Mohammad A. Ansari

Synthesis and structure of [(μ3-I)(μ3-WSe4){Ag(PMe2Ph)}3]

Reaction of [NPr 4 ] 2 [WSe 4 ] with [Ag(PMe 3 )I] 4 in CH 3 CN followed by addition of PMe 2 Ph affords the title compound, (μ 3 -iodo)(μ 3 -tetraselenidotungstide)tris(dimethylphenylphosphinesilver), [(μ 3 -I)(μ 3 -WSe 4 ){AgC 8 H 11 P)} 3 ] [systematic name: tris(dimethylphenylphosphine)-2κP,3κP,4κP-μ 3 -iodo-2:3:4κ 3 I-tri-μ 3 -selenido-1:2:3κ 3 Se; 1:2:4κ 3 Se; 1:3:4κ 3 Se-selenido-1κSe-trisilvertungsten], a neutral cubane cluster. The compound was characterized by a single-crystal X-ray structure determination

Isolation and structural characterization of the polymetallic zirconium alkoxide complexes, Zr3O(OCH2CMe3)9Cl, Zr3O(OCMe3)9(OH), and Na4Zr6O2(OEt)24

Abstract Three polymetallic zirconium alkoxide complexes have been isolated and structurally characterized which show that by proper combination of zirconium precursor and alkoxide, this small class of compounds can be expanded. The trimetallic neopentoxide complex [(NpO)2Zr]3(μ-ONp)3(μ3-Cl)(μ3-O), 1, (NpCH2CMe3) can be isolated from the reaction of ZrCl4 with four equivalents of KOCH2CMe3 in THF. The trimetallic tert-butoxide complex, [ ( t BuO ) 2 Zr ] 3 (μ- O t Bu ) 2 (μ- OH )(μ 3 - O t Bu )(μ 3 O ) , 2, can be isolated from the reaction of ZrCl4 with 3.3 equivalents of LiOCMe3 in THF. The reaction of Zr(OEt)4 with one equivalent of NaOSiMe3 in THF formed the mixed-metal polymetallic complex. {Na2[(EtO)Zr]3(μ-OEt)7(μ3-OEt)2(μ3-O)}2, 3. These results show that the common M3(μ-E)3(μ3-E)2 structural motif with E being a ligand donor atom can be obtained with zirconium alkoxides.

The reactivity of zirconium acetylacetonate with phenols

Abstract Although zirconium acetylacetonate, Zr[CH3C(O)CHC(O)CH3]4, 1, does not react with phenol, 4-methylphenol, or 2,6-dimethylphenol at reflux temperature in toluene or THF, it does react with p-nitrophenol in THF at room temperature to form (acac)3Zr(OC6H4NO2-4), 2, in 70% yield. 1 also reacts with 1,4-dihydroxybenzene to form bimetallic [(acac)3Zr]2(μOC6H4O-4), 3, in 90% yield. 2 crystallizes from THF to form a capped trigonal prismatic geometry around zirconium with the aryloxide ligand in the capping position. 3 crystallizes from THF/C6H6 to form a structure similar to that of 2 except that the aryloxide ligand occupies a trigonal prismatic vertex in the square face which is capped.

Isolation and structural characterization of tetra- and pentaheterometallic neodymium 4-methylphenoxide complexes

Abstract The compatibility of the special bridging abilities of the 4-methylphenoxide ligand, OC 6 H 4 Me-4, and alkylaluminum reagents have been examined. NdCl 3 reacts with KOC 6 H 4 Me-4 in THF to form K 3 Nd 2 (μ-OC 6 H 4 Me-4) 6 ( μ 4 -OC 6 H 4 Me-4) 3 (THF) 7 , 1 , which has a trigonal bipyramidal arrangement of metal atoms with neodymium in the apical sites. Six doubly-bridging aryloxide ligands connect each apical metal to an equatorial metal and three quadruply-bridging aryloxide ligands connect the apical metals with two equatorial sites. Two potassium atoms have two terminal THF ligands and the other metals each have one terminal THF. A suspension of 1 in hexanes reacts with Al 2 Me 6 to produce colorless crystals of [Me 2 Al(OC 6 H 4 Me-4)] n and blue crystals which have been crystallographically characterized as Nd[μ-OC 6 H 4 Me-4) 2 AlMe 2 ] 3 , 2 . The neodymium atom in 2 is surrounded by an octahedron of bridging aryloxide ligands and each aluminum is tetrahedral.

