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PubMed1981

Inhibition of in vitro nickel sulfate reaction by anti-HLA-D/DR antisera. Lack of demonstrable suppressor cells in peripheral blood in nickel unresponsiveness in man.

A nickel sulfate induced lymphocyte blast transformation reaction in vitro was specifically inhibited by anti-HLA-D/DR antisera, which indicates the requirement of HLA-D/DR antigens in cellular cooperation. Macrophages are effective antigen presenting cells in the in vitro nickel reaction and this step could be the site of an HLA-antigen function in the recognition of "self." It was shown that macrophages of an HLA identical, healthy sibling could offer proper "help" to macrophage-depleted lymphocytes of the nickel allergic subject in evoking a nickel reaction. Thus, in this respect, the function of macrophages in nickel allergy is not different from that in a nickel-unresponsive state. The nickel unresponsiveness in healthy subjects is probably not due to specific suppressor cells because HLA identical lymphocytes from the healthy siblings could not suppress the nickel induced blast transformation of the nickel allergic siblings. This suggests that a deletion of sensitized clones in the periphery is the more probable mechanism of unresponsiveness in healthy subjects.

Female↗
PubMed2005

Cross-reactivity between nickel and palladium demonstrated by systemic administration of nickel.

Concomitant patch test reactions to nickel and palladium have frequently been reported in patients undergoing investigation because of suspected allergic contact dermatitis. Theoretically, these reactions can be explained by multiple, concomitant, simultaneous sensitization as well as cross-sensitization. We studied whether concomitant reactions to nickel and palladium could represent cross-sensitization in females hypersensitive to combinations of nickel, palladium and cobalt. Females were patch tested with serial dilutions of nickel sulfate, cobalt chloride and palladium chloride on the upper back. 1 month later, when the patch test reactions were gone, the patients were randomized into 2 groups that were challenged orally with either nickel or placebo. 1 day later, the areas of previous positive patch test reactions were read in a blind way looking for flare-up reactions. Nickel provocation but not placebo yielded flare-up reactions on sites previously tested with nickel (P = 0.012) and palladium (P = 0.006), but were also observed on sites previously tested with cobalt, even though this was not statistically significant. Flare-up reactions of previous patch test reactions to nickel and palladium after oral challenge with nickel speak in favour of a cross-reactivity mechanism.

Administration, Oral↗
PubMed1991

Nickel concentrations in fingernails as a measure of occupational exposure to nickel.

The nickel concentration in fingernails from 2 groups of people occupationally exposed to nickel was determined. In one group, comprising 83 persons moderately exposed to nickel, the mean +/- standard deviation (SD) was 29.2 micrograms/g +/- 56.7 micrograms/g and the median 13.8 micrograms/g (range 0.926-396 micrograms/g). In the other group, comprising 51 persons heavily exposed to nickel, the mean +/- SD was 123 micrograms/g +/- 289 micrograms/g and the median 29.9 micrograms/g (range 1.95-1770 micrograms/g). Both levels were significantly different from the normal nickel concentration in nails (p less than 0.001). The difference between the 2 levels was also significant (p less than 0.001). No correlation between the nickel concentration in fingernails and the duration of exposure could be demonstrated. It was concluded that the higher the nickel level in the fingernails, the greater is the possibility that the person is occupationally exposed to nickel. Nail analysis is suggested as a measure of occupational exposure to nickel.

Adolescent↗
PubMed2002

Conserved low-affinity nickel-binding amino acids are essential for the function of the nickel permease NixA of Helicobacter pylori.

