AN ANALYSIS OF THE DNA DAMAGE INDUCED BY NICKEL COMPOUNDS IN CHINESE HAMSTER OVARY CELLS (CARCINOGENESIS, HETEROCHROMATIN, CYTOTOXICITY, REPLICATION, PROTEIN CROSSLINKING)

The carcinogenic activity of water-insoluble crystalline nickel sulfide requires phagocytosis and lysosome-mediated intracellular dissolution of the particles to yield Ni('2+). This study investigated the extent and nature of the DNA damage in Chinese hamster ovary cells treated with various nickel compounds using the technique of alkaline elution. Crystalline NiS and water-soluble NiCl(,2) induced single strand breaks that were repaired quickly and DNA-protein crosslinks that persisted up to 24 hr after exposure to nickel. The induction of single strand breaks was concentration dependent at both noncytotoxic and lethal amounts of nickel. The induction of DNA-protein crosslinks was concentration dependent but was absent at lethal amounts of nickel. The cytoplasmic and nuclear uptake of nickel was concentration dependent even at the toxic level of nickel. However, the induction of DNA-protein crosslinks by nickel required active cell cycling and occurred predominantly in mid-late S phase of the cell cycle, suggesting that the lethal amounts of nickel inhibited DNA-protein crosslinking by inhibiting active cell cycling. Since the DNA-protein crosslinking induced by nickel was resistant to DNA repair, the nature of this lesion was investigated using various methods of DNA isolation and chromatin fractionation in combination with SDS-polyacrylamide gel electrophoresis. High molecular weight, non-histone chromosomal proteins and possibly histone 1 were preferentially crosslinked to DNA by nickel. The crosslinked proteins were concentrated in a magnesium-insoluble fraction of sonicated chromatin (5% of the total) that was similar to heterochromatin in solubility and protein composition. Alterations in DNA structure and function, brought about by the effect of nickel on protein-DNA interactions, may be related to the carcinogenicity of nickel compounds. ^

DETERMINANTS OF THE SELECTIVE PHAGOCYTOSIS OF CARCINOGENIC PARTICULATE NICKEL COMPOUNDS

Certain inorganic nickel compounds such as crystalline NiS and Ni(,3)S(,2) are potent inducers of carcinogenesis and in vitro cell transformation, while several closely-related compounds such as amorphous NiS are essentially devoid of genotoxic activity. The phenomenon of selectivity of phagocytosis among such particulate nickel compounds has been hypothesized to account for their widely varying toxicological potency, yet the determinants of this selectivity have not been well characterized. Extracellular medium composition, particle dissolution, and particle surface charge were examined as potential determinants of selective phagocytosis for the carcinogenic crystalline and noncarcinogenic amorphous modifications of NiS. Selectivity and avidity of uptake of crystalline NiS by CHO cells was not dependent upon serum: phagocytosis of crystalline, but not amorphous NiS proceeded readily in a minimal salts/glucose medium at 37(DEGREES)C. The evolution of phagocytosis-inhibiting Ni(II) from the surface of amorphous NiS particles did not demonstrably contribute to the lower uptake of these noncarcinogenic particles despite their somewhat greater dissolution rate than the readily phagocytosed crystalline NiS particles. Significant differences in surface charge were noted between crystalline and amorphous NiS, the former being more negative in charge in distilled water suspension. Exposure of amorphous NiS particles to the vigorously reducing environment of a LiAlH(,4) solution under an inert atmosphere resulted in the particles' acquisition of a more negative surface charge. Amorphous NiS particles thus treated were phagocytosed by CHO cells to an extent similar to that of untreated crystalline NiS particles and likewise were shown to induce morphological transformation of primary Syrian hamster embryo cells with a similar potency. The potentiation of uptake characteristic of LiAlH(,4)-treated amorphous NiS was lost gradually upon storage of particles in ambient oxygenated atmosphere and was lost rapidly by apparent particle surface oxidation in aerated distilled water suspensions aged for up to 7 days. Concomitant with this loss of uptake there occurred a loss of negative surface charge. These results suggest the predominant role of particle surface charge rather than adsorbed serum components or particle dissolution as a determinant of selective phagocytosis among particulate nickel compounds. ^

SUPEROXIDE RADICAL AND TOXICITY OF ENVIRONMENTAL NICKEL EXPOSURE

Three nickel compounds were tested for pancreatic, hepatic and osteogenic damage in rats by a single i.m. injection Ni++ (7 mg kg(-1)). The nickel induced biochemical alterations included significantly increased levels of serum alkaline phosphatase in rats with NiS (75%) and NiO (50%). Amylase and aspartate transaminase were also increased, and lipoperoxide was increased in rats with NiO (5.6-fold) and NiS (3.4-fold). No serum changes were observed with NiCl2. Daily injection of Cu-Zn superoxide dismutase (SOD) conjugated with polyethylene glycol prevented the serum level changes, indicating that superoxide radical is an important intermediate in toxicity of nickel insoluble compounds.

