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At least 19 recordsLinked to original sources

PubMed2000

Nickel-induced cytokine production from mononuclear cells in nickel-sensitive individuals and controls. Cytokine profiles in nickel-sensitive individuals with nickel allergy-related hand eczema before and after nickel challenge.

Exposure to nickel is a major cause of allergic contact dermatitis which is considered to be an inflammatory response induced by antigen-specific T cells. Here we describe the in vitro analysis of the nickel-specific T-cell-derived cytokine response of peripheral blood mononuclear cells from 35 nickel-allergic and 30 non-nickel-allergic individuals. Peripheral blood mononuclear cells were stimulated with 10(-4) and 10(-5) mol/l NiSO4 for 6 days and then additionally with ionomycin and phorbol myristate acetate for 24 h. Culture supernatants were analysed for interleukin-4 (IL-4), IL-5, interferon-gamma (IFN-gamma) and tumour necrosis factor-alpha (TNF-alpha) by quantitative ELISA. The analysis showed that the synthesis of IL-4 and IL-5 but not of IFN-gamma or TNF-alpha was significantly higher in the nickel-allergic individuals. The finding of preferential synthesis of Th2 cytokines was somewhat of a surprise, since previous studies have suggested a Th1 response in nickel-mediated allergic contact dermatitis. Subsequently, the nickel-allergic individuals were randomized to experimental exposure to nickel or vehicle in a double-blind design. A daily 10-min exposure of one finger to 10 ppm nickel solution for 1 week followed by 100 ppm for an additional week evoked a clinical response of hand eczema in the nickel-exposed group. Blood samples were drawn on days 7 and 14 after the start of this exposure to occupationally relevant concentrations of nickel. No statistically significant differences were observed in the nickel-induced in vitro cytokine response during the exposure period. Our results indicate the possibility that IL-4 and IL-5 are involved in the pathogenesis of nickel-mediated contact dermatitis.

Cytokines↗

PubMed1989

Lung toxicity after 13-week inhalation exposure to nickel oxide, nickel subsulfide, or nickel sulfate hexahydrate in F344/N rats and B6C3F1 mice.

The relative toxicity of nickel oxide (NiO), nickel sulfate hexahydrate (NiSO4.6H2O), and nickel subsulfide (Ni3S2) was studied in F344/N rats and B6C3F1 mice after inhalation exposure for 6 hr/day, 5 days/week, for 13 weeks. Exposure concentrations used (as mg Ni/m3) were 0.4-7.9 for NiO, 0.02-0.4 for NiSO4.6H2O, and 0.11-1.8 for Ni3S2. No exposure-related effects on mortality and only minor effects on body weight gain were seen in rats or mice. The most sensitive parameter for nickel toxicity was histopathologic change in the lungs of exposed animals were chronic active inflammation, fibrosis, and alveolar macrophage hyperplasia were associated with nickel exposure. There was an exposure-related increase in lung weight in rats and mice. Equilibrium levels of nickel in the lung were reached by 13 weeks of nickel sulfate and nickel subsulfide exposure, whereas lung levels of nickel continued to increase throughout exposure to nickel oxide. Additional exposure-related histopathologic lesions in treated animals included atrophy of the olfactory epithelium after nickel sulfate and nickel subsulfide exposure. No nasal lesions were seen after nickel oxide exposure. Lymphoid hyperplasia of the bronchial lymph nodes developed in animals exposed to all three nickel compounds. The order of toxicity corresponded to the water solubility of the nickel compounds, with nickel sulfate being most toxic, followed by nickel subsulfide and nickel oxide.

Administration, Inhalation↗

PubMed1995

Comparative carcinogenic effects of nickel subsulfide, nickel oxide, or nickel sulfate hexahydrate chronic exposures in the lung.

