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At least 127 records · Page 7Linked to original sources
PubMed1996

Pre-treatment of nickel test areas with sodium lauryl sulfate detects nickel sensitivity in subjects reacting negatively to routinely performed patch tests.

A fair % of patients with a clinical history of nickel allergy show negative patch test results. To improve the response rate to NiSO4 5% pet. patch tests, a testing procedure utilizing pre-treatment of the test area by a 24-h application of sodium lauryl sulfate (SLS) was introduced. 46 women with a clinical history of nickel sensitivity, who exhibited negative reactions to nickel sulfate 5% pet. patch tests, were studied. Patients underwent 6 patch tests on adjacent sites on the volar surface of the forearms. 4 patch tests were performed with a 72-h application of 40 mg nickel sulfate 5% pet. While 1 of these patch tests served as control, 3 test areas underwent 24-h pre-treatment with 40 microliters SLS, 1 with 0.1% and 2 with 0.5% solution. To evaluate differences in the reactivity to SLS plus nickel sulfate related to the site on the forearm, 0.5% SLS pre-treatment was performed both on a proximal and on a distal test site. At the 72-h evaluation, 19 subjects out of 46 showed positive reactions to nickel sulfate 5% pet. at skin sites pre-treated with 0.1% SLS, whereas 23 patients reacted positively at 0.5% SLS pre-treated areas. Echographic values of skin thickness and of hypo-echogenic dermal areas at positive pre-treated nickel test areas were higher than at control test areas, confirming the clinical evidence of an increased response to NiSO4 after SLS pre-treatment. The inflammatory reaction, as evaluated clinically and echographically, was much higher at distal skin areas (0.1% SLS and distal 0.5% SLS) than at proximal 0.5% SLS ones.

Adult↗
PubMed2005

Nickel recovery from spent nickel catalyst.

A process for nickel recovery from a spent catalyst of definite composition has been developed using the hydro-metallurgical route. The processing steps includes direct sulphuric acid leaching followed by separation of iron as well as silica and other impurities. For a 152 microm particle size catalyst, extraction of about 98% nickel was achieved at 363 K in 2 h using a sulphuric acid concentration (v/v) of 8% and a pulp density of 10%. The dissolution of nickel followed diffusion-controlled leaching kinetics. Increase in temperature and sulphuric acid concentration resulted in increase in the nickel recovery. The activation energy for nickel dissolution was calculated to be 62.8 kJ mol(-1). Finally, nickel was recovered as value-added products such as sulphide and oxalate with overall recovery of 90 and 88% of nickel, respectively.

Catalysis↗
PubMed2001

Tolerance to nickel: oral nickel administration induces a high frequency of anergic T cells with persistent suppressor activity.

We adapted our mouse model of allergic contact hypersensitivity to nickel for the study of tolerance. Sensitization in this model is achieved by the administration of nickel ions with H(2)O(2); nickel ions alone are unable to prime naive T cells, but can restimulate primed ones. A 4-wk course of oral or i.p. administration of 10 mM NiCl(2) to naive mice induced tolerance, preventing the induction of hypersensitivity for at least 20 wk; long term desensitization of nickel-sensitized mice, however, required continuous NiCl(2) administration. When splenic T cells of orally tolerized donors, even after a treatment-free interval of 20 wk, were transferred to naive recipients, as with lymph node cells (LNC), they specifically prevented sensitization of the recipients. The LNC of such donors were anergic, because upon in vivo sensitization with NiCl(2) in H(2)O(2) and in vitro restimulation with NiCl(2), they failed to show the enhanced proliferation and IL-2 production as seen with LNC of mice not tolerized before sensitization. As few as 10(2) bulk T cells, consisting of both CD4(+) and CD8(+) cells, were able to specifically transfer tolerance to nickel. A hypothesis is provided to account for this extraordinarily high frequency of nickel-reactive, suppressive T cells; it takes into account that nickel ions fail to act as classical haptens, but form versatile, unstable metal-protein and metal-peptide complexes. Furthermore, a powerful amplification mechanism, such as infectious tolerance, must operate which allows but a few donor T cells to tolerize the recipient.