Highly selective nickel ethylene oligomerization catalysts based on sterically hindered tris(pyrazolyl)borate ligands

The reaction of TlTp' (Tp' = HB(3-mesitylpyrazolyl)(3)(-) (Tp(Ms)), HB(3-mesitylpyrazolyl)(2)(5-mesitylpyrazolyl)(-) (Tp(Ms)*)) with NiCl(2).6H(2)O affords Tp(Ms)NiCl (1) and Tp(Ms)*NiCl (2) in good yield. The compound 2 undergoes an isomerization process to form [{Tp(Ms)**}NiCl](2) (3) (Tp(Ms)** = HB(5-mesitylpyrazolyl)(2)(3-mesitylpyrazolyl)(-)) in 68% yield. Treatment of the tris(pyrazolyl)-borate nickel compounds 1 and 2 with alkylaluminum cocatalysts such as methylalumoxane (MAO) and trimethylaluminum (TMA) in toluene generates active catalysts for ethylene oligomerization. The compound 1 shows turnover frequencies in the range of (2.2-43.1) x 10(3) h(-1). Oligomerization reaction conditions can be adjusted that lead to selectivities as high as 81% for butene-1.

Protective effect of nickel chloride on superoxide damage: enhancement of CuZn superoxide dismutase affinity to the oxygen free radical.

The effect of nickel from soluble NiCl2 on Cu-Zn superoxide dismutase (SOD) activity, as well as on rate of nitro blue tetrazolium reduction, was studied in vitro since lipid peroxidation has been implicated in cell damage by nickel insoluble compounds, whose toxicity and carcinogenicity are well established. The physical and chemical nature of nickel compounds is one of the key determinations of its toxicity. Soluble nickel freely enter cells, but is just as readily excreted reducing the opportunity for production of lipid damage. Nickel from NiCl2 strongly activated SOD activity. In vitro addition of nickel chloride to a crude lung preparation altered the KM for SOD without changing the Vmax. Nickel chloride produced increased enzyme affinity to the substrate, because decreased (O2-) concentration that yields half-maximal velocity. The combination of nickel and SOD may contribute to stabilization of the particular conformation of SOD responsible for maximal catalytically activity.

Toxic effects of nickel exposure on heart and liver of rats

The role of air pollution as a health risk factor is of special interest. Numerous toxic pollutants, such as nickel, are being released to the environment as a result of combustion of fossil fuels, crude oil, and coal. Nickel in the atmosphere can be combined with other environmental pollutants, producing various nickel compounds, which have varying animal toxicity. A rat biossay validated for the identification of toxic effects of nickel revealed increased serum activities of total lactate dehydrogenase (LDH) and alanine transaminase (ALT) in rats that received intratracheal injection of Ni2+ in .09% saline solution of NiCl2. The total LDH activity was also increased in the heart, and the isoenzyme pattern showed the LDH1/LDH2 ratio elevated to greater than 1. We conclude that intratracheal administration of nickel induced cardiac and hepatic damage. The development of cardiac and hepatic damage and of increased enzymes' activities was only demonstrated when nickel had accumulated in these tissues, indicating that nickel depot is essential to its toxicity. Intratracheal administration of NiCl2 induced changes in LDH and ALT activities.