The relative toxicity and carcinogenicity of nickel sulfate hexahydrate (NiSO4.6H2O), nickel subsulfide (Ni3S2), and nickel oxide (NiO) were studied in F344/N rats and B6C3F1 mice after inhalation exposure for 6 h/day, 5 days/week for 2 years. Nickel subsulfide (0.15 and 1 mg/m3) and nickel oxide (1.25 and 2.5 mg/m3) caused an exposure-related increased incidence of alveolar/bronchiolar neoplasms and adrenal medulla neoplasms in male and female rats. Nickel oxide caused an equivocal exposure-related increase in alveolar/bronchiolar neoplasms in female mice. No exposure-related neoplastic responses occurred in rats or mice exposed to nickel sulfate or in mice exposed to nickel subsulfide. These findings are consistent with results from other studies, which show that nickel subsulfide and nickel oxide reach the nucleus in greater amounts than the do water-soluble nickel compounds such as nickel sulfate. It has been proposed that the more water-insoluble particles are phagocytized, whereas the vacuoles containing nickel migrate to the nuclear membrane, where they release nickel ions that effect DNA damage. The findings from these experimental studies show that chronic exposure to nickel can cause lung neoplasms in rats, and that this response is related to exposure to specific types of nickel compounds.

Animals↗

PubMed1993

Relationship between atmospheric and urinary nickel in workers manufacturing electrical resistances using nickel oxide: role of the bioavailability of nickel.

The daily concentrations of nickel in total (ie inhalable) and respirable airborne dust (personal sampling) and in post-shift and pre-shift urine samples were monitored during five consecutive work days in 20 workers exposed to NiO in a workshop manufacturing electrical resistances. The individual daily atmospheric nickel concentrations ranged from 0.5 to 9586 micrograms Ni/m3 (geometric mean 22.9) for total dust and from 0.2 to 332 micrograms Ni/m3 (geometric mean 3.5) for respirable dust. The results of the urinary excretion of nickel suggested that the occupationally-related systemic absorption of nickel strongly differed in one subject (worker E) compared to the other 19 workers. In the latter group the nickel concentration in urine never exceeded 5 micrograms Ni/g creatinine, it did not differ between post-shift and pre-shift samples (geometric means: 1.1 versus 1.2 micrograms Ni/g creatinine), and it was only slightly higher than that measured in a group of 17 non-exposed subjects (mean 0.5 micrograms Ni/g creatinine; range 0.1-1.7); furthermore their nickel elimination in urine did not change during the days off or after two weeks of holiday. In worker E, the nickel concentration ranged from 21 to 101 micrograms Ni/g creatinine in post-shift urine, the next morning (after 16 h) it had dropped on average by 50 per cent, it decreased further during the days off, and amounted still to 4.4 micrograms Ni/g creatinine after two weeks of holiday. These divergent patterns of elimination of nickel in urine are most likely related to differences in the nature of exposure to airborne nickel involving both particle size and bioavailability of nickel. Worker E was exposed to NiO powder of 1-8 microns particle size resulting in nickel levels of the respirable fraction on average about 50 times that measured for the 19 other workers (3 micrograms Ni/m3). Transformation of the initial NiO powder into particles of 150 to 600 microns size and associated changes in physicochemical properties of NiO in the particles of the respirable fraction may explain why the urinary excretion of nickel in the 19 workers is hardly influenced by their occupational exposure to this metal. The pattern of urinary nickel elimination in worker E, however, most likely reflects very recent exposure to NiO, suggesting that the degree of bioavailability of nickel from this particular physicochemical form of NiO powder is much higher than that usually accepted for poorly soluble nickel compounds.

Adult↗

PubMed1992

Nickel-dependent reconstitution of hydrogenase apoprotein in Bradyrhizobium japonicum Hupc mutants and direct evidence for a nickel metabolism locus involved in nickel incorporation into the enzyme.

