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Trinuclear Zinc(II) Complexes and Polymeric Cadmium(II) Complexes with the Ligand 2,5-Bis(2-pyridyl)pyrazine: Synthesis, Spectral Analysis, and Single-Crystal and Powder X-ray Analyses.

Three zinc compounds, [ZnCl(2)(bppz)(dmf)] (1), [Zn(3)(OAc)(6)(bppz)(2)](H(2)O) (2), and [Zn(3)(Cl)(6)(bppz)(3)](H(2)O) (3), and two cadmium complexes, {[Cd(OAc)(2)(bppz)](H(2)O)(5)}(n)() (4) and [Cd(NO(3))(2)(bppz)](n)() (5), where bppz is 2,5-bis(2-pyridyl)pyrazine, have been synthesized and characterized spectroscopically and crystallographically. The mononuclear complex 1, C(17)H(17)Cl(2)N(5)OZn, crystallizes in the monoclinic space group P2(1)/c, with a = 8.654(1) Å, b = 9.500(1) Å, c = 22.997(1) Å, beta = 97.99(1) degrees, and Z = 4; R1 for 2356 observed reflections [I > 2sigma(I)] was 0.058. The zinc atom has a distorted square planar coordination sphere with the ligand bppz connected in a mono-bidentate manner. The remaining coordination sites are occupied by the chloride counterions and by an oxygen atom of a solvent molecule. The trinuclear zinc compound 2, C(40)H(38)N(8)O(12)Zn(3).H(2)O, crystallizes in the triclinic space group P&onemacr;, with a = 12.238(4) Å, b = 12.986(3) Å, c = 15.470(4) Å, alpha = 75.65(1) degrees, beta = 97.99(1) degrees, gamma = 65.98(1) degrees, and Z = 2; R1 for 4511 observed reflections [I > 2sigma(I)] was 0.07. This complex consists of a linear arrangement of three zinc atoms. The central zinc atom, located on a crystallographic inversion center, is connected by six bridging acetate groups to two symmetry-related zinc atoms. It has an almost perfect octahedral coordination environment. The outer symmetry-related zinc atoms are in a square pyramidal environment, and they coordinate to three acetate groups and to one bppz molecule in a mono-bidentate manner. Compound 3, C(42)H(30)Cl(6)N(12)Zn(3).1.25H(2)O, a cyclic zinc(II) trimer, crystallizes in the cubic space group Ia&thremacr;d, with a = 26.311(1) Å and Z = 16; R1 for 692 observed reflections [I > 2sigma(I)] was 0.038. This trinuclear complex has a perfect triangular arrangement of the zinc atoms. Each zinc atom is connected to the other two by a bppz molecule. The coordination about the metal is best described as a distorted octahedral with four long distances in the basal plane, to two chlorines and to two nitrogen atoms, and two short distances in the axial direction, to two nitrogen atoms. With Cd(II) two polymeric complexes, 4 and 5 were obtained. Compound 4, C(18)H(16)N(4)O(4)Cd.5H(2)O, crystallizes in the triclinic space group P&onemacr;, a = 9.045(1) Å, b = 10.438(1) Å, c = 12.719(1) Å, alpha = 100.48(1) degrees, beta = 95.05(1) degrees, gamma = 95.86(1) degrees, and Z = 2; R1 for 3694 observed reflections [I > 2sigma(I)] was 0.029. The analogous Cd(NO(3))(2) complex with bppz, 5, could only be obtained in microcrystalline form, and its structure was solved by the use of X-ray powder diffraction methods. Compound 5, C(14)H(10)N(6)O(6)Cd, crystallizes in the monoclinic space group C2/c, with a = 11.6601(3) Å, b = 11.9870(3) Å, c = 12.1453(3) Å, beta = 103.348(2) degrees, and Z = 4. In both 4 and 5 the cadmium atoms are bridged by the ligand bppz, so forming uniform one-dimensional coordination polymers. The cadmium ions exhibit the rare coordination number of 8, with two coordinated ligand molecules and two chelating acetate (4) or nitrate (5) groups.

Journal Article↗

The biochemical and pathological changes produced by the intratracheal instillation of certain components of zinc-hexachloroethane smoke.

Zinc chloride which is formed by igniting a mixture of zinc oxide and hexachloroethane in the production of white smokes has been shown to produce oedema when given to rats as a single instillation. The oedematous reaction, as assessed by histopathology and measurements of alveolar surface protein in lavage fluid, is variable, dose-dependent, and maximal at 3 days but at sub-lethal doses it regresses after 7 days. The parent compound, zinc oxide, does not produce these effects. In some animals there is evidence of a fibrogenic response at 7 days post-exposure although it is currently unknown whether or not this effect is progressive.

