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PubMed1987

Oral challenge with nickel and cobalt in patients with positive patch tests to nickel and/or cobalt.

During a 3-year period, 146 patients with positive patch tests to nickel and/or cobalt, for whom a systemic cause of dermatitis was suspected, were challenged orally with a single dose of 2.5 mg nickel given as nickel sulphate and 1 mg cobalt given as cobalt sulphate using a double-blind, placebo-controlled method. No following-up was possible for 2 patients. Seventy-five of the remaining 144 (52%) had flares of their dermatitis after challenge with nickel and/or cobalt, while 45 patients (31%) had no reaction and 24 (17%) reacted only to the placebo or to the placebo in combination with nickel or cobalt. Seven out of 13 patients with positive patch tests to cobalt experienced flares of their dermatitis only after challenge with cobalt.

Administration, Oral↗
PubMed1989

Nickel allergy in relationship to previous oral and cutaneous nickel contact.

Potential relationships between the development of nickel allergy and previous ear piercing or orthodontic treatment with nickel-containing appliances were studied in 294 patients. We found 77 (31.2%) of 247 patients with pierced ears were allergic to nickel compared to only three (6.4%) patients without pierced ears (p = 0.001), which confirms earlier suggestions that nickel allergy (as assessed by patch testing) is promoted by ear piercing. If orthodontic treatment preceded the event of ear piercing, the frequency of nickel allergy was reduced from 36% to 25%. This supports the view that oral allergenic contacts may induce immunological tolerance.

Drug Hypersensitivity↗
PubMed1988

Nickel antigen induces IL-2 secretion and IL-2 receptor expression mainly on CD4+ T cells, but no measurable gamma interferon secretion in peripheral blood mononuclear cell cultures in delayed type hypersensitivity to nickel.

Nickel sulphate antigen-induced peripheral blood lymphocyte activation in vitro was characterized by lymphokine measurement (IL-2, IFN-gamma) and phenotyping of the IL-2 responsive cells. Mononuclear cells from nickel-sensitive patients synthesized more DNA, produced more IL-2 and had more IL-2 receptor positive cells in response to nickel than did those of the control subjects. On the other hand no IFN-gamma was detectable in the nickel supernatants, while PPD, used as the control antigen, induced pronounced quantities of IFN-gamma with an equal amount of DNA synthesis. The increase in IL-2 receptor positive cells was due to activation of CD4+ (helper/inducer) T cells. T cells with HLA-DR antigen surface markers were more numerous on each day of culture than cells with IL-2 receptors. These two activation markers were co-expressed on the same cells only to a certain extent, thus perhaps reflecting different types or phases of activation. In conclusion, nickel-induced peripheral blood mononuclear cell activation in vitro differs from microbial antigen-induced activation with respect to its modest or non-existent IFN-gamma response.

Adult↗
PubMed1988

[Evaluation of occupational exposure to nickel and other metals based on the analysis of air in the production of nickel alloys].

The measurements of air pollutions in the rolling mill of non-ferrous metals aimed at the evaluation of occupational exposure to nickel and other metals (Cu, Zn, Mn, Mg) used during the production of nickel alloys. It was found that nickel fumes and dusts concentration can be the only hazardous factor for the workers' health. The majority (ca 85%) of the crew of 28 workers is exposed to the nickel concentration in air exceeding 0.05 mg/m3. Smelters (8 persons) at the stand of 97-99% nickel smelting are at the highest risk of the loss of health; average exposure of this group during 8 hours' shift may surpass 2 mg Ni/m3. Mean concentration in air of the fumes and dusts of copper, zinc, manganese and magnesium do not make a hygienic problem.

Air Pollutants, Occupational↗
PubMed1984

Carcinogenicity and mutagenicity of nickel and nickel compounds.