A double mutant (JH103K10) was created from hydrogenase constitutive mutant (JH103) by replacement of a chromosomal 0.60 kb nickel metabolism related locus with a kanamycin resistance gene. The double mutant required 10 to 20 times more nickel (Ni) to achieve near parental strain levels of hydrogenase activity. In the absence of nickel, both JH103K10 and JH103 synthesized high levels of (inactive) hydrogenase apoprotein (large subunit, 65 kDa). With nickel, the double mutant JH103K10 synthesized the same level of hydrogenase apoenzyme (65-kDa subunit) as the JH103 parent strain; however, whole cell hydrogenase activity in JH103K10 was less than half of that in JH103, and the CPM (due to 63Ni in hydrogenase) of membranes and the calculated ratio of nickel per unit of hydrogenase enzyme of the double mutant were 40% of that in JH103. Therefore, the difference in hydrogenase activities between the double mutant and the Hupc strain can be accounted for by different abilities of the strains to incorporate nickel into the hydrogenase apoenzyme. The addition of nickel ions to previously Ni-starved and then chloramphenicol-treated Bradyrhizobium japonicum whole cells (JH103 and JH103K10) resulted in (an in vivo) restoration of hydrogenase activity, suggesting that the apoprotein synthesized in the Ni-free cultures could be activated by addition of nickel even in the absence of protein synthesis. The extent of reconstitution of active hydrogenase by nickel was greater in the absence of chloramphenicol. Hydrogenase apoprotein could not be activated by nickel in vitro even with the addition of ATP. The successful in vivo but not in vitro results suggest that enzymatic but cell-disruption labile factors are required for Ni incorporation into hydrogenase.

Apoenzymes↗

PubMed1994

The role of nickel and nickel-mediated reactive oxygen species in the mechanism of nickel carcinogenesis.

Increasing evidence demonstrates the reactive oxygen species (ROS) are implicated in metal carcinogenesis. Exposure of cultured Chinese hamster ovary (CHO) cells to several nickel compounds, i.e. NiS, Ni3S2, NiO (black and green), and NiCl2 has been shown to increase oxidation of 2',7-dichlorofluorescein to the fluorescent 2',7-dichlorofluorescein (DCF), suggesting that nickel compounds increased the concentration of oxidants in CHO cells. This fluorescence can be attenuated by addition of exogenous catalase to the extracellular media, indicating that H2O2 is one of the formed oxidants in this system. Fluorimetric measurements of chromogens following thiobarbituric acid reaction showed that nickel compounds also induce lipid peroxidation with a decreasing potency NiS, Ni3S2 > black NiO > green NiO > NiCl2. These results suggest that lipid hydroperoxides may also be produced through the action of nickel in intact cells. MgCl2, an antagonist of Ni-induced DNA strand breaks and cell transformation, has no effect on the formation of DCF fluorescence induced in CHO cells by nickel. The results suggest that nickel is an active inducer of ROS in intact mammalian cells and that the molecular mechanism of nickel carcinogenesis may involve multiple steps of nickel-mediated ROS.

Animals↗

PubMed2001

Influence of nickel supplementation from nickel sulphate hexahydrate and nickel-sodium monofluorophosphate on the performance of the West African dwarf kids.

The influence of nickel supplementation on the performance of the West African dwarf kids was studied. The investigation involved 12 kids, 3-4 months old with average weight of 5.99+/-0.18kg in a completely randomised design experiment. The treatments consisted of nickel in the forms of nickel-sodium monofluorophosphate (Ni-SMFP) and nickel sulphate hexahydrate (NiSO(4).6H(2)O) added to a corn-based diet at 10ppm of nickel. The control was the corn-based diet with no nickel supplement. Feeding was at 4% of body weight. Parameters for assessment were weight gain, feed intake, nitrogen intake and retention, urea, total protein, creatinine and glucose in serum, haemoglobin, erythrocyte and leucocyte counts. Feed intake, weight gain and nitrogen retention were affected (P<0.05) by treatment, Ni-SMFP having greater (P<0.05) influence than NiSO(4).6H(2)O. Nickel supplementation had no effect on serum creatinine, glucose, haemoglobin, erythrocyte and leucocyte counts. Ni-SMFP may be the better supplementary form of nickel in enhancing the performance of the young kid.

Journal Article↗

PubMed2004

Structural, spectroscopic, and electrochemical studies of the complexes [Ni2(mu-CNR)(CNR)2(mu-dppm)2](n+) (n = 0, 1, 2): unusual examples of nickel(0)-nickel(I) and nickel(0)-nickel(II) mixed valency.