Long-term toxicity following acute administration of nickel

Nickel compounds have high potential risk for the health of populations and for this reason their toxic effects should be urgently established. To determine the effect of nickel monosulfide in the muscle at the injection site on pancreatic, hepatic, and osteogenic lesions and the potential therapeutic effect of Cu-Zn superoxide dismutase (SOD), male Wistar rats received single intramuscular injections of nickel monosulfide (NiS - 7 mg Ni2+/Kg). A group of these experimental rats were injected intraperitoneally, with a single weekly dose of SOD covalently linked to polyethylene glycol (SOD-PEG). Rats were sacrificed at 2, 4, 6, and 8 months after Ni2+ injection. Nickel monosulfide produced tumors at the injection site. The increased phospholipid, alanine transaminase (ALT), alkaline phosphatase (ALP), and amylase levels in serum, in absence of SOD-PEG, reflected the toxic effects on pancreatic, hepatic, and osteogenic tissues of rats. SOD activity was increased in serum of rats receiving SOD-PEG throughout the experiment, and no significant difference was observed in biochemical parameters of control and experimental rats in presence of SOD- PEG. Superoxide radical generated by Ni2+ is of primary importance in the development of tumors at the injection site. Superoxide anion (O2 -) is also an important toxic intermediate with respect to hepatic, pancreatic, and osteogenic injury, since SOD-PEG has a potential therapeutic effect.

Thermal study of nickel(II) pyrazolyl complexes

The thermal behavior of the pyrazolyl complexes [NiCl2(HPz) 4] (1), [Ni(NCS)2(HPz)4] (2), [NiCl 2(HdmPz)4]·2H2O (3) and [Ni(NCS) 2(HdmPz)4]·2H2O (4) (HPz=pyrazole, HdmPz=3,5-dimethylpyrazole) has been studied by thermogravimetry (TG) and differential thermal analysis (DTA). The TG data indicated that the thermal stability of [NiX2(HL)4] (X=Cl, NCS) compounds varies depending on the pyrazolyl ligand in the following order HL=HPz>HdmPz. From the thermal decomposition of 3 and 4 it was possible to isolate the intermediate compounds [Ni(μ-Cl)2(HdmPz)2] (3a) and [Ni(μ-1,3-NCS) 2(HdmPz)2] (4a), respectively. The final products of the thermal decompositions of 1-4 were identified as NiO by X-ray powder diffraction. © 2005 Akadémiai Kiadó, Budapest.

Nickel in a tropical soil treated with sewage sludge and cropped with maize in a long-term field study

Sewage sludge produced by the SABESP wastewater treatment plant (Companhia de Saneamento Básico do Estado de São Paulo), located in Barueri, SP, Brazil, may contain high contents of nickel (Ni), increasing the risk of application to agricultural soils. An experiment was carried out under field conditions in Jaboticabal, SP, Brazil, with the objective of evaluating the effects on soil properties and on maize plants of increasing rates of a sewage sludge rich in Ni that had been applied for 6 consecutive years. The experiment was located on a Typic Haplorthox soil, using an experimental design of randomized blocks with four treatments (rates of sewage sludge) and five replications. At the end of the experiment the accumulated amounts of sewage sludge applied were 0.0, 30.0, 60.0 and 67.5 t ha-1. Maize (Zea mays L.) was the test plant. Soil samples were collected 60 d after sowing at depths of 0-20 cm for Ni studies and from 0 to 10 cm and from 10 to 20 cm for urease studies. Sewage sludge did not cause toxicity or micronutrient deficiencies to maize plants and increased grain production. Soil Ni appeared to be associated with the most stable fractions of the soil organic matter and was protected against strong extracting solutions such as concentrated and hot HNO3 and HCl. Ni added to the soil by sewage sludge increased the metal concentration in the shoots, but not in the grain. The Mehlich 3 extractor was not efficient to evaluate Ni phytoavailability to maize plants. Soil urease activity was increased by sewage sludge only in the layer where the residue was applied. © 2006 Elsevier Ltd. All rights reserved.

Sensor for diuron quantitation based on the P450 biomimetic catalyst nickel(II) 1,4,8,11,15,18,22,25-octabutoxy-29H,31H-phthalocyanine

A biomimetic sensor based on a carbon paste electrode modified with the nickel(II) 1,4,8,11,15,18,22,25-octabutoxy-29H,31H-phthalocyanine complex was developed as a reliable alternative technique for the sensitive and selective analysis of the herbicide diuron in environmental media. The sensor was evaluated using cyclic voltammetry and amperometric techniques. The best amperometric responses were obtained at 750 mV vs. Ag/AgCl (KClsat), using 0.1 mol L-1 phosphate buffer solution at pH 8.0. Under these conditions, the sensor showed a linear response for diuron concentrations between 9.9 × 10-6 and 1.5 × 10-4 mol L -1, a sensitivity of 22817 (±261) μA L mol-1, and detection and quantification limits of 6.14 × 10-6 and 2 × 10-5 mol L-1, respectively. The presence of the nickel complex in the carbon paste improved selectivity, stability, and sensitivity (which increased 700%), compared to unmodified paste. The applicability of the sensor was demonstrated using enriched environmental samples (river water and soil). © 2012 Elsevier B.V. All rights reserved.