A brief description of present concepts of tumour development and the most common genotoxicity tests is given. Data on the mutagenicity testing of nickel are summarized. They indicate that carcinogenic nickel compounds may bring about initiation by means of mutation, such as chromosome breakage and irregular distribution of genetic material. Compared with many mutagenic organic compounds, the efficacy of the nickel compounds is low. Extrapolation to man calls for great caution, since mutation tests involve short-term exposures, while the human situation is characterized by long-term exposure and very long cancer latency periods. The predictive value of mutagenicity tests in evaluating new environmental situations involving nickel compounds is limited. Positive findings identify a carcinogenic hazard, whereas negative findings do not exclude such a hazard. Experimental studies of transformation suggest that nickel compounds may also have promoting properties.

Animals↗
PubMed1995

Reduced uptake of nickel by a nickel resistant strain of Candida utilis.

A nickel resistant strain of the yeast Candida utilis was obtained by selection of spontaneous mutants on solid medium containing 3 mM Ni2+. In time-course experiments, non-growing suspensions of the mutant strain took up approximately 50% less nickel than the parent strain over 30 min incubation in MES buffer plus glucose at pH 5.5. Efflux of nickel from either strain was negligible. Uptake was reduced by omission of glucose from the uptake buffer in both strains but this was much more marked in the parent strain. Uptake of nickel in the presence of equimolar concentration of Mg2+ was reduced by 80% in both parent and mutant strains. It was concluded that resistance to nickel was due to an alteration in a transport system primarily responsible for uptake of magnesium.

Candida↗
PubMed1996

Polydentate N(2)S(2)O and N(2)S(2)O(2) Ligands as Alcoholic Derivatives of (N,N'-Bis(2-mercaptoethyl)-1,5-diazacyclooctane)nickel(II) and (N,N'-Bis(2-mercapto-2-methylpropane)-1,5-diazacyclooctane)nickel(II).

The synthesis, structural characterization, spectroscopic, and electrochemical properties of N(2)S(2)-ligated Ni(II) complexes, (N,N'-bis(2-mercaptoethyl)-1,5-diazacyclooctane)nickel(II), (bme-daco)Ni(II), and (N,N'-bis(2-mercapto-2-methylpropane)1,5-diazacyclooctane)nickel(II), (bme-daco)Ni(II), derivatized at S with alcohol-containing alkyl functionalities, are described. Reaction of (bme-daco)Ni(II) with 2-iodoethanol afforded isomers, (N,N'-bis(5-hydroxy-3-thiapentyl)-1,5-diazacyclooctane-O,N,N',S,S')halonickel(II) iodide (halo = chloro or iodo), 1, and (N,N'-bis(5-hydroxy-3-thiapentyl)-1,5-diazacyclooctane-N,N',S,S')nickel(II) iodide, 2, which differ in the utilization of binding sites in a potentially hexadentate N(2)S(2)O(2) ligand. Blue complex 1 contains nickel in an octahedral environment of N(2)S(2)OX donors; X is best modeled as Cl. It crystallizes in the monoclinic space group P2(1)/n with a = 12.580(6) Å, b = 12.291(6) Å, c = 13.090(7) Å, beta = 97.36(4) degrees, and Z = 4. In contrast, red complex 2 binds only the N(2)S(2) donor set forming a square planar nickel complex, leaving both -CH(2)CH(2)OH arms dangling; the iodide ions serve strictly as counterions. 2 crystallizes in the orthorhombic space group Pca2(1) with a = 15.822(2) Å, b = 13.171(2) Å, c = 10.0390(10) Å, and Z = 4. Reaction of (bme-daco)Ni(II) with 1,3-dibromo-2-propanol affords another octahedral Ni species with a N(2)S(2)OBr donor set, ((5-hydroxy-3,7-dithianonadiyl)-1,5-diazacyclooctane-O,N,N',S,S')bromonickel(II) bromide, 3. Complex 3 crystallizes in the orthorhombic space group Pca2(1) with a = 15.202(5) Å, b = 7.735(2) Å, c = 15.443(4) Å, and Z = 4. Complex 4.2CH(3)CN was synthesized from the reaction of (bme-daco)Ni(II) with 1,3-dibromo-2-propanol. It crystallizes in the monoclinic space group P2/c with a = 20.348(5) Å, b = 6.5120(1) Å, c = 20.548(5) Å, and Z = 4.

