Theoretical study on the activation of C-H bond in ethane by PdX+ (X = F, Cl, Br, H, and CH3) in the gas phase.

The mechanism of C-H bond activation of ethane was catalyzed by palladium halide cations (PdX+ (X = F, Cl, Br, H, and CH3)), which was investigated using density functional theory (DFT) at B3LYP level. The reaction mechanism was taken into account in triplet and singlet spin state potential energy surfaces. For PdF+, PdCl+, and PdBr+, the high spin states were the ground states, whereas the ground states were the low spin states in PdH+ and PdCH3+. The reaction of PdF+, PdCl+, and PdBr+ with ethane occurred via a typical "two-state reactivity" mechanism. In contrast, for PdH+ and PdCH3+, the overall reaction performed on the ground state PESs in a spin-conserving manner. The crossing points between two potential energy surfaces were observed and effectively decreased the activation barrier in PdX+/C2H6 (X = F, Cl, and Br). The minimum energy crossing points (MECP) were obtained used the algorithm in Harvey method. The natural valence electron configuration calculations were analyzed by natural bond orbital. The distribution and contribution of the front molecular orbital of the initial complexes could be further understand by the density of states. The feature of the bonding evolution in the main pathways was studied using topological analysis including localized orbital locator and atoms in molecules.

Enhancement of the Catalytic Activities of Heteronuclear Bimetallic Cations for the C-H Bond Activation of Cyclohexane.

Heterometallic cations NiCu+ and CoNi+ can easily induce triple dehydrogenation of cyclohexane with high yield, and monometallic cations Ni+ and Co+ only give rise to double dehydrogenation with low yield. Reaction mechanisms of the six C-H bond activations for cyclohexane are systematically investigated by comparing the difference between bimetallic cations and monometallic ones. Fragment molecular orbital analysis clearly indicates that charge transfer (CT) occurs from the occupied interacting orbital of the metallic cation to the σ*-antibonding orbital of the first, third, and fifth activated C-H bonds in transition states. The synergistic effects of heteronuclear bimetallic cations result in the destabilization of the occupied interacting orbital in bimetallic cations, which raise the reactivity of bimetallic cations and enhance the CT between catalysts and substrates. Contrary to the absence of the third dehydrogenation product in the mononuclear metallic cation catalytic reaction, a significant amount of the third dehydrogenation product is observed in the presence of heteronuclear cations (NiCu+ and CoNi+). π back-bonding between Ni of heteronuclear metallic cations and the substrate cyclohexadiene plays an essential role in lowering the energies of transition states, which accelerate the third dehydrogenation. The reasons why heteronuclear bimetallic cations are more reactive than monometallic ones are discussed in detail.

[Effects of long-term oral administration of lanthanum nitrate on the liver of rats].

OBJECTIVE: To probe the effects of long-term oral administration of lanthanum nitrate [La(NO(3))(3)] on morphological change in the liver, aftereffect of deposited La in the liver and their mechanism in rats. METHODS: Young Wistar rats were divided into two groups, one fed with 0.1, 0.2, 2.0, 10.0 and 20.0 mg/kg of La(NO(3))(3) for six months and the other for the control. Changes in ratio of liver to body weight were observed after exposure to La(NO(3))(3) at varied doses for six months and one month after six-month exposure, as well as morphology of the liver in the rats with routine histochemistry and transmission electron microscopy (TEM) technique. Content of La in the liver was measured with inductively coupled plasma-mass spectrometry (ICP-MS). RESULTS: Ratio of liver to body weight was significantly higher in the male rats exposed to 20.0 mg/kg of lanthanum for six months than that in the control group. Ratio of liver to body weight restored to normal in the rats exposed to 20.0 mg/kg of La one month after six-month exposure. Infiltration of inflammatory cells in the portal region of the liver, small amount of fat drops in hepatocytic cytoplasm, increased density of mitochondria stroma, lysosome containing highly-electronic-density bodies and dense granules, normal nucleus and slightly deformed nucleus of hepatocytes could be found in the rats exposed to 20.0 mg/kg. Areas of the liver deposited with glycogen after six-month exposure to 20.0 mg/kg of La accounted for (26.1 +/- 1.5)% and (4.1 +/- 1.4)%, respectively for male and female rats, significantly lower than those in the control group [(31.3 +/- 1.4)% and (39.4 +/- 0.9)%, respectively], with a statistical significance and very statistical significance, respectively. There was a little infiltration of inflammatory cells in the portal region of the liver one month after six-month exposure to 20.0 mg/kg of La, and amount of the dense bodies was lower in the rats exposed to La for six months. Liver contents of La in the rats of all experimental groups were lower one month after six-month exposure than those in the rats exposed for six months. CONCLUSIONS: Exposure to a dose of 20.0 mg/kg La(NO(3))(3) for a long term could damage the liver structure to certain extent, but lanthanum deposited in the liver could be eliminated from the body gradually.

Experimental study of subchronic toxicity of lanthanum nitrate on liver in rats.

Wistar rats were divided into six groups, which were given La (NO(3))(3) at 20.0, 10.0, 2.0, 0.2, and 0.1 mg/kg, and the control group, which was given physiological saline, respectively, for six months. Pathological changes of liver were observed via light microscopy and transmission electron microscopy. Glutamic-oxalacetic transaminase, glutamic-pyruvic transitanase, gamma-glutamyl transferase, and alkline phosphatase activities in the serum were measured. Superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), and malondialdehyde of liver were determined. The metabolic accumulation of lanthanum in rat liver was investigated via inductively coupled plasma mass spectrometry. Results showed no abnormal biochemical changes. In the group of 20.0 mg/kg La(NO(3))(3), there were loss of weight, decrease of glycogen in the hepatocytes, denser matrix of the mitochondria, and deformation of the nuclei of some hepatocytes with different degrees and infiltration of inflammatory cells in the portal area. The higher was the dose, the higher was the number of bodies contain high electronic dense gravel-like granules, and secondary lysosomes with dense bodies were observed. In the group fed 0.1 mg/kg La(NO(3))(3), intracellular glycogen showed an increasing tendency, particularly increased animal growth and increased activities of SOD and GSH-Px. The content of La in the liver increased regularly with increase in dose and time of administration. The results further proved that low-dose La(NO(3))(3) produced some specific biologic effects. This study illustrated the influence of La(NO(3))(3) on rat liver at cellular and subcellular levels and it provides an experimental basis for the purpose of setting a reasonable standard for safely utilizing rare earth elements.

1H NMR analysis for metabolites in serum and urine from rats administrated chronically with La(NO3)3.

1H NMR spectroscopy has been used to assess long-term toxicological effects of a rare earth. Male Wistar rats were administrated orally with La(NO3)3 at doses of 0.1, 0.2, 2.0, 10, and 20 mg/kg body wt, resp., for 3-6 months. Urine was collected at 1, 2, and 3 months and serum samples were taken after 6 months. Numerous low-M(r) metabolites in rats serum and rats urine, including creatinine, citrate, glucose, ketone bodies, trimethylamine N-oxide (TMAO), and various amino acids, were identified on 400- and 500-MHz 1H NMR spectra. La3+-induced renal and liver damage is characterized by an increase in the amounts of the excreted ketone bodies, amino acids, lactate, ethanol, succinate, TMAO, dimethylamine, and taurine and a decrease in citrate, glucose, urea, and allantoin. Information on the molecular basis of the long-term toxicity of La(NO>3)3 was derived from the abnormal patterns of metabolite excretions. An assay of some biochemical indexes and analysis of some enzymes in plasma supported NMR results.