Recycling nickel electroplating rinse waters by low temperature evaporation and reverse osmosis /

"Contract no. CR-815829."

Oxide reduction in NiO-containing solid solution systems during transmission electron microscopy

The effects of electron irradiation on NiO-containing solid solution systems are described. Partially hydrated NiO solid solutions, e. g. , NiO-MgO, undergo surface reduction to Ni metal after examination by TEM. This surface layer results in the formation of Moire interference patterns.

Occupational determinants of pancreatic cancer

Objective and background. Tobacco smoking, pancreatitis and diabetes mellitus are the only known causes of pancreatic cancer, leaving ample room for yet unidentified determinants. This is an empirical study on a Finnish data on occupational exposures and pancreatic cancer risk, and a non-Bayesian and a hierarchical Bayesian meta-analysis of data on occupational factors and pancreatic cancer. Methods. The case-control study analyzed 595 incident cases of pancreatic cancer and 1,622 controls of stomach, colon, and rectum cancer, diagnosed 1984-1987 and known to be dead by 1990 in Finland. The next-of-kin responded to a mail questionnaire on job and medical histories and lifestyles. Meta-analysis of occupational risk factors of pancreatic cancer started off with 1,903 identified studies. The analyses were based on different subsets of that database. Five epidemiologists examined the reports and extracted the pertinent data using a standardized extraction form that covered 20 study descriptors and the relevant relative risk estimates. Random effects meta-analyses were applied for 23 chemical agents. In addition, hierarchical Bayesian models for meta-analysis were applied to the occupational data of 27 job titles using job exposure matrix as a link matrix and estimating the relative risks of pancreatic cancer associated with nine occupational agents. Results. In the case-control study, logistic regressions revealed excess risks of pancreatic cancer associated with occupational exposures to ionizing radiation, nonchlorinated solvents, and pesticides. Chlorinated hydrocarbon solvents and related compounds, used mainly in metal degreasing and dry cleaning, are emerging as likely risk factors of pancreatic cancer in the non-Bayesian and the hierarchical Bayesian meta-analysis. Consistent excess risk was found for insecticides, and a high excess for nickel and nickel compounds in the random effects meta-analysis but not in the hierarchical Bayesian meta-analysis. Conclusions. In this study occupational exposure to chlorinated hydrocarbon solvents and related compounds and insecticides increase risk of pancreatic cancer. Hierarchical Bayesian meta-analysis is applicable when studies addressing the agent(s) under study are lacking or very few, but several studies address job titles with potential exposure to these agents. A job-exposure matrix or a formal expert assessment system is necessary in this situation.

Polypropylene as a carbon source for the synthesis of multi-walled carbon nanotubes via catalytic combustion

Multi-walled carbon nanotubes (MWCNTs) were efficiently synthesized by catalytic combustion of polypropylene (PP) using nickel compounds (such as Ni2O3, NiO, Ni(OH)(2) and NiCO3 (.) 2Ni(OH)(2)) as catalysts in the presence of organic-modified montmorillonite (OMMT) at 630-830 degrees C. Morphologies of the sample undergoing different combustion times were observed to investigate actual process producing MWCNTs by this method. The obtained MWCNTs were characterized by X-ray diffraction (XRD), transmission electron microscope and Raman spectroscopy. The yield of MWCNTs was affected by the composition of PP mixtures with OMMT and nickel compounds and the combustion temperature. The proton acidic sites from the degraded OMMT layers due to the Hoffman reaction of the modifiers at high temperature played an important role in the catalytic degradation of PP to supply carbon sources that are easy to be catalyzed by nickel catalyst for the growth of MWCNTs. The XRD measurements demonstrated that the nickel compounds were in situ reduced into the Ni(0) state with the aid of hydrogen gas and/or hydrocarbons in the degradation products of PP, and the Ni(O) was really the active site for the growth of MWCNTs. The combination of nickel compounds with OMMT was a key factor to efficiently synthesize MWCNTs via catalytic combustion of PP.

Kondo-attractive-Hubbard model for the ordering of local magnetic moments in superconductors

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)