Journal Article↗
PubMed1999

Spectrophotometric Study of the Equilibria between Nickel(II) Schiff-Base Complexes and Alkaline Earth or Nickel(II) Cations in Acetonitrile Solution.

Adduct formation between M(ClO(4))(2) and nickel(II) complexes of tetradentate Schiff-base ligands ([NiL]) have been investigated in acetonitrile by means of UV-vis spectrophotometric analysis (M(2+)= Mg(2+), Ca(2+), Sr(2+), Ba(2+), Ni(2+); [NiL] = [Ni(salen)] = [N,N'-ethylenebis(salicylideneiminato)]nickel(II), [Ni(salphen)] = [N,N'-o-phenylenebis(salicylideneiminato)]nickel(II), [Ni(salpren)] = [N,N'-propylenebis(salicylideneiminato)]nickel(II)). [NiL] complexes act as bidentate oxygen-donor ligands forming adducts of the type [(NiL)M](2+) and [(NiL)(2)M](2+) whose general order of increasing stability was correlated to the dimensions of the M(2+) cations. Complexes of general composition 2[Ni(salen)].M(ClO(4))(2) were isolated as powders in the solid state (M = Sr, Ca, Mg). X-ray structures of the crystalline complexes [{Ni(salen)}(2)Ba(ClO(4))(2)(thf)] (1) (thf = tetrahydrofuran) and [{Ni(salen)}(2)Ni(H(2)O)(2)](ClO(4))(2) (2) are reported. 1 crystallizes in the space group P2(1)/c (a = 10.995 Å; b = 20.830 Å; c = 19.567 Å, beta = 116.94 degrees ) and 2 in C2/c (a = 10.3020 Å; b = 21.818 Å; c = 17.796 Å; beta = 118.98 degrees ). Two [Ni(salen)] units act as oxygen bidentate ligands in both the compounds. The barium is coordinated to eight oxygen atoms in a distorted square antiprismatic geometry. An 8-fold coordination is completed by a molecule of tetrahydrofuran and two perchlorate anions acting as bi- and monodentate O-ligands, respectively. In 2, the nickel atom, coordinated to two [Ni(salen)] complexes, has a distorted octahedral geometry and completes its coordination by linking two molecules of water.

Journal Article↗
PubMed2005

Control of expression of a periplasmic nickel efflux pump by periplasmic nickel concentrations.

There is accumulating evidence that transenvelope efflux pumps of the resistance, nodulation, cell division protein family (RND) are excreting toxic substances from the periplasm across the outer membrane directly to the outside. This would mean that resistance of Gram-negative bacteria to organic toxins and heavy metals is in fact a two-step process: one set of resistance factors control the concentration of a toxic substance in the periplasm, another one that in the cytoplasm. Efficient periplasmic detoxification requires periplasmic toxin sensing and transduction of this signal into the cytoplasm to control expression of the periplasmic detoxification system. Such a signal transduction system was analyzed using the Cnr nickel resistance system from Cupriavidus (Wautersia, Ralstonia, Alcaligenes) metallidurans strain CH34. Resistance is based on nickel efflux mediated by the CnrCBA efflux pump encoded by the cnrYHXCBAT metal resistance determinant. The products of the three genes cnrYXH transcriptionally regulate expression of cnr. CnrY and CnrX are membrane-bound proteins probably functioning as anti sigma factors while CnrH is a cnr-specific extracytoplasmic functions (ECF) sigma factors. Experimental data provided here indicate a signal transduction chain leading from nickel in the periplasm to transcription initiation at the cnr promoters cnrYp and cnrCp, which control synthesis of the nickel efflux pump CnrCBA.

