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PubMed1986

Nickel dermatitis: the reaction to oral nickel challenge.

Pompholyx in nickel-sensitive subjects can be induced by orally-administered nickel, but only by a high dose. Ingestion of 5.6 mg nickel consistently worsened the pompholyx, often with a mild toxic erythema or patch test site flare, but lower doses of nickel failed to excite reactions more frequently than did a placebo, in a double-blind study. The metabolism of nickel is complex and there was considerable variation between three normal individuals in their absorption and excretion of an orally-administered nickel load. Patients may show similar variability which could be of importance clinically, although in only one of five subjects with acute eczema was the serum nickel raised, and then only marginally. The exact role of dietary nickel in perpetuating the hand dermatitis of sensitive subjects remains unclear.

Administration, Oral↗
PubMed1992

Effects of nickel-chrome dental alloys used in dentistry on saliva and serum nickel levels, peripheral T-lymphocytes and some other blood parameters.

Epidemiological investigations have shown that nickel is a potent sensitivity producing agent. However, it is not known if intra-oral use of nickel-chrome alloys can cause any sensitization reaction. The purpose of this study was to determine if nickel-chrome alloys used in dentistry influence nickel levels in saliva and serum and whether there were associated changes of some blood parameters such as lymphocyte, T-lymphocyte, neutrophil, eosinophil, basophil and monocyte. The study was performed on 10 patients all of whom had no medical and dental history of using nickel containing drugs or restorations. Four unit fixed partial prostheses containing 22.97% nickel and 22.65% chrome were constructed and worn by the patients. Blood and unstimulated whole saliva samples were taken from the patients before insertion of the prostheses and then 1 month and 6 months post-insertion. Hematocrit determinations, total and differential leucocyte count, total T-lymphocyte counts and serum nickel concentrations were determined from the blood samples and salivary nickel concentrations from the saliva samples. It was found that there were no significant changes in circulating T-lymphocyte and monocyte population but a decrease was found in circulating eosinophil and an increase in circulating neutrophil and basophil populations.

Adult↗
PubMed1985

Patch testing for nickel allergy. The influence of the vehicle on the response rate to topical nickel sulphate.

A group of 43 patients with a clinical history of nickel allergy who exhibited an equivocal or no allergic reaction to a patch test at 48 h were further challenged using several different formulations of nickel sulphate. This experimental test battery comprised aqueous, dimethyl sulphoxide (DMSO) and propylene glycol (PG) solutions of nickel sulphate, and nickel sulphate incorporated into cetomacrogol cream and yellow soft paraffin (PMF). Although some of these vehicles were irritant, a formulation-dependent test response was observed, such that in terms of the number of responses per unit weight of nickel sulphate applied to the skin, the vehicles could be ranked: DMSO greater than PG greater than aqueous solution greater than cetomacrogol cream greater than PMF preparations. This ranking could be correlated with the relative ease with which nickel sulphate could be dialysed from each vehicle in vitro. This study demonstrates that for nickel sulphate, the vehicle can influence the outcome of patch testing apparently by modifying the quantity of nickel released into the skin for elicitation of the allergic response.

Dermatitis, Atopic↗
PubMed1993

Concentration threshold of non-occluded nickel exposure in nickel-sensitive individuals and controls with and without surfactant.

Most cases of primary nickel sensitization are caused by occluded exposure to nickel released from earrings, buttons, etc. Nickel-sensitive females are both domestically and occupationally exposed to trace amounts of nickel. The present study was designed to define the minimum eliciting threshold concentration of nickel exposure in previously nickel-sensitized individuals, after open application on normal forearm skin with and without surfactant. A dilution series of NiCl2, ranging from 0.1 to 4000 ppm nickel with and without 4% sodium lauryl sulfate, was applied to healthy volar forearm skin. None reacted with definite allergic reactions to 100 ppm and below. Follicular reactions were seen in the concentration range from 0.1-100 ppm in a few patients and 1 healthy control. The results are discussed in relation to consumer products containing 1-10 ppm nickel.

Dermatitis, Allergic Contact↗
PubMed1994

Nickel release from nickel-plated metals and stainless steels.