Adjuvants, Immunologic↗
PubMed1990

Nickel contact allergy and a nickel-restricted diet.

More than half of nickel-allergic patients develop secondary eruptions, that is, dermatitis in areas of the skin that are not in obvious contact with nickel-plated items. Similar eruptions occur after placebo-controlled oral challenge with inorganic nickel salts. The possible relationship between ingestion of nickel in food and secondary eruptions in nickel-sensitive patients is discussed, making reference to the available literature. Recommendations are given for the management of patients suspected to have nickel dermatitis aggravated by nickel in food.

Administration, Oral↗
PubMed1977

[Nickel content of human lymphoblastoid cells cultured in a nickel sulfate-enriched medium].

Nickel is titrated by atomic absorption in nuclear and non-nuclear fractions of cells cultured in media supplemented by nickel sulphate. The living cell percentages are estimated in the same culture conditions. We try to connect the nickel presence in cellular fractions and the living cell percentages. These used cells seem to have mortality probability when nuclear fraction has 55 x 10(-6) of nickel and non-nuclear fraction has 33 x 10(-6) of nickel. We discuss the nickel stimulating effect for the start of DNA synthesis and the nickel penetration into cells.

Cell Nucleus↗
PubMed2002

Nickel accumulation and nickel oxalate precipitation by Aspergillus niger.

A strain of Aspergillus niger isolated from a metal-contaminated soil was able to grow in the presence of cadmium, chromium, cobalt, copper, and unusually high levels of nickel on solid (8.0 mM) and in liquid (6.5 mM) media. This fungus removed >98% of the nickel from liquid medium after 100 h of growth but did not remove the other metals, as determined by inductively coupled plasma spectroscopy. Experiments with non-growing, live fungal biomass showed that nickel removal was not due to biosorption alone, as little nickel was bound to the biomass at the pH values tested. Furthermore, when the protonophore carbonyl cyanide p-(trifluoremetoxy) phenyl hydrazone (FCCP) was added to the actively growing fungus nickel removal was inhibited, supporting the hypothesis that energy metabolism is essential for metal removal. Analytical electron microscopy of thin-sectioned fungal biomass revealed that metal removed from the broth was localized in the form of small rectangular crystals associated with the cell walls and also inside the cell. X-ray and electron diffraction analysis showed that these crystals were nickel oxalate dihydrate.

Aspergillus niger↗
PubMed1991

Nickel-induced renal lipid peroxidation in different strains of mice: concurrence with nickel effect on antioxidant defense systems.

Lipid peroxidation (LPO) and active oxygen-detoxifying enzymes, catalase (CAT), glutathione peroxidase (GSH-Px), and superoxide dismutase (SOD), as well as glutathione (GSH) and some related enzymes, glutathione-S-transferase (GST) and glutathione reductase (GSSG-R) were assayed in kidneys of BALB/cAnNCr (BALB/c), C3H/HeNCr-MTV- (C3H), B6C3F1, and C57BL/6NCr (C57BL) mice 3-48 h after a single intraperitoneal injection of 170 mumol nickel (II) acetate (NiAcet)/kg body wt. In control mice that received 340 mumol sodium acetate/kg, the levels of enzymes and GSH did not significantly vary in time but were different in various strains. The basal activities of CAT and SOD in in the controls were highest in BALB/c and lowest in C57BL mice (1.8:1.0 and 1.4:1.0 respectively) in contrast to that of GSH-Px which was highest in B6CF1 and lowest in BALB/c (1.3:1.0; P less than 0.05). The strain ranking of control concentrations of renal GSH was B6C3F1 greater than C3H greater than or equal to C57BL greater than BALB/c (2.8:2.4:2.3:1.0), and that of GSSG-R was C3H greater than or equal to BALB/c greater than B6C3F1 greater than or equal to C57BL [corrected] (1.5:1.4:1.1:1.0). The basal activity of renal GST in control mice was 25% lower in C3H than in any of the other 3 strains. The renal LPO levels in the control mice did not vary among strains. Nickel treatment transiently increased renal LPO levels in the control mice did not vary among strains. Nickel treatment transiently increased renal LPO in the BALB/c mice by 100%, in B6C3F1 by 30%, and in C57BL by 20% (P less than 0.05), with no significant effect in C3H mice. Thus, the magnitude of nickel-induced renal LPO was greatest in the strain that is lowest in GSH and GSH-Px, but not in CAT and SOD. Nickel effects on GSH and the enzymes were time-dependent and included transient inhibition or enhancement of different proportions with no apparent strain- and/or base level-related patterns, or concurrence with LPO. The results emphasize the importance of GSH and GSH-Px for preventing nickel-induced oxidative cell damage.