Biological Transport↗
PubMed2003

Interaction of nickel with 4-(2'-benzothiazolylazo) salicylic acid (BTAS) and simultaneous first-derivative spectrophotometric determination of nickel(II) and iron(III).

The solution properties of nickel complex with 4-(2'-benzo-thiazolylazo) salicylic acid (BTAS) have been studied by zero-order absorption spectrophotometry in 40% (v/v) ethanol at 20 degrees C and an ionic strength of 0.1 mol dm(-3) (KNO(3)). The equilibria that exist in solution were established and the basic characteristics of complexes formed were determined. A new direct spectrophotometric method for the determination of trace amounts of the nickel is proposed based on the formation of the Ni (BTAS) complex at pH 7.0. The absorption maximum, molar absorbtivity, and Sandell's sensitivity of 1:1 (M:L) complex are 525 nm, 0.6 x 10(4) l mol(-1) cm(-1) and 2.824 x 10(-9) microg cm(-2), respectively. The use of first-derivative spectrophotometry eliminates the interference of iron and enables the simultaneous determination of nickel and iron using BTAS. Quantitative determination of Ni(II) and Fe(III) is possible in the range (0.59-7.08) and (2.1-8.4) microg ml(-1), respectively with a relative standard deviation of 0.5%. The proposed method has been successfully applied to the simultaneous spectrophotometric determination of nickel and iron in steel alloys and aluminum alloys.

Alloys↗
PubMed2002

Nickel(II) complexes with tetra- and pentadentate aminopyridine ligands: synthesis, structure, electrochemistry, and reduction to nickel(I) species.

A series of nickel(II) complexes with polydentate aminopyridine ligands N,N,N'-tris-[2-(2'-pyridyl)ethyl]ethane-1,2-diamine (L1), N,N,N'-tris-[2-(2'-pyridyl)ethyl]-N'-methylethane-1,2-diamine (L2), and N,N'-bis-[2-(2'-pyridyl)ethyl]-N,N'-dimethylethane-1,2-diamine (L3) were synthesized and characterized by elemental analysis and spectroscopic methods. Single-crystal X-ray diffraction studies showed that the Ni(II) ions have five-coordinate square-pyramidal geometry in [NiL2](ClO(4))(2), similar to that previously found in [NiL1](ClO(4))(2) x CH(3)NO(2) (Hoskins, B. F.; Whillans, F. D.J. Chem. Soc., Dalton Trans. 1975, 657), and square-planar geometry in [NiL3](ClO(4))(2). All three nickel(II) complexes are reduced by sodium borohydride or sodium amalgam in organic solvents to nickel(I) species, which were identified by highly anisotropic EPR spectra at 100 K: g(1) = 2.239, g(2) = 2.199, and g(3) = 2.025 for [NiL1](+); g(axially) = 2.324 and g(radially) = 2.079 for [NiL2](+) and [NiL3](+). Cyclic voltammetry of the nickel(II) complexes in acetonitrile exhibited reversible reduction waves at -1.01 V for [NiL1](2+), -0.91 V for [NiL2](2+), and -0.83 V for [NiL3](2+) versus SCE, potentials which are significantly less negative than those of most previously characterized Ni(II) complexes with nitrogen-only donor atoms. Complexes [NiL1](2+) and [NiL2](2+) showed high catalytic activity in the electroreduction of 1,2-trans-dibromocyclohexane to cyclohexene.

Aminopyridines↗
PubMed1978

Low nickel diet in the treatment of patients with chronic nickel dermatitis.