Nickel release from nickel-plated metals often induces allergic contact dermatitis, but, for nickel-containing stainless steels, the effect is not well-known. In this paper, AISI 304, 316L, 303 and 430 type stainless steels, nickel and nickel-plated materials were investigated. 4 tests were performed: patch tests, leaching experiments, dimethylglyoxime (DMG) spot tests and electrochemical tests. Patch tests showed that 96% of the patients were intolerant to Ni-plated samples, and 14% to a high-sulfur stainless steel (303), while nickel-containing stainless steels with a low sulfur content elicited no reactions. Leaching experiments confirmed the patch tests: in acidic artificial sweat, Ni-plated samples released about 100 micrograms/cm2/week of nickel, while low-sulfur stainless steels released less than 0.03 microgram/cm2/week of nickel, and AISI 303 about 1.5 micrograms/cm2/week. Attention is drawn to the irrelevance of the DMG spot test, which reveals Ni present in the metal bulk but not its dissolution rate. Electrochemical experiments showed that 304 and 316 grades remain passive in the environments tested, while Ni-plated steels and AISI 303 can suffer significant cation dissolution. Thus, Ni-containing 304 and 316 steels should not induce contact dermatitis, while 303 should be avoided. A reliable nitric acid spot test is proposed to distinguish this grade from other stainless steels.

Chemistry Techniques, Analytical↗
PubMed1995

Patch test results with serial dilutions of nickel sulfate (with and without detergent), palladium chloride, and nickel and palladium metal plates.

Clinical experience suggests the existence of different degrees of sensitivity in nickel-allergic patients. For quantification of this phenomenon, 462 consecutive patients with previously diagnosed or strongly suspected nickel allergy were tested with serial dilution patch tests with 5 ppm to 5% nickel sulfate in pet. (Ni), and 5 ppm to 1% nickel sulfate in pet. with 1% detergent (Ni/D). Additionally, nickel and palladium metal plates were tested in 103, and cobalt salts, dichromate and palladium chloride (PdCl2) in most patients. 332 patients reacted positively to Ni or Ni/D. The influence of a concomitantly administered detergent was not significant. A significant correlation was found between positive reactions to low concentrations of Ni (or Ni/D), i.e., 0.1% or less (N = 166), and concomitant reactions to nickel metal plates, cobalt salts and PdCl2 and a history of ear piercing with metal intolerance. The clinical relevance of reactions to PdCl2 is at present not clear. A subgroup of nickel-allergic patients with "high sensitivity" can be defined. In future studies further addressing the clinical relevance of high versus low sensitivity, patch testing with 0.01, 0.1, 1.0 and 5% nickel sulfate in pet. is recommended instead of routine tests with 5% only.

Adult↗
PubMed1998

An in vitro study of the use of chelating agents in cleaning nickel-contaminated human skin: an alternative approach to preventing nickel allergic contact dermatitis.

The purpose of this study was to investigate the efficacy of organic ligands in cleaning human skin contaminated with nickel. 4 ligands were investigated, 5-chloro-7-iodoquinolin-8-ol (either as HL(1) or NaL(1)), ethylenediaminetetraacetic acid (either as H4L(2) or Na2H2L(2)), sodium diethyldithiocarbamate (NaL(3)) and L-histidine (HL(4)). The cytotoxicity of these ligands was assessed using HaCaT cells (a transformed human keratinocyte cell line). The cytotoxicity order of the ligands was NaL(1) >Na2H2L(2)>NaL(3)>HL(4). An in vitro methodology for examining nickel removal from viable human skin was developed. This methodology was then used to compare the efficiency of the ligands in removing nickel from skin, both alone and in combination with soap solutions. HL(1) and NaL(3) were no more effective than control solutions in removing nickel over the pH range 2-11. In contrast, both H4L(2) and HL(4) removed between 74 and 87% (mean=82+/-3%) of nickel from human skin over the same pH range. Nickel removal from skin by sodium lauryl ethoxy sulfate (SLES, the active ingredient in most liquid skin cleansers) was independent of concentration and no more effective than phosphate-buffered saline (PBS). The amount of nickel removed by PBS solutions of Na2H2L(2) and HL(4) was significantly greater than the amount removed by SLES and was concentration dependent. An evaluation of nickel removal from skin by commercial solid soap, liquid soap and PBS, both alone and with added Na2H2L(2) or HL(4), was conducted. Commercial liquid soap with added HL(4) was more effective than the untreated soap. PBS with either added Na2H2L(2) or HL(4) was more effective than PBS alone.

Buffers↗
PubMed1998

Patch testing with nickel sulfate: comparison between 2 nickel sulfate preparations and 2 different test sites on the back.