Animals↗

Zinc hydroxide stimulates superoxide production by rat alveolar macrophages.

The effect of zinc hydroxide on superoxide (O2-) production by rat alveolar macrophages was determined by chemiluminescence and by cytochrome c reduction. Zinc ions had no effect on the chemiluminescence of unstimulated alveolar macrophages. By contrast, zinc hydroxide (ZnOH2), a neutralized form of zinc ions, increased the chemiluminescence level and O2- release. Increased O2- release was inhibited by pertussis toxin, isoquinoline sulfonamide and pretreatment with EGTA. These findings indicate that zinc hydroxide formation from zinc compounds can stimulate the O2- production by alveolar macrophages by receptor-mediated and Ca(2+)-dependent process.

Animals↗

Effect of zinc-carnosine chelate compound (Z-103), a novel antioxidant, on acute gastric mucosal injury induced by ischemia-reperfusion in rats.

The protective effect of a novel synthetic zinc-carnosine chelate compound, zinc N-(3-aminopropionyl)-L-histidine (Z-103), on the gastric mucosal injury induced by ischemia-reperfusion was studied in rats. Ischemia and reperfusion injury was produced on the rat stomach by applying a small clamp to the celiac artery for 30 min and by removal of the clamp for 30 min. The decrease in the gastric mucosal blood flow was not influenced by the treatment with Z-103. The increase in total area of the erosions on the stomach after ischemia-reperfusion and the increase in lipid peroxides in the gastric mucosa were significantly inhibited by the oral administration of Z-103. In addition, Z-103 inhibited lipid peroxidation of rat brain homogenate and liver microsome in vitro. These results suggest that the protective effect of Z-103 against the aggravation of gastric mucosal injury induced by ischemia-reperfusion may be due to its inhibitory effect on lipid peroxidation.

Animals↗

In vitro cytotoxicity testing of three zinc metal salts using established fish cell lines.

The utilisation of fish cell lines has proven to be a valuable, rapid and cost-effective tool in the ecotoxicological assessment of chemicals and environmental samples. The main objective of this study was to investigate the value of multiple endpoint measurements in evaluating the cytotoxicity of three divalent zinc salts in three established fish cell lines (EPC, CHSE and RTG-2) and the potential for their employment as effective screening tools for zinc contaminated environmental samples. A significant stimulatory effect was detected with the neutral red assay in EPC and RTG-2 cells exposed to the lower doses of some zinc compounds. Significant (p < or = 0.01) lactate dehydrogenase release was detectable only with the highest exposure concentration of ZnCl2. Toxicity ranking based on IC50 values calculated from the neutral red and coomassie blue assay data found that in general, ZnC2 was the most cytotoxic metal compound to the cell lines employed. Differential cell sensitivities were observed to be dependant on the particular compound tested and the endpoint employed. It was found that the use of light microscopy in the identification of cell morphological changes was a valuable adjunct in verifying the results of colorimetric tests. In conclusion, careful consideration should be given to study design and statistics applied and use of a battery style approach is recommended for toxicological screening studies.

Animals↗

Chemical vapor synthesis of size-selected zinc oxide nanoparticles.

ZnO can be regarded as one of the most important metal oxide semiconductors for future applications. Similar to silicon in microelectronics, it is not only important to obtain nanoscale building blocks of ZnO, but also extraordinary purity has to be ensured. A new gas-phase approach to obtain size-selected, nanocrystalline ZnO particles is presented. The tetrameric alkyl-alkoxy zinc compound [CH(3)ZnOCH(CH(3))(2)](4) is chemically transformed into ZnO, and the mechanism of gas-phase transformation is studied in detail. Furthermore, the morphological genesis of particles via gas-phase sintering is investigated, and for the first time a detailed model of the gas-phase sintering processes of ZnO is presented. Various analytical techniques (powder XRD, TEM/energy-dispersive X-ray spectroscopy, magic-angle spinning NMR spectroscopy, FTIR spectroscopy, etc.) are used to investigate the structure and purity of the samples. In particular, the defect structure of the ZnO was studied by photoluminescence spectroscopy.

Gases↗

Inhibition of HIV-1 infection by zinc group metal compounds.

