Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “NICKEL”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 145 records · Page 8Linked to original sources
PubMed1990

Nickel in intercellular fluid. Comparison between nickel-allergic patients and controls.

Twelve non-atopic women with nickel allergy and allergic contact dermatitis (pompholyx type) were compared with matched controls without any known allergy. Intercellular fluid was obtained by the suction blister technique, and sufficient material for analysis was available from 10 women from each group. The median nickel concentration was 16 nmol/l in the patient group and 39 nmol/l in the controls (p less than 0.02). Calculated dietary intake of nickel during the week before examination was similar in the two groups, but the fluid intake was larger in the control group. Urine was collected in the morning before examination by 11 women in each group; the nickel concentrations showed no difference between the two groups. These observations suggest that cellular uptake of nickel in sensitized patients may be sufficient to influence the kinetics of nickel in the body.

Dermatitis, Contact↗
PubMed1992

[Oral nickel provocation and a nickel-free diet. Indications and practical implementation].

In spite of some unsolved questions, an influence of orally ingested nickel on some forms of chronic eczema is generally accepted. In cases of chronic relapsing dermatitis with typical location, positive nickel patch test and positive oral nickel challenge, a nickel-restricted diet may be recommended for a limited period of time. Regional nutritional habits should be considered in the design of diets. Indications, practice and evaluation criteria for oral nickel challenge and nickel-reduced diets are described.

Administration, Oral↗
PubMed1991

Systemic effects of nickel-containing dental alloys: analysis of nickel levels in serum, liver, kidney, and oral mucosa of guinea pigs.

For economic reasons, nickel alloys are in widespread use in dentistry. However, allergic reactions have been observed in nickel-sensitive patients. In this study, absorption of nickel in the serum, liver, kidney and oral mucosa of guinea pigs was examined. Guinea pigs experimentally sensitized to nickel showed significantly higher level of nickel in serum than did control animals. Levels of nickel in experimental and control animals were found to increase over time.

Analysis of Variance↗
PubMed1982

The possible chelating effect of sodium diethyldithiocarbamate (DDC) in nickel allergic patients. Patch test procedures with nickel on DDC pretreated skin.

Encouraged by some reports about the chelating effect of p.o. given sodium diethyldithiocarbamate (DDC) in nickel allergic patients, some experiments were performed to determinate the blocking effect of locally applied DDC on positive patch test reactions with nickel. Two groups of nickel allergic patients were patch tested with different concentrations of nickel sulphate on with DDC treated skin. Control patch tests were done on areas which were pretreated with the creambase only. In one group 10% DDC in the cream was applied under 24 h occlusion; in this group also a nickel coin was tested. In the second group of patients the DDC cream was rubbed four times during 24 h without occlusion. In both groups there were no statistical differences regarding the reactions on skin pretreated with DDC and with the cream base. From this investigation it may be concluded that there is no indication that a DDC-containing barriercream will be of great help in patients with occupational dermatitis, which is especially due to nickel sensitization.

Administration, Topical↗
PubMed1991

Nickel mutagenesis: alteration of the MuSVts110 thermosensitive splicing phenotype by a nickel-induced duplication of the 3' splice site.

We investigated DNA damage caused by carcinogenic metals in a murine sarcoma virus (MuSV)-based mutagenicity assay in which mutations targeted to v-mos expression can be selected. Nickel chloride treatment of NRK cells (termed 6m2 cells) infected with MuSVts110, a retrovirus conditionally defective in viral RNA splicing and cell transformation, caused the outgrowth of transformed "revertants" with changes in the MuSVts110 RNA splicing phenotype. Cadmium and chromium treatment of 6m2 cells resulted in the selection of a second class of revertants with what appeared to be frameshift mutations allowing the translation of a readthrough gag-mos protein. In both classes of metal-induced revertants, viral gene expression was distinct from that observed in revertants arising in untreated 6m2 cultures, arguing that metal treatment did not simply enhance the rate of spontaneous reversion. In one representative nickel revertant line the operative nickel-induced mutation affecting MuSVts110 RNA splicing was a duplication of 70 bases surrounding the 3' splice site. The effect of this mutation was to direct splicing to the most downstream of the duplicated 3' sites and concomitantly relax its characteristic thermosensitivity. These data establish the mutagenic potential of nickel and provide the first example of a defined nickel-induced mutation in a mammalian gene.

Animals↗
PubMedDate not supplied

Superoxide dismutase activity and novel reactions with hydrogen peroxide of histidine-containing nickel(II)-oligopeptide complexes and nickel(II)-induced structural changes in synthetic DNA.