Nickel acquisition is necessary for urease activity, a major virulence factor of the human gastric pathogen Helicobacter pylori. The nickel permease NixA of H. pylori is a member of the single-component nickel-cobalt transporter family. To identify functionally relevant amino acids of NixA, single-site exchanges were introduced into NixA via PCR-based mutagenesis. This study investigated one of the recognition motifs for this family in transmembrane segment III and other conserved amino acids, mostly with possible nickel-binding capacities. The mutant alleles were expressed in Escherichia coli, and activity of the altered permeases was analyzed by measuring nickel accumulation and urease activity. Expression was checked by immunoblotting after sodium dodecyl sulfate-polyacrylamide gel electrophoresis with a NixA-specific antibody. Replacement of Phe-75 and His-79-both part of the characteristic sequence motif-and of Asn-127, Thr-195, and Ser-197 with alanine abolished nickel uptake in the E. coli system. The results were unchanged if these amino acids were replaced with residues more similar to the original amino acid. The phenotype of the null mutants was independent of the culture medium. Mutation of Val-82, Tyr-242, Thr-260, His-181, and His-15 strongly affected uptake activity under nickel limitation on complex Luria-Bertani medium but had little effect in minimal medium. Eight other conserved amino acids (Ser-80, Ser-81, Phe-119, Trp-180, Tyr-183, Trp-244, Pro-249, and Asn-256) were found to be dispensable for the function of NixA. These results show that atypical nickel-binding amino acids play an important function in nickel uptake and that most of the essential amino acids are clustered in conserved motifs.

Amino Acid Motifs↗
PubMed1996

Exposure to nickel compounds and smoking in relation to incidence of lung and nasal cancer among nickel refinery workers.

OBJECTIVES: To investigate the relation between occupational hazards among nickel refinery workers and their exposure to different forms of nickel over time and the interaction between smoking and total exposure to nickel. METHODS: The cohort consisted of 379 workers with first employment 1916-40 and at least three years of employment and 4385 workers with at least one year of employment 1946-83. Data on smoking (ever or never) were available for almost 95% of the cohort. Two analyses were used, indirect standardisation from observed and expected numbers and Poisson regression. RESULTS: During the follow up 1953-93, 203 new cases of lung cancer were observed v 68 expected (standardised incidence ratio (SIR) 3.0, 95% confidence interval (95% CI) 2.6-3.4) and 32 cases of nasal cancer were observed v 1.8 expected (SIR 18.0, 95% CI 12-25). The Poisson regression analysis showed an excess risk of lung cancer in association with exposure to soluble forms of nickel, with a threefold increase in relative risk (RR) (P < 0.001) and a multiplicative effect of smoking and exposure to nickel. The RRs were 1.1 (95% CI 0.2-5.1) for exposed workers who had never smoked and 5.1 (95% CI 1.3-20.5) for exposed workers who smoked. CONCLUSION: It is not possible to state with certainty which specific nickel compounds are carcinogenic, but a significant excess risk was found for workers exposed to soluble nickel alone or in combination with other forms of nickel. The present study suggests a multiplicative effect of smoking and nickel exposure.

Follow-Up Studies↗
PubMed1980

Jack been urease (EC 3.5.1.5). II. The relationship between nickel, enzymatic activity, and the "abnormal" ultraviolet spectrum. The nickel content of jack beans.

At low pH, EDTA promotes the loss of the tightly bound nickel ions from jack bean urease. The specific activity of soluble enzyme after partial EDTA-promoted inactivation is a linear function of the nickel content. The results are consistent with the presence of 2.0 nickel ions per 97 000-dalton subunit in pure urease. The time scale for loss of enzymatic activity and nickel under these conditions is similar to that for loss of the "abnormal" tail absorption in the ultraviolet and visible absorption spectrum of urease (including the shoulder at approximately 420 nm). This indicates that nickel in urease is essential for enzymatic activity and establishes that the metal ions are in part responsible for the tail absorption in the ultraviolet spectrum of urease. After partial inactivation in the presence of EDTA either at low pH or in 2.5 M guanidinium chloride at neutral pH, urease did not regain activity in the presence of Ni2+. As yet apourease has not been produced reversibly. Jack bean seeds grown hydroponically without added nickel were low in both urease activity and nickel (10 and 6%, respectively, of parent seeds). Several other metal ions were readily available. This result suggests that metal ions other than nickel cannot substitute for nickel in the formation of normally active urease.

Diacetyl↗
PubMed2000

Early DNA synthesis and cytokine expression in the nickel activation of peripheral blood mononuclear cells in nickel-allergic subjects.