Among patients routinely undergoing patch testing for suspected allergic contact dermatitis (ACD), nickel is the most frequently sensitizing hapten, with a clear predominance in the female population. However, some patients who report the appearance of dermatitis upon exposure to metal objects show negative patch test results to a nickel sulfate 5% pet. application. In some cases, a positive response to nickel can be observed simply by repeating the patch test. The objective of our study was to assess if, during routine patch testing, positive responses to nickel sulfate are missed owing to contingent problems, referring to application site, patch test execution or variations in skin reactivity. To this end, we applied 2 different patch test materials containing nickel sulfate 5% pet. to 3040 consecutive patients, undergoing patch testing for suspected allergic contact dermatitis, during the same session. The rôle of the test site was also investigated by applying the preparation on 2 different sites of the back in 30 patients. Of the whole, 612 patients (20%) showed positive patch test responses. The 2 nickel materials were almost equivalent: 78% of nickel-sensitive patients had positive reactions to both, whereas 11% showed a positive response to 1 preparation alone. No variations in patch test responses in relation to application site were observed. Our data show that false-negative patch test responses to nickel are frequent. The use of 2 different preparations during the same patch test session increases the response rate by 10%.

Adolescent↗
PubMed1995

Distribution of nickel in body fluids and organs of rats chronically exposed to nickel sulphate.

1. Male and female rats were given 100 mg Ni L-1 (as nickel sulphate) in drinking water for 6 months. 2. The feeding of nickel was associated with an increased concentration of nickel in body fluids and organs. The highest concentrations of nickel were found in the liver of both male and female rats. In male rats nickel levels decreased in the order: liver > kidney = whole blood = serum > testes > urine. In female rats the decreasing order was similar: liver > kidney = whole blood = serum = plasma > urine > ovaries. 3. No significant differences were found between nickel concentrations in organs (except ovaries), blood and urine of rats exposed for 3 months and those exposed for 6 months indicating the reaching of a steady state of nickel in the rat during long-term exposure. 4. The urinary excretion of the orally administered nickel was only 2% of absorbed dose (supposing 1% Ni absorption).

Administration, Oral↗
PubMed2006

Nickel release, a possible indicator for the duration of antiplatelet treatment, from a nickel cardiac device in vivo: a study in patients with atrial septal defects implanted with an Amplatzer occluder.

UNLABELLED: The present study was undertaken to evaluate the safety and release of nickel after implantation of a nickel device (Amplatzer occluder) in patients with an atrial septal defect (ASD) receiving antiplatelet therapy. METHODS: Blood and urine samples were obtained from 24 patients with ASD before occluder implantation (baseline) and during a 12-month post closure period. Antiplatelet drugs were administered for the initial 6-month period post implantation. The nickel content in the specimens was determined using electrothermal atomic absorption spectroscopy. The clinical, sonographic and magnetic resonance imaging follow-ups were carried out 1 week, 1 month, 6 months and 12 months post implantation. RESULTS: Mean baseline concentrations of nickel in serum and urine were within normal range with values of 0.6 +/- 0.2 microg/l and 3.1 +/- 1.2 microg/l, respectively. During the 6-week post closure period, the time needed for the formation of neointima on the surface of the graft, nickel levels in serum increased up to 5-fold (p < 0.01 versus baseline). Mean concentrations in serum and urine returned to baseline levels within 4-6 months post implantation. All patients showed satisfactory clinical improvements and there was no sonographic evidence of complications. CONCLUSIONS: The initial dissolution of nickel from the Amplatzer occluder is not a specific cardiovascular risk and is temporarily linked to the formation of the non-thrombogenic neointima on the surface of the graft. The antiplatelet drug regimen used (300 mg aspirin + 75 mg clopidogrel daily for 3 months in the initial phase and 100 mg aspirin daily for a further 3 months) appears to cover the period of neointima formation on the nickel device when nickel levels are significantly elevated. However, further studies in a larger number of patients and over a period greater than 12 months are needed to confirm the validity of these conclusions and to formulate definitive recommendations on the duration of the antiplatelet treatment.

Adult↗
PubMed1999

Nickel allergy in mice: enhanced sensitization capacity of nickel at higher oxidation states.