Reaction of Ni(COD)(2) (COD = cyclooctadiene) with dppm (dppm = bis(diphenylphosphino) methane) followed by addition of alkyl or aryl isocyanides yields the class of nickel(0) dimers Ni(2)(mu-CNR)(CNR)(2)(mu-dppm)(2) (R = CH(3) (1), n-C(4)H(9) (2), CH(2)C(6)H(5) (3), i-C(3)H(7) (4), C(6)H(11) (5), t-C(4)H(9) (6), p-IC(6)H(4) (7), 2,6-(CH(3))(2)C(6)H(3) (8)). The cyclic voltammograms of the dimers exhibit two sequential single electron oxidations to the +1 and +2 forms. Specular reflectance infrared spectroelectrochemical (IRSEC) measurements demonstrate reversible interconversions between the neutral Ni(0) dimers and their +1 and +2 forms. Bulk samples of the +2 forms are prepared by chemical oxidation using [FeCp(2)][PF(6)], while the +1 forms are prepared by the comproportionation of neutral and +2 forms. The neutral complexes 6 and 8 were characterized by X-ray diffraction as symmetric, locally tetrahedral binuclear Ni(0) complexes. The +2 forms of these complexes, 6(2+) and 8(2+), have asymmetric structures with one locally square planar and one locally tetrahedral metal center, evidence for a Ni(II)-Ni(0) mixed valence state. The X-ray structural characterization of 6(+) is symmetrical and qualitatively similar to that of the neutral complex 6. The +1 forms all exhibit intense near IR electronic absorptions that are assigned as intervalence charge transfer (IVCT) bands. On the basis of structural, spectroscopic, and electrochemical data, the +1 forms of the complexes, 1(+)-8(+), are assigned as Robin-Day class III, fully delocalized Ni(+0.5)-Ni(+0.5) mixed valence complexes.

Journal Article↗

PubMed1993

Dose-response testing with nickel sulphate using the TRUE test in nickel-sensitive individuals. Multiple nickel sulphate patch-test reactions do not cause an 'angry back'.

The aim of this study was to employ the TRUE test assay to confirm the presence or absence of the 'angry back' phenomenon, i.e. that a strong positive patch-test reaction heightens adjacent patch-test response. In addition, we wished to establish the dose-response relationship for nickel sulphate patch tests among nickel-sensitive patients. Seventy-two nickel-sensitive patients, 36 in Odense and 36 in Stockholm, were tested with a 10-step nickel sulphate dilution series (TRUE test) and two placebo patches. The position of the patches was rotated, to provide a balanced spatial distribution of the different concentrations. Readings were performed blind. The results were analysed by means of polynomial multiple-regression methods and a logistic dose-response model. Half the patients (38/72) had a threshold patch-test concentration for nickel sulphate in the range of 3-0.3 microgram/cm2. The 'angry back' phenomenon was not apparent in this study, as the spill-over effect was not statistically significant. Strong reactions to high concentrations of nickel sulphate did not enhance the response to adjacent lower concentrations of nickel sulphate.

Dermatitis, Allergic Contact↗

PubMed1983

Carcinogenesis tests of nickel arsenides, nickel antimonide, and nickel telluride in rats.

Carcinogenicity of nickel arsenides (NiAs, Ni11As8, Ni5As2, NiAsS), nickel antimonide (NiSb), and nickel telluride (NiTe) was tested by IM administration to male Fischer rats (14 mg Ni/rat). Three negative control groups received similar IM injections of glycerol vehicle, ferronickel alloy (NiFe), or nickel titanate (NiTiO3); two positive control groups received nickel oxide (NiO) or ferronickel sulfide (Ni4FeS4) at equivalent dosages (14 mg Ni/rat). Within 2 years, the incidences of sarcomas at the injection site were: 0/20 (0%) in NiAs-treated rats, 8/16 (50%) in Ni11As8-treated rats; 17/20 (85%) in Ni5As2-treated rats; 14/16 (85%) in NiAsS-treated rats; 17/29 (59%) in NiSb-treated rats; and 14/26 (54%) in NiTe-treated rats. No local sarcomas occurred in the negative control groups, including 40 glycerol-treated rats, 16 NiFe-treated rats, and 20 NiTiO3-treated rats; in the positive control groups, local sarcomas occurred in 14/15 (93%) of NiO-treated rats and 15/15 (100%) of Ni4FeS4-treated rats. The 99 sarcomas that were induced by the various nickel compounds included 67 rhabdomyosarcomas, 11 fibrosarcomas, 15 osteosarcomas, 1 fibrous histiocytic sarcoma, and 5 undifferentiated sarcomas; metastases were found in 57 sarcoma-bearing rats. This study demonstrates that Ni11As8, Ni5As2, NiAsS, NiSb, and NiTe are carcinogenic for rats. Since Ni11As8, Ni5As2, and NiAsS are likely to be formed during oil shale retorting, environmental contamination by nickel arsenides in spent shale products could conceivably pose a carcinogenic hazard if large-scale production of petroleum from oil share is established.