Examination of the LnCl3/RLi alkylation system for organic synthesis using yttrium as a probe including the X-ray crystal structure of Li2Y8Cl18O4(THF)12

Abstract The LnCl3/RLi reagent system commonly used with Ln=Ce for organic alkylation reactions has been studied with Ln=Y to make use of the 89Y nucleus (I = 1/2) in NMR analyses. The ‘YCl’ obtained by the current literature methods of dehydrating LnCl3(H2O)x reagents in the LnCl3/RLi system contains water by elemental analysis, by reactivity with LiCH2SiMe3 and LiMe, and by X-ray analysis of recrystallized material which proved to be [YCl2(H2O)6]Cl. The complexity of the intermediates that may be present in these systems when reagents are not rigorously purified is shown by the structure of Li2Y8Cl18O4(THF)12, which was isolated from a YCl3/LiCH2SiMe3 reaction. The complex contains a tetracapped tetrahedron of yttrium atoms with two outlying lithium atoms all of which are connected by four μ4-O, fourteen μ2-Cl and two μ3-Cl atoms. Each lithium and each capping yttrium are ligated by two THF groups.

Endogenous opioids and TSH secretion in azotemic male rats.

The role of endogenous opioids in the control of thyroid-stimulating hormone (TSH) secretion in uremic male rats was investigated using the narcotic antagonist naloxone. In order to eliminate the effect of weight loss due to uremia-induced anorexia as a cause of altered TSH secretion in uremia, we also studied a group of normal control animals who were pair-fed with the uremic animals, so that their weights were comparable to that of the uremic animals. Naloxone administration produced a significant increase in the basal concentration of TSH response to TRH (5 micrograms i.v.) was significantly blunted in the uremic animals compared to the normal controls and the starved animals. Naloxone administration did not alter the peak thyrotropin-releasing hormone (TRH) stimulated TSH response in any of the experimental groups of rats. Because of the possibility that the effects of naloxone on TSH secretion in the uremic rats were related to impaired clearance of the naloxone in those animals, an additional group of normal rats was given twice the dose of naloxone administered to the uremic animals. The higher dose of naloxone was similarly without effect on the basal or TRH-stimulated TSH secretion in this group. The data suggest that experimental renal failure is associated with diminished sensitivity of the thyrotroph to TRH stimulation and that this blunted sensitivity cannot be abolished by blockade of endogenous opioids by naloxone. Opioid blockade does, however, increase basal TSH secretion in uremic animals, suggesting an increase in endogenous opioidergic tone in uremia.(ABSTRACT TRUNCATED AT 250 WORDS)

Dopamine and TSH Secretion in Uremic Male Rats

The role of dopamine in the dysregulation of TSH secretion in uremic male rats was investigated using the dopamine antagonist, pimozide. In order to obviate the effect of weight loss due to uremia-induced anorexia as a cause of altered TSH secretion in uremia, we also studied a group of normal animals whose food intake was restricted and who demonstrated weight loss comparable to that of the uremic animals. Baseline TSH concentrations were not significantly different in the normal, uremic or starved animals. Pimozide administration produced no change in the baseline TSH concentrations in any of the groups of rats. The peak TSH response to TRH (5 micrograms IV) was significantly blunted in the uremic animals compared to the normal controls and the starved animals. Pimozide administration did not alter the peak TRH-stimulated TSH response in either the normal animals or the starved animals. However, the peak TRH-stimulated TSH response was significantly increased in the uremic animals and was comparable to the peak TSH response seen in the pimozide-untreated control animals. The data suggest that experimental renal failure in rats is associated with diminished sensitivity of the thyrotroph to TRH stimulation, and that this blunted sensitivity may be dopamine-dependent since it can be abolished by pharmacologic dopamine blockade.

Gonadotropin secretion in azotemic male rats--effect of opioid blockade.