Attempts to induce contact hypersensitivity to nickel in mice using, e.g., Ni(II)Cl2 often failed. Here, we report that sensitization was achieved by injecting Ni(II)Cl2 in combination with either CFA or an irritant, such as SDS and PMA, or IL-12, or by administering nickel at higher oxidation states, i.e., Ni(III) and Ni(IV). Although Ni(II), given alone, was ineffective in T cell priming, it sufficed for eliciting recall responses in vivo and in vitro, suggesting that Ni(II) is able to provide an effective signal 1 for T cell activation, but is unable to provide an adequate signal 2 for priming. Immunization of mice with nickel-binding proteins pretreated with Ni(IV), but not with Ni(II), allowed them to generate nickel-specific CD4+ T cell hybridomas. Ni(II) sufficed for restimulation of T cell hybridomas; in this and other aspects as well, the hybridomas resembled the nickel-specific human T cell clones reported in the literature. Interestingly, restimulation of hybridomas did not require the original Ni(IV)-protein complex used for priming, suggesting either that the nickel ions underwent ligand exchange toward unknown self proteins or peptides or that nickel recognition by the TCR is carrier-independent. In conclusion, we found that Ni(III) and Ni(IV), but not Ni(II) alone, were able to sensitize naive T cells. Since both Ni(III) and Ni(IV) can be generated from Ni(II) by reactive oxygen species, released during inflammation, our findings might explain why in humans nickel contact dermatitis develops much more readily in irritated than in normal skin.

Animals↗
PubMed1987

Nickel-specific T lymphocyte clones derived from allergic nickel-contact dermatitis lesions in man: heterogeneity based on requirement of dendritic antigen-presenting cell subsets.

Inflammatory skin T cells were cloned in an antigen-independent way from lesions of patients with experimentally induced nickel-contact dermatitis. In three experiments 7-15% of the CD4+8- T lymphocyte clones (TLC) appeared to be specific for nickel in a proliferation assay. These proliferative response of nickel-specific TLC required the presence of antigen-presenting cells (APC) and were restricted by HLA class II molecules. All TLC recognized nickel presented by APC from epidermal skin. Remarkably, 5 out of 8 nickel-specific TLC exclusively recognized nickel when presented by these skin-specific APC whereas 3 out of these 8 clones could also recognize nickel presented by APC from peripheral blood. The critical APC within the fractions of epidermal cells and peripheral blood appeared to belong to the family of dendritic cells, i.e. Langerhans cells and circulating dendritic cells, respectively.

Antigen-Presenting Cells↗
PubMed2003

[Decrease in nickel sensitization in young patients--successful intervention through nickel exposure regulation? Results of IVDK, 1992-2001].

BACKGROUND: In the early 1990s, the prevalence of nickel contact allergy was high-almost 20% on a population level, and some 40% in contact dermatitis patients. Around that time, nickel exposure was starting to be regulated. PATIENTS/METHODS: Descriptive and bivariate analyses of patch test results of all patients tested with nickel sulfate (5% pet.) in the departments joining the Network of Departments of Dermatology (IVDK) 1992-2001 (n=82,991, women: 52,709; men: 30,282). The annual frequency of sensitization to nickel was analyzed in women and men in four age subgroups (<31/31 to <44/44 to 58= or >58). RESULTS: In young women less than 31 (n=13.909) the prevalence of contact allergy to nickel decreased significantly from 36.7% in 1992 to 25.8% in 2001. In young men in the same age group (n=7087), the prevalence dropped from 8.9% in 1992 to 5.2% in 2001. CONCLUSIONS: The observed decline indicates that measures to limit the release of nickel from costume jewelry helped reduce the prevalence of nickel allergy. In general term, allergen elimination or reduction is an effective primary prevention strategy which does not depend on individual behavior modifications.

Adolescent↗
PubMed1991

Nickel-induced lipid peroxidation in the liver of different strains of mice and its relation to nickel effects on antioxidant systems.

After a single intraperitoneal injection of 170 mumol nickel(II)acetate/kg body wt., the activity of hepatic catalase (CAT) decreased by 25-56% in a strain- and time-dependent manner, the most susceptible being C57BL/6NCr greater than C3H/HeNCr-MTV- greater than B6C3F1 greater than or equal to BALB/cAnNCr mice. The glutathione (GSH) levels in all 4 strains were inhibited by nickel with the C57BL/6NCr mice showing the biggest decrease (68%) followed by BALB/cAnNCr (46%) greater than or equal to B6C3F1 (42%) greater than C3H/HeNCr-MTV- (22%). The response of hepatic glutathione peroxidase (GSH-Px) to nickel was variable and included 30% enhancement in C3H/HeNCr-MTV- or lack of biologically significant effect (max. +/- 10% variations in time) in the remaining strains. The activity of glutathione reductase (GSSG-R) increased gradually by up to 30% (48 h post-injection) in B6C3F1 and C3H/HeNCr-MTV- mice or, transiently, by 15-18% (3 h), in C57BL/6NCr and BALB/cAnNCr mice. Also, in some strains, nickel significantly affected superoxide dismutase (SOD) (14-19% loss in C57BL/6NCr and B6C3F1 mice, respectively), and GSH-S-transferase (GST) (26% loss in C3H/HeNCr-MTV- mice). Lipid peroxidation (LPO) in the liver reached its highest value 24 h after nickel treatment in C57BL/6NCr (549% over the control) greater than or equal to BALB/cAnNCr (519%) greater than B6C3F1 (426%) much greater than C3H/HeNCr-MTV- (39%). In conclusion, the magnitude of nickel-induced LPO shows a reverse correlation with the extent and direction of nickel effect on GSH, GSH-Px and GSSG-R, but not on CAT, SOD or GST.

