3,5-di-tert-butyl-2-hydroxybenzylideneamino)phenyl] sulfone were reacted to form the complexes with 2:1 copper:ligand ratio, Cu2[B(t-Bu) (OMe)BAPS](u-OCH3)2 (4) and with 2:2 copper:ligand ratio, Cu2[B(t-Bu)2BAPS]2 (5), respectively. Structures of 4 and 5 were determined based on IR, UV-Vis, and FAB-MS data in comparison with previously characterized related copper complexes. The two complexes 4 and 5 were utilized in the oxidation of the substrates 2,4- and 2,6-di-tert-butylphenol (dtbp) at -50C with H2O2 in CH2CI2. The coupling products are preferred in biphenol were achieved with the use 4 and 5, respectively. For 2,6-dtbp, yields of 1,900% and 400% of 3,3,5,5-tetra-tert-butyl-4,4-biphenol were realized utilizing 4 and respectively. These show that the methoxy groups activated the complex. Based on low temperature UV-vis results, a u-n2;n2-peroxo or a u-hydroperoxo intermediate was possibly formed by the reaction of 4 with the H2O2. This effected the oxidation of the 2,4-and 2,6- dtbp substrates but also resulted in the attack of other complexes which acted as substrates. A proposed oxidation mechanism using complex 4 and related complexes is presented

Synthesis, characterization and reactivity of a series of dinuclear copper complexes bearing the ligand bis[3-(2-hydroxybenzylideneamino)phenyl] sulfone and derivatives

The ligands bis[3-(X-2-hydroxybenzylideneamino)phenyl] sulfones (X=none: BHBAPS, X=3-tert-butyl: BH(t-Bu)BAPS and X=3,5-dichloro: BHCl2BAPS) were prepared. These, together with Cu(OAc)2 were used in the syntheses of the dinuclear copper complexes Cu2(BBAPS)(μ-OMe)2 (1), Cu2[B(t-Bu)BAPS] (μ-OH)2 (2), and Cu2[BCl2BAPS] (μ-OMe)2 (3). Complex 1 was crystallographically characterized. The structures of 2 and 3 are similar to 1 by comparison of IR, UV–Vis, FAB-MS and elemental analyses results. Complexes 1–3 (1 mol%) were used in the oxidation of 2,4- and 2,6-di-t-butylphenol (dtbp) at −50 °C with H2O2. The results show that (1) the coupling products are preferred when CH2Cl2 is used; and (2) the quinone yield increases when THF is utilized. In CH2Cl2 with 2,4-dtbp, the yield of the coupling product based on the complex amount, is in the order 2, 1, and 3 with yields of 6300, 4700 and 200%, respectively. Low temperature UV–Vis results of the reaction of 1 with H2O2 showed the growth of peaks at 390 and 580 nm indicative of a μ-η2:η2-peroxo or μ-η1:η1-hydroperoxo intermediate. At −50 °C, this spectrum does not change. But when warmed to 0 °C, a spectrum similar to the original spectrum was obtained. This probably indicates hydrogen radical abstractions of the peroxo intermediate from solvents, and if excess H2O2 is present, the peroxo intermediate may again be formed. This reusability of the complex explains the high yield using 1 and 2. The ligands bis[3-(X-2-hydroxybenzylideneamino)phenyl] sulfones (X=none: BHBAPS, X=3-tert-butyl: BH(t-Bu)BAPS and X=3,5-dichloro: BHCl2BAPS) were prepared. These, together with Cu(OAc)2 were used in the syntheses of the dinuclear copper complexes Cu2(BBAPS)(μ-OMe)2 (1), Cu2[B(t-Bu)BAPS](μ-OH)2 (2), and Cu2[BCl2BAPS](μ-OMe)2 (3). Complex 1 was crystallographically characterized. The structures of 2 and 3 are similar to 1 by comparison of IR, UV–Vis, FAB-MS and elemental analyses results. Complexes 1–3 (1 mol%) were used in the oxidation of 2,4- and 2,6-di-t-butylphenol (dtbp) at −50 °C with H2O2

Iron-restricted pair-feeding affects renal damage in rats with chronic kidney disease.

BACKGROUND:We have previously shown that dietary iron restriction prevents the development of renal damage in a rat model of chronic kidney disease (CKD). However, iron deficiency is associated with appetite loss. In addition, calorie restriction is reported to prevent the development of end-stage renal pathology in CKD rats. Thus, the beneficial effect of iron restriction on renal damage may depend on calorie restriction. Here, we investigate the effect of pair-feeding iron restriction on renal damage in a rat model of CKD. METHODS:First, to determine the amount of food intake, Sprague-Dawley (SD) rats were randomly given an ad libitum normal diet or an iron-restricted diet, and the food intake was measured. Second, CKD was induced by a 5/6 nephrectomy in SD rats, and CKD rats were given either a pair-feeding normal or iron-restricted diet. RESULTS:Food intake was reduced in the iron-restricted diet group compared to the normal diet group of SD rats for 16 weeks (mean food intake; normal diet group and iron-restricted diet group: 25 and 20 g/day, respectively). Based on the initial experiments, CKD rats received either a pair-feeding normal or iron-restricted diet (20 g/day) for 16 weeks. Importantly, pair-feeding iron restriction prevented the development of proteinuria, glomerulosclerosis, and tubulointerstitial damage in CKD rats. Interestingly, pair-feeding iron restriction attenuated renal expression of nuclear mineralocorticoid receptor in CKD rats. CONCLUSIONS:Pair-feeding iron restriction affected renal damage in a rat model of CKD