BACKGROUND AND OBJECTIVE: Nickel sulphate stimulates the proliferation of lymphocytes in nickel-allergic subjects. However, nickel-induced stimulation of lymphocytes from control persons without clinical symptoms of nickel allergy has also been reported. The aim of the present study was to correlate T cell activity, measured by DNA synthesis and the expression of Th1 [interleukin (IL)-2, tumour necrosis factor (TNF)-beta and interferon (IFN)-gamma] and Th2 (IL-4) cytokines, in short-term (up to 72 h) culture of nickel-stimulated peripheral blood mononuclear cells (PBMC) from nickel-allergic patients compared to control subjects. METHODS: DNA synthesis was measured by the incorporation of [methyl-(3)H]thymidine. The production of IL-2, TNF-beta, IFN-gamma and IL-4 was measured in the supernatants of the cultures by ELISA. In situ hybridization for mRNA was performed using oligonucleotide probes for IL-4, IFN-gamma and TNF-beta in cell smears. RESULTS: Already after 24 h and proceeding through the remaining culture period, there was a statistically significant (p<0.001) difference in the concentrations of IL-2 between patients and controls. There was a significant (p<0.01) difference in DNA synthesis (stimulation index) between the patients and control subjects at 72 h, and also at the same time a difference in the concentrations of TNF-beta (p<0.05) and IL-4 (p<0.01). In the in situ hybridization study, TNF-beta was found to be the only one of the studied cytokines that differed between the nickel-allergic and control subjects, this difference being most evident at 72 h (p<0.01). CONCLUSIONS: Our results indicate a difference between nickel-allergic and non-allergic subjects in the synthesis of DNA and production of cytokines when PBMC are stimulated by nickel sulphate, and IL-2 may be regarded as a critical and early-occurring cytokine.

Adult↗
PubMed1990

Nickel in nails, hair and plasma from nickel-hypersensitive women.

The concentrations of nickel in finger-nails, toe-nails, hair and plasma from 71 nickel-hypersensitive women and 20 non-hypersensitive women were determined. Nickel concentrations in finger-nails were significantly higher than in toe-nails in both the nickel-hypersensitive group and the control group. Nickel-sensitive women had significantly higher levels of nickel in toe-nails, hair and plasma than had control subjects, whereas there was no significant difference in nickel concentration in finger-nails between the two groups. No correlation could be demonstrated between nickel levels in any combination of nails, hair and plasma in the nickel-hypersensitive or in the control group.

Adolescent↗
PubMedDate not supplied

Urinary and fecal elimination of nickel in relation to air-borne nickel in a battery factory.

Nickel in urine and in air from the breathing zone of 18 male workers in a battery factory was determined weekly during 11 consecutive weeks. The study started immediately following three weeks of Christmas vacation. The nickel levels in air varied but did not increase with time. The average urinary excretion of nickel showed an increase during the first weeks, after which a steady state seemed to have been reached. There was a considerable individual variation in both exposure levels and urine nickel levels. However, a correlation between the averages of nickel in air and urine could be demonstrated on a group basis. In a second study, during one week, measurements of nickel in air and feces were made on 15 of the workers. A significant correlation was found between nickel in air and fecal nickel. Smoking habits did not seem to influence neither urinary nor fecal nickel concentrations.

Adult↗
PubMed1978

Lymphocyte transformation induced by nickel sulphate: an in vitro study of subjects with and without a positive nickel patch test.

Lymphocytes from 8 patients with contact dermatitis and a positive nickel patch test, 7 patients with contact dermatitis due to other factors and with a negative nickel patch test, and 9 other subjects, 7 of whom suffered from other dermatological disorders, were tested with the lymphocyte transformation test (LTT), using nickel sulphate in various concentrations. All execpt one of the nickel allergics showed a significant response to nickel, whereas the controls showed borderline (3 patients) or no response (12 patients). These observations confirm previous findings indicating that nickel hypersensitivity can be diagnosed in vitro. This may be of importance in cases of acute contact dermatitis where patch testing is undesirable. Some individuals with a negative nickel patch test responded significantly though weakly to nickel in the LTT, indicating that apart from acting as a specific antigen (hapten?) nickel sulphate may also have weak non-specific mitogenic properties.

Allergens↗
PubMed2003

Porous titanium-nickel for intervertebral fusion in a sheep model: part 2. Surface analysis and nickel release assessment.