At physiologic pH values, histidine-containing nickel(II) oligopeptides reduced the flux of superoxide anion (O2-) generated in the hypoxanthine/xanthine oxidase system. The postulated involvement of the Ni(III)/Ni(II) redox couple in this apparent dismutation receives indirect support from electron-spin resonance data. These complexes also catalyzed the disproportionation of hydrogen peroxide, a process which generates active intermediates capable of hydroxylating p-nitrophenol and oxidizing uric acid to allantoin. An oxene moiety, namely [Nio]2+, is postulated as the active species in these H2O2-dependent reactions. Spectral analysis showed that monovalent, divalent and trivalent ions induced cooperative conformational changes in synthetic polydeoxynucleotides. For the nickel(II) ion, resistance to DNase-I activity clearly showed that an alternating G-C sequence is required for the observed transitions. It is concluded that the ability of nickel(II) peptide complexes to participate in active oxygen biochemistry suggests a possible role for nickel as a chemical promoter of cancer, whereas the capacity of the nickel(II) ion to induce conformational changes in DNA could, in principle, affect gene expression. Of course, the validity of both hypotheses require that the observed reactions be verified as biologically significant.

Catalysis↗
PubMed1993

Mutagenic responses of nickel oxides and nickel sulfides in Chinese hamster V79 cell lines at the xanthine-guanine phosphoribosyl transferase locus.

Mutagenesis of several insoluble nickel compounds--crystalline nickel sulfide NiS, nickel subsulfide Ni3S2, nickel oxides (black and green) and soluble NiCl2 was studied in three Chinese hamster cell lines--at the hprt gene of the well-defined V79 cell line, and at gpt in two transgenic derivative cell lines G12 and G10. The transgenic cell line G12 responded very strongly to the insoluble Ni compounds, such that the gpt mutagenesis was at least 20 times higher than the spontaneous mutagenesis and in some experiments was even higher. In contrast the response of the G10 cells was much lower--the mutant frequencies only increased 2-3 times over the controls. In V79 cells, NiS and NiO (black) did not induce a mutagenic response at hprt. Soluble NiCl2 also exhibited no mutagenic activity in V79 cells and induced considerably lower activity than the insoluble compounds in the transgenic G12 cells. Following vitamin E pretreatment of G12 cells for 24 h prior to nickel exposure, increased cell survival was observed for several insoluble Ni compounds whereas vitamin E had no effect on NiCl2 cytotoxicity. With vitamin E pretreatment, significantly lower mutagenic responses in G12 cells were also noted for some insoluble Ni compounds, while no such effect was observed for NiCl2.

Animals↗
PubMed2003

Nickel immobilization in ceramic matrix admixed with waste nickel hydroxide.

WAXS examinations performed with nickel hydroxide samples heated to various temperatures showed that freshly settled wet nickel hydroxide sample contains some amount of crystalline beta-Ni(OH)(2) structure and its share increased when sample was dried during 3 weeks at ambient temperature. However, the share significantly decreased when the sample was dried at 110 degrees C and more so at 250 degrees C. Crystalline phase traces of Ni(OH)(2) disappeared after sample burning at 980 degrees C and instead the distinct presence of crystalline NiO was determined. The above samples were examined for solubility in stoichiometric amount of sulphuric acid diluted with water to pH 1.9 and 2.8. Solubility was determined by measuring nickel ion concentration in leachate by the AAS method. The dissolving rate was found to decrease with the rise of temperature to which the nickel hydroxide samples were heated. The solubility of Ni(OH)(2) sample burnt at 980 degrees C was undetectable during 90 h solubility-testing time likely due to its transformation into sparingly soluble crystalline NiO. The latter is considered to be the reason for effective immobilization of waste nickel hydroxide in ceramic prepared by blending with clay and sintering at 980 degrees C.

Aluminum Silicates↗
PubMed1992

Th1 lymphokine production profiles of nickel-specific CD4+T-lymphocyte clones from nickel contact allergic and non-allergic individuals.

Panels of nickel-specific T-lymphocyte clones (TLC) were prepared from nickel-allergic and non-allergic donors. TLC from both panels showed similar levels of expression of TCR alpha/beta, CD4, CD2, CD25, and CD29 and recognized nickel in association with class II HLA molecules with restriction determinants in HLA-DR, HLA-DP, and HLA-DQ. The lymphokine secretion was analyzed in TLC from both panels upon antigen-specific or non-specific stimulation and was compared with the secretion profiles of representants of pre-established human atopen-specific Th1 and Th2 cells. Nickel-specific TLC from both panels showed a lymphokine secretion pattern similar to the atopen-specific Th1 cells, although there was some variation from clone to clone. Most TLC secreted substantial amounts of IFN-gamma, IL-2, TNF-alpha, and GM-CSF, but little or no IL-4 and IL-5. The variation observed mainly concerned IL-2 secretion that could be low or absent in some of the TLC. The general secretion pattern did not change upon different modes of stimulation, including activation via CD3, CD2, or CD28. Because nickel-specific TLC from allergic and non-allergic individuals show a similar Th1 secretion pattern, the present results give no evidence that aberrant lymphokine secretion by CD4+T cells determines the contact allergic state, as was found for atopic allergy in a previous study.