Of 28 patients with chronic nickel dermatitis 17 experienced aggravation following oral ingestion of 2.5 mg nickel, but not a placebo tablet. The dermatitis of 9 of the 17 patients improved during a period of 6 weeks on a low nickel diet. The dermatitis of 7 of the 9 patients flared again when a normal diet was resumed. Nickel excretion over a 24-h period was measured for 14 of the 17 patients by atomic absorption spectrophotometry before, during, and after the diet. Reduced excretion was seen during the diet with no statistically significant difference between patients whose dermatitis improved during the diet and those whose dermatitis showed no change.

Chronic Disease↗
PubMed1985

Isolated late asthmatic reaction due to nickel sulphate without antibodies to nickel.

A worker with occupational exposure to nickel developed asthma a few months after starting work. Skin prick tests to nickel sulphate were negative. Inhalation challenge with nickel sulphate, at a concentration of 10 mg/ml for 30 min induced a late asthmatic reaction, starting 3 hr after the end of exposure leading to severe nocturnal attack. Tests for antibodies with nickel reactivity were negative.

Adult↗
PubMed1976

Nickel dermatitis--nickel excretion.

Nickel excretion in urine in four females sensitive to nickel with an intermittent dyshidrotic eruption was measured with flameless atomic absorption. Excretion of nickel was found to be increased in association with outbreaks of vesicles. The results support the idea that the chronic condition was maintained by ingestion of nickel in food.

Adult↗
PubMed1979

Effect on growth and nickel content of cabbage plants watered with nickel solutions.

Chinese cabbage plants were watered with different concentrations of NiCl2 solutions and the effect on growth and uptake of nickel in the plants were studied. No toxic effect on plant growth was observed. A higher content of nickel was found in the plants exposed to more concentrated nickel solutions. Nickel contamination and its clinical consequences are discussed.

Brassica↗
PubMed1989

Allergy to nickel or cobalt: tolerance to nickel and cobalt samples in man and in the guinea pig allergic or sensitized to these metals.

The aim of this study was to evaluate, in animals and humans sensitive to nickel or cobalt, the tolerance to manufactured metal samples of nickel and cobalt of a defined metallographic structure, plated or not with a layer of chrome or copper/chrome of a determined thickness. Under the defined experimental conditions, a guinea pig sensitized to one metal (nickel or cobalt) was intolerant to both metals (nickel and cobalt). A plating of chrome or copper/chrome did not act as a protection. In the human, it was not the same: the tolerance to metal samples was determined by the specific sensitivity. A plating of chrome or copper/chrome did not act as protection.

Animals↗
PubMed2005

Nickel and cobalt resistance engineered in Escherichia coli by overexpression of serine acetyltransferase from the nickel hyperaccumulator plant Thlaspi goesingense.

The overexpression of serine acetyltransferase from the Ni-hyperaccumulating plant Thlaspi goesingense causes enhanced nickel and cobalt resistance in Escherichia coli. Furthermore, overexpression of T. goesingense serine acetyltransferase results in enhanced sensitivity to cadmium and has no significant effect on resistance to zinc. Enhanced nickel resistance is directly related to the constitutive overactivation of sulfur assimilation and glutathione biosynthesis, driven by the overproduction of O-acetyl-L-serine, the product of serine acetyltransferase and a positive regulator of the cysteine regulon. Nickel in the serine acetyltransferase-overexpressing strains is not detoxified by coordination or precipitation with sulfur, suggesting that glutathione is involved in reducing the oxidative damage imposed by nickel.

Cobalt↗
PubMed2001

NreB from Achromobacter xylosoxidans 31A Is a nickel-induced transporter conferring nickel resistance.

There are two distinct nickel resistance loci on plasmid pTOM9 from Achromobacter xylosoxidans 31A, ncc and nre. Expression of the nreB gene was specifically induced by nickel and conferred nickel resistance on both A. xylosoxidans 31A and Escherichia coli. E. coli cells expressing nreB showed reduced accumulation of Ni(2+), suggesting that NreB mediated nickel efflux. The histidine-rich C-terminal region of NreB was not essential but contributed to maximal Ni(2+) resistance.

Alcaligenes↗