Porous titanium-nickel (PTN) devices represent an alternative to traditional cage implants. PTN materials possess an interconnecting network of pores with capillarity properties that may promote bone ingrowth, long-term fixation, and intervertebral fusion without the need for bone grafting. However, their considerable surface area and nickel content may elicit concerns over sensitization potential. Therefore, PTN surface corrosion and nickel release resistance must be carefully studied. To evaluate this possibility, a PTN interbody fusion device (IFD) was compared to a conventional nonporous cage made of TiAlV, a well-known biocompatible biomaterial, in a sheep model. PTN and TiAlV IFDs were inserted at two non-contiguous lumbar sites for 3, 6, and 12 months postsurgery. Their surface was then evaluated by scanning electron microscopy (SEM) combined with backscattered electron analysis (BSE). No evidence of surface corrosion was observed either pre- or postimplantation, regardless of device type. Dosage of nickel ions was also performed with the use of inductively coupled plasma-mass spectrometry (ICP-MS). Blood nickel levels were observed to be within acceptable levels at all postinstrumentation times. Nickel content in PTN-adjacent tissue, as well as in detoxification and remote organs, was equivalent both in PTN-treated and control sheep. Therefore, porous titanium-nickel demonstrated resistance to both in vivo surface corrosion and nickel ion release and compared very well with a conventional titanium implant in the course of a 12-month sheep study.

Alloys↗
PubMed1999

Nickel-induced activation of T cells in individuals with negative patch test to nickel sulphate.

Contact hypersensitivity to nickel is the most common form of allergic contact dermatitis. To gain insight into the induction of this frequent disease, T cell reactivity towards nickel was investigated in "nonallergic" individuals defined as those with no skin manifestations and a negative patch test towards NiSO4. Surprisingly, we found that nickel induced proliferation of peripheral blood mononuclear cells (PBMC) from 16 of 18 adult individuals tested. This activation was specific, and no stimulation of PBMC was observed using control stimulants at equimolar concentrations. Furthermore, the NiSO4-induced activation required the presence of professional antigen-presenting cells. To describe the functional capacity of the nickel-inducible T cells, cytokine release was investigated in both nickel-allergic and nonallergic individuals. The T cells from both groups released interferon-gamma but no interleukin-4 upon stimulation with nickel, suggesting that the functional capacities of these cell populations were similar in nickel-allergic and nonallergic individuals. Thus, at this level, no qualitative differences could be demonstrated between T cells obtained from nickel-allergic and nonallergic individuals.

Adult↗
PubMed2006

Urinary elimination of nickel and cobalt in relation to airborne nickel and cobalt exposures in a battery plant.

OBJECTIVE: To estimate the relationship between Ni concentrations in the ambient air and in the urine, at a battery plant using nickel hydroxide. METHODS: Workers occupationally exposed to a mixture of nickel hydroxide, metallic cobalt and cobalt oxyhydroxide dust were studied during two consecutive workdays. Air levels of Ni and Co in total dust were determined by personal sampling in the breathing zone. Both metals in air were sampled by Teflon binder filters and analyzed by inductively coupled plasma absorption emission spectrophotometry. Urine was collected from 16 workers immediately before and after the work shift. Urinary Ni and Co concentrations were measured by electrothermal atomic absorption spectrometry. RESULTS: A poor correlation was seen between Co in the air and in post-shift urine (r = 0.491; P < 0.01), and no correlation was found between Ni in the air and in post-shift urine (r = 0.272; P = 0.15), probably due to the use of respiratory protection. The subjects were exposed to higher levels of Ni than Co (Ni (mg/m(3)) = -0.02 + 7.41 Co (mg/m(3)), r = 0.979, P < 0.0001). Thus, exposure to Co at 0.1 mg/m(3) should produce a Ni level of 0.7 mg/m(3). According to section XIII of the German list of MAK and BAT Values, a relationship between exposure to Co and urinary Co excretion, Co (microg/l) = 600 Co (mg/m(3)), has been established and the relationship between soluble or insoluble Ni salts in the air and Ni in urine was as follows: Ni (microg/l) = 10 + 600 Ni (mg/m(3)) or Ni (microg/l) = 7.5 + 75 Ni (mg/m(3)). Assuming nickel hydroxide to be soluble and to be insoluble, the Ni concentrations corresponding to Ni exposure at 0.7 mg/m(3) were calculated as 430 and 60 microg Ni/l, respectively. Similarly, exposure to Co at 0.1 mg/m(3) should result in Co urinary concentrations of 60 microg Co/l. On the other hand, a good correlation was found between Co and Ni in post-shift urine (Ni (microg/l) = 9.9 + 0.343 Co (microg/l), r = 0.833, P < 0.0001). On the basis of this relationship, the corresponding value found in our study was 0.343 x 60 microg Co/l + 9.9 = 30.5 microg Ni/l. This value was close to that calculated by the equation for a group of insoluble compounds, but about 14 times lower than that calculated by the equation for a group of soluble compounds. CONCLUSIONS: Our results suggest that exposure to nickel hydroxide yields lower urine nickel concentrations than the very soluble nickel salts, and that the grouping of nickel hydroxide might be reevaluated. Therefore, to evaluate conclusively the relationship between nickel hydroxide dust in the air and Ni in post-shift urine, further studies are necessary.