CD4-Positive T-Lymphocytes↗
PubMed1991

Reduced frequency of nickel allergy upon oral nickel contact at an early age.

From animal studies we know that oral administration of T-dependent antigens before sensitization effectively induces systemic immune unresponsiveness. Such 'oral tolerance' is persistent, dose-dependent, antigen-specific and presumably T suppressor cell-mediated. Oral tolerance induction could be an effective way to prevent undesired T cell-mediated immune functions, such as playing a role in allograft reaction, autoimmune and allergic diseases. In the present study allergic contact hypersensitivity (ACH) to nickel, currently presenting the most frequent contact allergy in man, was chosen to establish the feasibility of oral prevention of undesired T cell-mediated immunity in man. Potentially tolerizing (oral nickel contacts via orthodontic braces) as well as sensitizing (ear piercing) events were studied retrospectively in 2176 patients attending nine European patch test clinics. Patients were interviewed by means of a confidential questionnaire. The results show that ear piercing strongly favoured development of nickel ACH. More importantly, patients having had oral contacts with nickel-releasing appliances (dental braces) at an early age, but only if prior to ear piercing, showed a reduced frequency of nickel hypersensitivity. Frequencies of other hypersensitivities, in particular to fragrance, were not affected. These results support our view that induction of specific systemic immunologic tolerance by timely oral administration of antigens is feasible in man.

Adolescent↗
PubMed1984

The application of scanning transmission electron microscopy (STEM) to the study of thin anodic films on nickel and nickel-molybdenum alloys.

Anodized thin-film samples of nickel, molybdenum and a nickel-13 w/o molybdenum alloy have been analysed by scanning transmission electron microscopy, using selected area diffraction, microdiffraction and X-ray micro-analysis. Thin-film samples were obtained by ion thinning with argon and by electropolishing in acetic acid-perchloric acid. Electropolishing is the preferred technique for these studies, producing a surface with roughness on a scale of 1 nm. The anodized films on nickel and nickel 13 w/o molybdenum alloy exhibit a rugosity with a 'particle' size of 3 nm. The crystal structure of the films is similar to f.c.c. nickel oxide. Molybdenum enrichment was detected in the anodized alloy surfaces but there is no electron diffraction evidence for a crystalline molybdenum oxide. The electron diffraction pattern from anodized pure molybdenum suggests that the surface film is amorphous.

Alloys↗
PubMed1991

The nickel content of certain commercially available metallic patch test materials and its relevance in nickel-sensitive subjects.

The nickel contamination of the metallic patch test substances from 3 commercial sources was estimated by atomic absorption spectrophotometry. Contamination was generally greatest in the cobalt patch test substances. To determine whether the levels of contamination encountered were sufficient to produce a false positive patch test, 20 nickel-sensitive patients were patch tested to various concentrations of free elemental nickel in aqueous solution. The level of nickel contamination was less than that required to produce a false positive patch test in our patients, but was at a level which could produce false positive reactions in subjects highly sensitive to nickel.

Adolescent↗
PubMed1994

Nickel levels in serum and urine in five different groups of eczema patients following oral ingestion of nickel.

Patients with nickel allergy and different types of eczema with and without atopy were given a single oral dose of nickel sulfate. Blood levels and urinary excretion were determined by atomic absorption spectrophotometry. Urinary excretion of nickel was found to be dependent on age, decreasing with increasing age. When difference in age between the eczema groups was taken into account, the level of nickel in urine was significantly (p < 0.005) higher in the two atopy groups compared to the controls. This may indicate a higher intestinal absorption of nickel in atopic skin disease.

Administration, Oral↗
PubMed1982

Nasal histology and nickel concentration in plasma and urine after improvements in the work environment at a nickel refinery in Norway.

Nasal histology and nickel concentration in the plasma and urine of nickel workers were reexamined after 4 a for an evaluation of the effect of improvements in the refining process and work conditions. Ninety-eight (31%) nickel workers who were part of a previous study were reexamined. In addition, 33 of the original 38 workers with nasal epithelial dysplasia were studied for possible regression of the histological changes. Reduction in the atmospheric content of nickel and improved hygienic conditions lowered the concentration of nickel in plasma and urine by approximately 50%. The mean histological score and frequency of dysplasia was virtually the same in the two investigations, 12 and 13%, respectively. Nasal biopsies are of limited diagnostic value in the examination of individual cases. However, the method seems to be of value in identifying and monitoring groups of persons with increased risk of developing nasal carcinoma.

Adult↗
PubMed1992

GGT to GTT transversions in codon 12 of the K-ras oncogene in rat renal sarcomas induced with nickel subsulfide or nickel subsulfide/iron are consistent with oxidative damage to DNA.