Animals↗

PubMed1988

Comparative toxicity of nickel oxide, nickel sulfate hexahydrate, and nickel subsulfide after 12 days of inhalation exposure to F344/N rats and B6C3F1 mice.

The relative toxicity of nickel oxide (NiO), nickel sulfate hexahydrate. (NiSO4.6H2O), and nickel subsulfide (Ni3S2) was studied in F344/N rats and B6C3F1 mice after inhalation exposure for 6 h/day, 5 days/week for 12 exposure days. Exposure concentrations used (as mg Ni/m3) were 0.9-23.6 for NiO; 0.8-13.3 for NiSO4.6H2O, and 0.4-7.3 for Ni3S2. For each compound there were 5 exposure groups plus a control group. NiSO4.6H2O was the most toxic compound with exposure related mortality seen at exposure concentrations of 13.3 mg/m3 in rats and 1.6 mg/m3 and above in mice. For Ni3S2, mortality was seen in mice (but not in rats) at the highest exposure concentration (7.3 mg/m3). No mortality was seen after NiO exposure. Lesions of the lung and nasal cavity were seen in both rats and mice after exposure to NiSO4.6H2O and Ni3S2 at the 4 highest exposure concentrations. Lesions of the lung were seen primarily at the highest exposure concentrations after NiO exposure. The amount of nickel in the lungs at the end of exposure varied in relation to the water solubility of the compounds. Based on these 2-week studies, the toxicity ranking was NiSO4.6H2O greater than Ni3S2 much greater than NiO. Additional studies are in progress to assess the relative toxicities of these three nickel compounds after 90-day exposures.

Administration, Inhalation↗

PubMed1975

Tissue nickel levels and nickel dermatitis. I. Nickel in hair.

The determination of nickel by instrumental neutron activation is presented. The 58Ni (n, p) 58Co reaction and high-resolution gamma spectroscopy were employed in these measurements. The nickel content of human hair was found to be more dependent upon the sex of the donor than upon other parameters. Mean values for males (1.01 +/- 0.23 ppm) and females (4.21 +/- 0.54 ppm) agreed with values for the nickel content of hair obtained by other methods in most cases. Nickel sensitivity was not reflected in the nickel contents of hair in the female.

Dermatitis, Contact↗

PubMed1988

Nickel dermatitis and diet: clinical improvement and a reduction in blood and urine nickel levels with a low-nickel diet.

A 27-year-old nickel-sensitive female who had had continuous spontaneous flare-ups of eczema, including at sites of previous metal contact, experienced a clearing of her eruption after commencing a low-nickel diet. When on the diet, whole-blood and urinary nickel levels fell to half or less of pre-diet values and this coincided with the clinical improvement. Low-nickel diets should be considered for patients who are highly nickel sensitive.

Adult↗

PubMed1994

Enhanced generation of hydroxyl radical and sulfur trioxide anion radical from oxidation of sodium sulfite, nickel(II) sulfite, and nickel subsulfide in the presence of nickel(II) complexes.