Adult↗
PubMed1990

Nickel induced lipid peroxidation in the rat: correlation with nickel effect on antioxidant defense systems.

Lipid peroxidation (LPO) and alterations in cellular systems protecting against oxidative damage were determined in the liver, kidney and skeletal muscle of male F344/NCr rats, 1 h to 3 days after a single intraperitoneal (i.p.) injection of 107 mumol nickel(II)acetate per kg body weight. At 3 h, when tissue nickel concentrations were highest, the following significant (at least, P less than 0.05) effects were observed: in kidney, increased LPO (by 43%), increased renal iron (by 24%), decreased catalase (CAT) and glutathione peroxidase (GSH-Px) activities (both by 15%), decreased glutathione (GSH) concentration (by 20%), decreased glutathione reductase (GSSG-R) activity (by 10%), and increased glutathione-S-transferase (GST) activity (by 44%); the activity of superoxide dismutase (SOD) and gamma-glutamyl transferase (GGT), as well as copper concentration, were not affected. In the liver, nickel effects included increased LPO (by 30%), decreased CAT and GSH-Px activities (both by 15%), decreased GSH level (by 33%), decreased GSSG-R activity (by 10%) and decreased GST activity (by 35%); SOD, GGT, copper, and iron remained unchanged. In muscle, nickel treatment decreased copper content (by 43%) and the SOD activity (by 30%) with no effects on other parameters. In blood, nickel had no effect on CAT and GSH-Px, but increased the activities of alanine-(ALT) and aspartate-(AST) transaminases to 330% and 240% of the background level, respectively. In conclusion, nickel treatment caused profound cell damage as indicated by increased LPO in liver and kidney and leakage of intracellular enzymes, ALT and AST to the blood. The time pattern of the resulting renal and hepatic LPO indicated a possible contribution to its magnitude from an increased concentration of nickel and concurrent inhibition of CAT, GSH-Px and GSSG-R, but not from increased iron or copper levels. The oxidative damage expressed as LPO was highest in the kidney and lowest in the muscle, which concurs with the corresponding ranking of nickel uptake by these tissues.

Alanine Transaminase↗
PubMedDate not supplied

Human nickel exposure in an area polluted by nickel refining: the Sør-Varanger study.

Sør-Varanger municipality in northern Norway is located close to two Russian nickel refineries that cause nickel and sulfur dioxide pollution. To investigate individual nickel exposure and possible health effects from the pollution, the authors invited all adults who were 18-69 y of age to a health survey in 1994. Urine samples were collected from 3671 participants (participation rate = 59.4%), and nickel concentrations were determined for 902 of them. Mean and median nickel concentrations were 0.9 microg/l and 0.6 microg/l, respectively. Individuals who lived in the rural areas closest to the refineries had lower nickel concentrations than individuals who lived in the more urban areas. Independent risk factors for nickel concentrations in urine were (a) being an urban dweller and (b) living close to areas with high-density traffic. The authors concluded that nickel exposure attributable to air pollution from Russian refineries was of minor importance for people who lived in Sør-Varanger.

Adolescent↗