Thirty-seven metal compounds were examined for inhibitory activities against infection with human immunodeficiency virus type 1 (HIV-1). Zinc group metal compounds, namely, zinc acetate, zinc chloride, zinc nitrate, cadmium acetate and mercury chloride, showed anti-HIV-1 activities. Cadmium and mercury compounds at 1-10 microg/ml and zinc compounds at 100 microg/ml strongly inhibited HIV-1 infection, although the cadmium, mercury and zinc compounds had severe cytotoxities at 100, 100 and 1000 microg/ml, respectively. They inhibited transcription of HIV-1 RNA and HIV-1 production at concentrations at which they did not affect the growth of HIV-1-producing cells. They had little effect on syncytium formation resulting from cocultivation of uninfected with HIV-1-producing cells. Nor did they affect HIV-1 DNA synthesis following HIV-1 infection. The metal compounds may owe their anti-HIV-1 effects to inhibition of HIV-1 DNA to RNA transcription, rather than inhibition of the adsorption, penetration or reverse transcription step of HIV-1 infection.

Antiviral Agents↗

Dephosphorylation of MnDPDP and related compounds by acid and alkaline phosphatase.

The enzymatic dephosphorylation of the magnetic resonance imaging contrast agent Teslascan was studied in in vitro experiments with acid phosphatase (prostatic, from human semen) and alkaline phosphatase (from human placenta). The active component, MnDPDP (manganese (II)-N,N'-dipyridoxylethylenediamine-N,N'-diacetate-5,5'-bis(phosphate), was dephosphorylated by both enzymes to the monophosphate MnDPMP and the totally dephosphorylated compound MnPLED. The corresponding zinc compound, ZnDPDP (which is a result of in vivo metabolism), was also dephosphorylated by both enzymes to ZnDPMP and ZnPLED. In separate experiments, both enzymes dephosphorylated MnDPMP and ZnDPMP. With the same amount of enzyme units, alkaline phosphatase was almost four times more active than acid phosphatase in dephosphorylating MnDPDP and ZnDPDP with only minor differences whether the substrate contained Mn or Zn. A similar difference in enzymatic activity was seen with the monophosphates, MnDPMP and ZnDPMP. This, taken together with the approximately 50 times higher activity of alkaline phosphatase than acid phosphatase in serum shows that alkaline phosphatase is responsible for most of the dephosphorylation of MnDPDP and its metabolites in vivo.

Acid Phosphatase↗

An analysis of candidates for addition to the Clean Air Act list of hazardous air pollutants.

There are 188 air toxics listed as hazardous air pollutants (HAPs) in the Clean Air Act (CAA), based on their potential to adversely impact public health. This paper presents several analyses performed to screen potential candidates for addition to the HAPs list. We analyzed 1086 HAPs and potential HAPs, including chemicals regulated by the state of California or with emissions reported to the Toxics Release Inventory (TRI). HAPs and potential HAPs were ranked by their emissions to air, and by toxicity-weighted (tox-wtd) emissions for cancer and noncancer, using emissions information from the TRI and toxicity information from state and federal agencies. Separate consideration was given for persistent, bioaccumulative toxins (PBTs), reproductive or developmental toxins, and chemicals under evaluation for regulation as toxic air contaminants in California. Forty-four pollutants were identified as candidate HAPs based on three ranking analyses and whether they were a PBT or a reproductive or developmental toxin. Of these, nine qualified in two or three different rankings (ammonia [NH3], copper [Cu], Cu compounds, nitric acid [HNO3], N-methyl-2-pyrrolidone, sulfuric acid [H2SO4], vanadium [V] compounds, zinc [Zn], and Zn compounds). This analysis suggests further evaluation of several pollutants for possible addition to the CAA list of HAPs.

Air Pollutants↗

Interaction of zinc with dental mineral.

As some currently available toothpastes contain zinc compounds, the reaction of zinc with dental mineral and its effect on crystal growth rates were studied using three synthetic calcium-deficient hydroxyapatites (HAP) as being representative of dental mineral. Zinc was readily acquired by all HAP samples in the absence of added calcium, the amount adsorbed being proportional to the HAP surface area; about 9 mumol Zn/m2 was adsorbed at high zinc concentrations. As zinc was acquired, calcium was released, consistent with 1:1 Ca:Zn exchange. Soluble calcium reduced zinc uptake and similarly, calcium post-treatment released zinc. Pretreatment of HAP with 0.5 mM zinc reduced its subsequent ability to undergo seeded crystal growth, as did extracts of a toothpaste containing 0.5% zinc citrate, even in the presence of saliva. The reverse reaction, i.e. displacement of adsorbed zinc by salivary levels of calcium, however, indicates the mechanism by which zinc can reduce calculus formation in vivo by inhibiting plaque mineralisation without adversely affecting the anti-caries effects of fluoride.