Animals↗
PubMed1978

Repeated failure of nickel-containing prosthetic heart valves in a patient allergic to nickel.

Life-threatening peri-prosthetic incompetence developed with two successive nickel-containing mitral-valve prostheses in a patient allergic to nickel. Neither prosthesis had been incorporated satisfactorily. Her present nickel-free prosthesis seems to be satisfactory 22 months after insertion. Since allergy to nickel may have been involved in the failure of these prostheses, it is recommended that nickel-sensitive patients should be given nickel-free prostheses.

Female↗
PubMed2003

Nickel removal from nickel plating waste water using a biologically active moving-bed sand filter.

Efficient removal of dissolved nickel was observed in a biologically active moving-bed 'MERESAFIN' sand filter treating rinsing water from an electroless nickel plating plant. Although nickel is fully soluble in this waste water, its passage through the sand filter promoted rapid removal of approximately 1 mg Ni/l. The speciation of Ni in the waste water was modelled; the most probable precipitates forming under the conditions in the filter were predicted using PHREEQC. Analyses of the Ni-containing biosludge using chemical, electron microscopical and X-ray spectroscopic techniques confirmed crystallisation of nickel phosphate as arupite (Ni3(PO4)2 x 8H2O), together with hydroxyapatite within the bacterial biofilm on the filter sand grains. Biosorption contributed less than 1% of the overall sequestered nickel. Metabolising bacteria are essential for the process; the definitive role of specific components of the mixed population is undefined but the increase in pH promoted by metabolic activity of some microbial components is likely to promote nickel desolubilisation by others.

Biofilms↗
PubMed1983

Carcinogenicity of nickel(II)hydroxides and nickel(II)sulfate in Wistar rats and its relation to the in vitro dissolution rates.

During a two year experiment, local sarcomas developed in 5 of 20 rats injected intramuscularly (i.m.) with 120 mumol of nickel(II)hydroxide air-dried gel (DRY), in 3 of 20 rats similarly injected with 120 mumol of crystalline industrial nickel(II)hydroxide (CRST) and in 16 of 20 rats injected i.m. with 40 mumol of nickel subsulfide (Ni3S2). I.m. injections of 120 mumol of freshly precipitated colloidal nickel(II)hydroxide (COL) did not produce tumors. No tumors were found in animals which had been injected i.m. with 15 doses of 4.4 mumol of nickel(II)sulfate (NiSO4) (total dose equalled 66 mumol/rat) or sodium sulfate (Na2SO4; controls). Statistical analysis ranked the tumor yields as follows: Ni3S2 greater than CRST = DRY greater than COL = NiSO4. The in vitro solubilization rates of the hydroxides and nickel subsulfide in human blood serum, artificial lung fluid and ammonium acetate buffer, pH 7.4, were found to increase in the following order: Ni3S2 less than CRST less than DRY less than COL. Hence, an inverse relation may exist between the tumor yield and rate of solubilization of the compounds tested.

Animals↗
PubMed2005

Can lung cancer risk among nickel refinery workers be explained by occupational exposures other than nickel?