Animals↗
PubMed2006

Microbial nickel metalloregulation: NikRs for nickel ions.

Nickel is a required co-factor for several microbial enzymes; however, because of its potential toxicity, nickel import and homeostasis must be tightly controlled. Recent biophysical and biochemical studies have revealed that NikR proteins are a new type of metalloregulatory protein that utilize allostery and coordination geometry to sense nickel ions and regulate transcription of genes involved in nickel import and processing. Nickel import into bacteria occurs through either ABC-type transporters (NikABCDE) or HoxN type permeases (NixA). Recent structural evidence suggests that nickel is transported through NikABCDE as a metallophore (akin to a siderophore). Nickel storage is accomplished via the HPN protein, a histidine-rich protein similar to metallothionein.

Bacterial Proteins↗
PubMed1979

Nickel feeding in nickel-sensitive patients with hand eczema.

Ten women with vesicular hand eczema and delayed hypersensitivity to nickel were given 0.5 mg nickel supplements to their diets. The double-blind controlled supplements were given on Monday and Tuesday of each week for at least 1 month. The nickel supplement was lower than that used in previous studies, and only one subject had reproducible flaring of her vesicular dermatitis. We conclude that dietary restriction of nickel is not warranted based on nickel supplement studies, but nickel's role in hand eczema could be clarified by depleting nickel from body stores with chelating agents.

Acute Disease↗
PubMed2003

The protein complex composed of nickel-binding SrnQ and DNA binding motif-bearing SrnR of Streptomyces griseus represses sodF transcription in the presence of nickel.

Nickel-responsive transcriptional repression of sodF, which codes for iron- and zinc-containing superoxide dismutase of Streptomyces griseus, was mediated through an operator (-2 to +15) spanning over the 5' end (+1) of the transcript. Two open reading frames, SrnR (12,343 Da) and SrnQ (12,486 Da), with overlapping stop-start codons were identified downstream from sodF and found responsible for the repression of sodF. The deduced amino acid sequence of SrnR revealed a DNA binding motif and showed homology to the transcriptional regulators of ArsR family, whereas SrnQ did not show any similarity to any known proteins. When srnRQ DNA was maintained in trans in S. griseus on a multicopy plasmid, sodF transcription was highly repressed by nickel, but neither srnR nor srnQ alone showed the effect. Consistently, the sodF transcription of srnR-interrupted mutant was no longer repressed by nickel, which was complemented only with srnRQ DNA. Nickel-dependent binding of SrnR and SrnQ to the sodF operator DNA was observed only when the two proteins were provided together. The maximum protein-DNA interaction was shown when SrnR and SrnQ were present in one-to-one stoichiometric ratio. The two proteins appear to constitute an octamer composed of four subunits of each protein. SrnR directly interacted with SrnQ, and the protein interaction did not require nickel. The conformation of SrnQ was changed upon nickel binding, which was in the ratio of one Ni(2+) ion per protein molecule. A model is proposed in which SrnQ of the protein complex senses nickel and subsequently enhances the DNA binding activity of SrnR through the protein-protein interaction.

Amino Acid Motifs↗
PubMed1994

The effect of repeated open exposure to low levels of nickel on compromised hand skin of nickel-allergic subjects.

Nickel is a very common contact allergen, with some reports showing that more than 10% of women are affected. It is therefore important to be able to assess the risk of elicitation of nickel dermatitis in such individuals, particularly in relation to repeated exposure to low levels of this metal. It has been shown previously that under the conditions of a 48-h occluded patch test, some subjects will react to as little as 0.5 ppm nickel on compromised skin. In the present study, the effect of repeated open nickel application combined with repeated treatment with the anionic surfactant sodium dodecyl sulphate has been evaluated on the hand skin of 4 nickel-allergic subjects. Despite 2 of these being known to be particularly sensitive, there was no evidence of a nickel-allergic reaction following 2x daily immersion of hand skin sites in up to 1 ppm nickel over a period of 23 days.

Adult↗