Nickel is a toxic, mutagenic, and carcinogenic metal of significant occupational and environmental concern. Although several cellular targets of nickel have been identified, considerable evidence suggests that it can act indirectly upon DNA by inducing the formation of oxidized purines or pyrimidines that constitute promutagenic lesions. In this study, we examined nickel subsulfide (Ni3S2)- or Ni3S2/iron-induced renal sarcomas in F344 rats for the presence of transforming mutations in the K-ras oncogene. Selective oligonucleotide hybridization analysis of K-ras gene sequences amplified by polymerase chain reaction revealed that 1 of 12 primary tumors induced with Ni3S2 and 7 of 9 primary tumors induced with Ni3S2/iron contained exclusively GGT to GTT activating mutations in codon 12. These mutations are consistent with the known ability of nickel, in the presence of an oxidizing agent, to catalyze formation of 8-hydroxydeoxyguanosine, which in turn promotes misincorporation of dATP opposite the oxidized guanine residue. The presence of GGT to GTT transversions was confirmed by direct sequencing of the polymerase chain reaction products. Sequencing also revealed that there were no transforming mutations in codons 13 or 59-61. Additionally, a direct correlation between shortened tumor latency and the presence of activating ras mutations was noted. These results show that, in rat kidney, Ni3S2 can induce transforming mutations that are consistent with the ability of nickel to produce oxidative lesions and that iron, which exacerbates the extent of cellular oxidative damage, can enhance the frequency of these transforming mutations.

Animals↗
PubMed2006

Isolation and characterization of nickel uptake by nickel resistant bacterial isolate (NiRBI).

OBJECTIVE: Bioremediation technology has gained importance because microbes could be the convenient source of bio-absorption/bioaccumulation of metals from effluent streams. METHODS: The nickel-resistant bacterial isolates (NiRBI) were selected from various bacterial isolates from industrial effluent and grown in nutrient broth containing different concentrations of nickel sulfate (0.3-3.0 mmol/L) and their capability of accumulating metal from the medium. RESULTS: Well-defined growth of NiRBI was observed in the medium containing up to 2.5 mmol/L of nickel. The isolate was identified using 16S rRNA and closely related to Pseudomonas fragi. Maximum accumulation of nickel (0.59 mg/g dry weight of bacterial cells) was observed when NiRBI was grown in media containing 2 mmol/L of nickel. The protein profile of the NiRBI cellular extract by SDS-PAGE showed two metal stress-induced proteins of molecular weight 48 KD and 18 KD with a simultaneous down regulation of four proteins of 46.7 KD, 42.2 KD, 19.7 KD, and 4.0 KD. CONCLUSION: 48 KD and 18 KD proteins play a role in metal resistance mechanism by NiRBI.

Biodegradation, Environmental↗
PubMed1990

Carcinogenesis bioassays of nickel oxides and nickel-copper oxides by intramuscular administration to Fischer-344 rats.

Five nickel oxides and nickel-copper oxides, with chemical compositions, physicochemical properties, and biological characteristics that were previously reported, were tested for carcinogenicity by administration to groups of male Fischer-344 rats as a single im injection (20 mg Ni/rat). Two additional groups of rats received injections of the glycerol vehicle (Negative Controls) or nickel subsulfide (alpha Ni3S2, 20 mg Ni/rat, Positive Controls). Within the observation period of 2 yr post-injection, the following numbers of sarcomas developed at the injection site: Negative Controls, 0/15; Positive Controls, 15/15; Compound A (INCO black NiO, prepared at less than 650 degrees C), 6/15; Compound B (grey NiO, calcined at 735 degrees C), 0/15; Compound F (green NiO, calcined at 1,045 degrees C), 0/15; Compound H (oxidized Ni-Cu matte, Ni/Cu = 2.5:1, calcined at 850 degrees C), 13/15; Compound I (oxidized Ni-Cu matte, Ni/Cu = 5:1, calcined at 850 degrees C), 15/15. The Ni- and Ni/Cu-oxides that induced sarcomas (Compounds A, H, and I) had measurable dissolution rates in body fluids and were strongly positive in an erythrocytosis stimulation assay, demonstrating Ni bioavailability. Compound A contained detectable Ni[III] and Compounds H and I contained Cu, plus traces of Fe, Co and S, which may all promote oxygen free-radical reactions. In contrast, the compounds that did not induce sarcomas (Compounds B and F) were essentially insoluble in body fluids, did not stimulate erythrocytosis, and were practically devoid of Ni[III], Cu, Fe, Co, or S. Thus, the bioavailability of nickel and the presence of constituents that promote oxygen free-radical reactions evidently influence the carcinogenicity of nickel oxides and related compounds.

Animals↗