BACKGROUND: Exposures in nickel refineries represent complex chemical mixtures, but only the effect of nickel has been evaluated quantitatively in epidemiologic studies of nickel workers. METHODS: For a Norwegian refinery, time- and department-specific exposure estimates were developed for arsenic, sulfuric acid mists, and cobalt in air on the basis of personal measurements and chemical data on raw materials and process intermediates. Exposure to asbestos, as well as employment in high-risk occupations outside the refinery, were assessed. We conducted a case-control study nested in a cohort of refinery workers, with 213 cases (diagnosed 1952-1995) and 525 age-matched controls. We analyzed lung cancer risk, adjusted for smoking, by cumulative exposure and duration of work. RESULTS: There was a substantial association between cumulative exposure to water-soluble nickel and lung cancer risk. Weaker effects were suggested for exposure to arsenic at the refinery and for occupational exposures outside the refinery for 15 years or more. No detectable excess risk was found for refinery exposure to asbestos or sulfuric acid mists, and no dose-related increase in risk was seen from cobalt. CONCLUSIONS: Exposure to water-soluble nickel remained the most likely explanation for the excess lung cancer risk in the cohort. Other occupational exposures did not confound the strong dose-related effect of nickel to any appreciable degree.

Air Pollution, Indoor↗
PubMed1990

The discrimination between nickel-sensitive and non-nickel-sensitive subjects by an in vitro lymphocyte transformation test.

A lymphocyte transformation test (LTT) was able to distinguish between nickel-sensitive subjects and non-nickel-sensitive controls. Sixty-one out of 66 (92%) nickel-sensitive subjects had positive stimulation indices in 6- and/or 7-day assays using 5 micrograms/ml of nickel sulphate, whereas none of the 43 controls gave positive results. Stimulation indices were not enhanced by the patch testing of subjects to nickel before performing the LTT. A weak correlation was seen between the results of the LTT and the macroscopic degree of patch-test reactivity. The concentration of nickel sulphate used (5 micrograms/ml) did not have a significant non-specific mitogenic effect.

Adult↗
PubMed1990

Nickel-sensitive patients with vesicular hand eczema: oral challenge with a diet naturally high in nickel.

Oral challenge with nickel sulphate indicated that vesicular hand eczema in nickel-sensitive patients may be exacerbated by nickel occurring naturally in the diet. Twelve nickel-sensitive females with vesicular hand eczema were challenged with a supplementary high nickel diet for 4 days in a single-blind cross-over study. The diet had about five times the average nickel content of the daily Danish diet. An aggravation of the hand eczema was observed in six out of 12 patients on day 4 after the start of the challenge. By day II, the hand eczema was worse in 10 out of 12 patients, and remained unchanged in two.

Adult↗
PubMed1988

Epidemiology of nickel allergy: results of a follow-up analysis of patients with positive patch tests to nickel.

In a previous paper, we reported on nickel sensitivity in 2400 consecutive patients in 5 countries. 3 years later, we reassessed 104 of the 157 nickel-positive patients of this former study and found 13 now to be negative to nickel sulphate. Nearly all the others can no longer tolerate nickel contact. 68 patients were free from nickel dermatitis, 16 showed a very mild eczema or dyshidrosis, and 13 were suffering from chronic hand dermatitis. 42 of 104 patients had changed their occupation, 36 successfully, with clearance of skin lesions. Rehabilitation by avoidance of nickel-containing costume jewelry, wrist-watches and clothing buckles, and by change of occupation, is possible and necessary.

Dermatitis, Contact↗
PubMed1996

Long-lasting allergic patch test reactions to nickel sulfate: analysis by nickel quantification and immunocytochemistry.

We previously showed the median duration of positive patch test reactions to nickel sulfate (5% pet.) was 9 days, and defined as long-lasting (LLAPTR) the 14.3% of reactions that persisted for 17 days or longer. The pathomechanisms of LLAPTR are unclear, but may involve either localized antigen persistence or abnormal downregulation of the cellular immune response. In this study, we compared (a) the nickel concentration and (b) the immunocytochemical nature of the local immune reaction, between biopsies from LLAPTR (n = 8) and normally resolving allergic patch test reactions (NRAPTR) (n = 8) to nickel sulfate. The concentration of nickel in LLAPTR (median 0.56 microgram/g, range 0.25-3.87 micrograms/g, mean 0.83 microgram/g, 95% CI 0.35-1.31) and NRAPTR (median 0.58 microgram/g, range 0.2-1.85 micrograms/g, mean 0.88 microgram/g, 95% CI 0.02-1.74) was similar. Activated T lymphocytes, expressing surface IL-2 receptor, HLA DR, DR alpha 1, DP, DQ, and CD2 > CD8 > CD4 antigens, were seen throughout the dermis and occasionally infiltrating the suprabasal layer of the epidermis in all biopsies. CD1 and HLA DR, DR alpha 1, DP, and DQ-expressing Langerhans cells were present throughout the epidermis and occasionally seen in the papillary dermis. HLA DR, DR alpha 1, DP, and DQ antigen expression were also seen on the surface of non-dendritic cells in the epidermis (probably either keratinocytes or T lymphocytes) and vascular endothelial cells in the papillary dermis. There were no significant qualitative or quantitative differences in the immunocytochemical nature of the localized immune reaction between LLAPTR and NRAPTR. These findings suggest that the pathomechanism of LLAPTR to nickel sulfate is unlikely to be explained simply on the basis of nickel concentration or the nature of the localized immune reaction at the patch test site.