The role of endogenous opioids in the control of gonadotropin secretion in uremic male rats was investigated using the narcotic antagonist, naloxone. In order to eliminate the effect of weight loss due to uremia-induced anorexia as a cause of previously described altered gonadotropin secretion in uremia, we also studied a group of normal pair-fed control animals who exhibited a weight loss comparable to that of the uremic animals. Naloxone administration had no effect on the basal or LRH-stimulated peak concentrations of LH and FSH in the normal or the uremic rats. Basal and LRH-stimulated gonadotropin responses in the pair-fed rats were comparable to those seen in the normal rats. Similarly, opioid blockade produced no change in the basal or LRH-stimulated gonadotropin responses in the pair-fed animals. Testosterone concentrations were significantly lower in the uremic and pair-fed animals compared to the normal rats. The data suggest that experimental renal failure is not associated with altered opioidergic tone, as it relates to gonadotropin secretion, or to diminished sensitivity of the gonadotroph to LRH stimulation. The decreased testosterone concentration seen in the uremic and pair-fed rats may reflect abnormalities in gonadal hormone secretion due to primary pathology occurring at the level of the gonad. These abnormalities may be reflected as diminished Leydig cell sensitivity to LH. The inappropriately low concentrations of LH in the presence of low testosterone together with normal gonadotropin response to exogenous LRH also suggest an abnormal secretion of endogenous LRH. It is not clear whether this presumed abnormality in LRH secretion is a primary event or is related to decreased testosterone production by the testes in the uremic and pair-fed rats.

Relationship between β-Endorphin/β-Lipotropin, Hyperglycemia, and Hyperinsulinemia in Obese Male Zucker Rats

Abstract The relationship between β-endorphin(β-EP)/β-lipotropin(β-LP) and insulin secretion in the basal state and after glucose challenge was studied in obese male Zucker rats and their lean littermates. Baseline plasma β-EP/β-LP concentrations were similar in the two groups of animals. Baseline plasma insulin and serum glucose concentrations were significantly higher in the obese animals. Following glucose challenge, the increase in plasma β-EP/β-LP concentrations was significantly lower in the obese animals than in their lean littermates. Opioid blockade with naloxone failed to alter the baseline hyperinsulinemia and hyperglycemia seen in the obese animals. The data suggest that the hyperinsulinemia in the obese Zucker rat is not due to endogenous hyperendorp hinemia as shown in humans with polycystic ovary syndrome. The obese rats showed dissociation between glucose-stimulated plasma levels of β-EP/β-LP and insulin levels which may contribute to the hyperinsulinemia and insulin restance in these animals.

Gamma-aminobutyric acid and dysregulation of TSH secretion in uremic male rats.

The role of gamma-aminobutyric acid (GABA) in the abnormal secretion of thyrotropic hormone (TSH) in uremia was studied in male Sprague-Dawley rats rendered renally insufficient by subtotal nephrectomy. Baseline TSH concentrations in normal control animals and in the uremic animals were similar. The peak TSH response to thyrotropin-releasing hormone (TRH; 5 micrograms i.v.) was significantly blunted in the uremic animals compared to the controls. Pretreatment of the uremic animals with the specific GABA antagonist, bicuculline (1.5 mumol i.v.) resulted in normalization of the peak TSH response to TRH. Bicuculline pretreatment, however, did not alter the basal secretion of TSH in either the normal or the uremic animals, and it also did not augment the TRH-stimulated TSH response in the normal animals. Sham-operated animals demonstrated basal and TRH-stimulated TSH responses comparable to the control group. In order to assess whether the weight loss associated with uremia could have accounted for the blunted TRH-stimulated TSH secretion in the uremic animals, a group of rats were starved so that their weights were comparable to those of the uremic animals. Basal and TRH-stimulated TSH responses in this group were not significantly different from the controls. Bicuculline pretreatment of the starved animals also failed to alter the basal and TRH-stimulated TSH responses. These data indicate that an increase in central gabaergic tone may be partly responsible for the blunted TSH response to TRH seen in uremia, but that GABA is not an important modulator of TSH secretion in the normal rat.