Acetates↗

Beta-alanyl-L-histidinato zinc prevents skeletal unloading-induced disorder of bone metabolism in rats.

The effect of a new zinc compound beta-alanyl-L-histidinato zinc (AHZ) on the disorder of bone metabolism caused by skeletal unloading was investigated. Skeletal unloading was designed using the model of hind-limb hang in rats. Skeletal unloading for up to 4 days caused a remarkable decrease of zinc content, alkaline phosphatase activity, and DNA content in the femoral diaphysis of rats. Oral administration of AHZ (2.5, 5.0, and 10.0 mg/100 g) caused a significant increase in zinc, DNA, and calcium contents in the femoral diaphysis of rats with the skeletal unloading. Bone alkaline phosphatase activity was significantly increased by doses of 5.0 and 10.0 mg/100 g. These results clearly indicate that skeletal unloading-induced disorder of bone metabolism is prevented by the oral administration of AHZ. AHZ may be useful as a therapeutic tool in bone disorder.

Alkaline Phosphatase↗

Effect of beta-alanyl-L-histidinato zinc on bone metabolism in rats with adjuvant arthritis.

The effect of a new zinc compound, beta-alanyl-L-histidinato zinc (AHZ), on osteopenia was investigated in rats with adjuvant arthritis. Arthritis was induced in female rats by administering 1% Mycobacterium butyricum (MB) into the subplantar surface of the right hind paw. AHZ (10, 30 and 100 mg/kg body weight) was orally administered to MB-treated rats 28 times at 24-h intervals, and the rats were bled 24 h after the last administration. Treatment with MB caused a remarkable increase in paw volume and a corresponding decrease in the ratio of albumin per globulin in serum, indicating that the treatment induces inflammation. These alterations were not significantly changed by the administration of AHZ (10, 30 and 100 mg/kg). Serum calcium and zinc concentrations are significantly decreased in rats with adjuvant arthritis. These decreases were completely restored by the administration of AHZ (30 and 100 mg/kg). Furthermore, the inflammation-induced decreases in alkaline phosphatase activity and calcium content in the femoral diaphysis were clearly blocked by the administration of AHZ (30 and 100 mg/kg). Also, the larger doses of AHZ (30 and 100 mg/kg) produced a significant increase in femoral-diaphyseal deoxyribonucleic acid and in the zinc content in rats with adjuvant arthritis. These results suggest that AHZ has a stimulating effect on bone formation in the femoral diaphysis of rats with adjuvant arthritis, although the compound did not have an anti-arthritic effect.

Alkaline Phosphatase↗

On the preparation of coordination polymers by controlled thermal decomposition: synthesis, crystal structures, and thermal properties of zinc halide pyrazine coordination compounds.

The five zinc(II) halide pyrazine coordination compounds poly-bis(mu2-pyrazine)-dichloro-zinc(II) (I), poly-(mu2-pyrazine-N,N')-dichloro-zinc(II) (II), poly-bis(mu2-pyrazine-N,N')-dibromo-zinc(II) (III), catena-(mu2-pyrazine-N,N')-dibromo-zinc(II) (IV), and catena-(mu-pyrazine)-diiodo-zinc(II) (V) were prepared by the reaction of ZnX2 (X = Cl, Br, I) with pyrazine in acetonitrile. In the crystal structure of compound I, the zinc atoms are coordinated by two chlorine atoms and two pyrazine ligands within distorted tetrahedra. The zinc atoms are linked by the N-donor ligands into layers. The crystal structure of compound III is very similar to that of compound I. The structure of compound III was originally reported in space group Ccca with similar a and b axes, but it was proved that the correct space group is I4/mmm. Ligand-poor compound V is isotypic to compound IV, in which ZnX2 units (X = Br, I) are connected by the pyrazine ligands into chains. It was originally reported in the noncentrosymmetric space group P2(1), but we found that the correct space group is P2(1)/m. If ligand-rich 1:2 compounds I and III are heated in a thermobalance, different mass steps are observed. We have proven that in the first step, ligand-poor compounds II and IV are formed in quantitative yields. On further heating, a second mass step occurs that leads to the formation of two new compounds of composition (ZnCl2)2(pyrazine) (VI) and (ZnBr2)2(pyrazine) (VII). However, the mass step is not well-resolved. and the new compounds are not phase-pure after the thermal event. If ligand-poor 1:1 compound V is investigated by thermogravimetry, a not-well-resolved single mass step is observed in which new ligand-poor 2:1 compound (ZnI2)2(pyrazine) (VIII) is formed. On further heating, all 2:1 compounds lose their remaining ligands and transform into the pure zinc(II) halides.

Journal Article↗