Adult↗
PubMed1982

Nickel allergy and nickel-containing dental alloys.

Test pieces from five cobalt-chromium casting alloys intended for use in removable partial dentures were attached to the skin of 10 women with known allergy to nickel. Patch tests were also performed with nickel and cobalt salts. Nine of the 10 women showed clear-cut or strong patch test reactions to the alloy with 7% nickel, one patient also to one of the other alloys (less than 1% nickel). In five patients with contact allergy reactions to both nickel and cobalt salts mild or marked responses to some of the other alloys were observed. Corresponding observations were made in three out of the five patients with contact allergy reactions to nickel salt but not cobalt salt.

Adult↗
PubMed1988

Nickel affects expression of the nickel-containing hydrogenase of Alcaligenes latus.

The effects of nickel on the expression of hydrogenase in the hydrogen-oxidizing bacterium Alcaligenes latus were studied. In the absence of added nickel, both hydrogenase activity, measured as O2-dependent H2 uptake, and hydrogenase protein, measured in a Western immunoblot, were very low compared with the levels in cells induced for hydrogenase in the presence of nickel. Hydrogenase activity and protein levels were dependent on the added nickel concentration and were saturated at 30 nM added Ni2+. The amount of hydrogenase protein in a culture at a given nickel concentration was calculated from the H2 uptake activity of the culture at that Ni2+ concentration. Between 0 and 30 nM added Ni2+, the amount of hydrogenase protein (in nanomoles) was stoichiometric with the amount of added Ni2+. Thus, all of the added Ni2+ could be accounted for in hydrogenase. Between 0 and 50 nM added Ni2+, all the Ni present in the cultures was associated with the cells after 12 h; above 50 nM added Ni2+, some Ni remained in the medium. No other divalent metal cations tested were able to substitute for Ni2+ in the formation of active hydrogenase. We suggest two possible mechanisms for the regulation of hydrogenase activity and protein levels by nickel.

Alcaligenes↗
PubMed2002

Distinct mechanisms of oxidative DNA damage induced by carcinogenic nickel subsulfide and nickel oxides.

The U.S. National Toxicology Program has shown clear evidence of carcinogenicity of nickel subsulfide (Ni(3)S(2)) and some evidence of carcinogenicity of NiO (green) in rats. In the present study, DNA damage in cultured cells and in lungs of rats induced by nickel compounds was investigated to clarify the mechanism of nickel carcinogenesis. In cultured HeLa cells, Ni(3)S(2) induced a significant increase in 8-hydroxydeoxyguanosine (8-OH-dG) formation, whereas NiO (black), NiO (green), and NiSO(4) did not. On the other hand, in rats, intratracheal instillation of all these nickel compounds significantly increased 8-OH-dG content in the lungs. The disparities in DNA damage between cultured cells and animals could be accounted for by two different mechanisms for nickel-induced oxidative DNA damage in lungs of rats. One is direct oxidative DNA damage: Ni(II) enters the cells and then reacts with endogenous and/or nickel sulfide-produced hydrogen peroxide (H(2)O(2)) to give reactive oxygen species that cause DNA damage. This mechanism is supported by oxidative damage to isolated DNA treated with Ni(II) and H(2)O(2). The other mechanism is indirect oxidative DNA damage due to inflammation. This double mechanism for DNA damage may explain the relatively high carcinogenic risk associated with Ni(3)S(2).

Animals↗