Electron spin resonance (ESR) spin trapping was utilized to investigate the generation of free radicals from oxidation of sodium sulfite, nickel(II) sulfite, and nickel subsulfide (Ni3S2) by ambient oxygen or H2O2 at pH 7.4. The spin trap used was 5,5-dimethyl-1-pyrroline-N-oxide (DMPO). Under ambient oxygen, a solution of sodium sulfite alone generated predominantly sulfur trioxide anion radical (.SO3-) due to the autoxidation of sulfite. Addition of nickel(II) chloride [Ni(II)] enhanced the .SO3- yield about 4-fold. Incubation of sulfite with Ni(II) in the presence of chelators such as tetraglycine, histidine, beta-alanyl-3-methyl-L-histidine (anserine), beta--L-histidine (carnosine), gamma-aminobutyryl-L-histidine (homocarnosine), glutathione, and penicillamine did not have any significant effect on that enhancement. In contrast, albumin, and especially glycylglycylhistidine (GlyGlyHis), augmented the enhancing effect of Ni(II) by factors of 1.4 and 4, respectively. Computer simulation analysis of the spin-adduct spectrum and formate scavenging experiment showed that the mixture of sodium sulfite, Ni(II), and GlyGlyHis generated both hydroxyl (.OH) radical and .SO3- radical, in the ratio of approximately 1:2. The free-radical spin adduct intensity reached its saturation level in about 5 min. The yield of the radical adducts could be slightly reduced by deferoxamine and very strongly reduced by diethylenetriaminepentaacetic acid (DTPA). Aqueous suspensions of sparingly soluble nickel(II) sulfite in the presence of air and GlyGlyHis generated surface-located .SO3- and .OH radicals. The same radicals were generated in Ni3S2 suspension in the presence of GlyGlyHis and H2O2, indicating sulfite production by oxidation of the sulfide moiety of this compound.(ABSTRACT TRUNCATED AT 250 WORDS)

Amino Acid Sequence↗

PubMed1979

In vitro lymphocyte transformation to nickel: a study of nickel-sensitive patients before and after epicutaneous and oral challenge with nickel.

An in vitro lymphocyte transformation test (LTT) was performed in 8 patients with nickel contact dermatitis and in 4 control persons. The mitogenic response was of the same magnitude before patch testing, after patch testing and after oral challenge with nickel. When purified protein derivative (PPD) was used as the antigen, there was no difference between the LTT response of patients and controls before and after patch testing. After oral challenge with nickel, however, the patients' responses to PPD were significantly increased when compared with the responses after patch testing. The responses of the controls were unchanged. The LTT levels of the patients were approximately the same before and after patch testing, but were markedly increased after oral challenge.

Administration, Oral↗

PubMed2003

Molecular mechanisms of nickel carcinogenesis: gene silencing by nickel delivery to the nucleus and gene activation/inactivation by nickel-induced cell signaling.

We have summarized the molecular and cellular events involved in nickel (Ni) compound induced carcinogenesis. The major hypothesis for nickel carcinogenic action has involved the ability of the Ni compound to deliver high concentrations of Ni intracellularly, enter the nucleus and interact with chromatin. Ni has been found to selectively damage heterochromatin, and a major action of Ni is its ability to silence the expression of genes located near heterochromatin by inducing a loss of histone H4 and H3 acetylation and DNA hypermethylation. When Ni silences critical genes, such as tumor suppressor genes, the cell is altered to a greater state of neoplastic transformation. The carcinogenic hazard of Ni compounds has been directly related to the ability of that Ni compound to raise the intracellular Ni ions. The mechanisms of Ni-induced gene silencing will be discussed. However, recently it has been found that soluble Ni ions can interact with the cell surface receptors and activate cell signaling resulting in the induction of a variety of cellular genes. In particular, the Ca and hypoxia inducible factor pathway is activated in all cells exposed to soluble Ni ions. In the case of HIF-1 induction, a cell is now equipped with the expression of a variety of genes that will allow the cell to survive the lack of oxygen and thus should enable a previously initiated cancer cell to progress into a full malignant state and metastasize. These new findings support the view that soluble Ni ions exhibit carcinogenic potential by activating cell promotion and lend strength to the epidemiological data showing soluble Ni to be associated with cancer risk in Ni refinery workers.

Calcium Signaling↗

PubMed1988

Acute nickel toxicity in electroplating workers who accidently ingested a solution of nickel sulfate and nickel chloride.

Thirty-two workers in an electroplating plant accidently drank water contaminated with nickel sulfate and chloride (1.63 g Ni/liter). Twenty workers promptly developed symptoms (e.g., nausea, vomiting, abdominal discomfort, diarrhea, giddiness, lassitude, headache, cough, shortness of breath) that typically lasted a few hours but persisted 1-2 days in 7 cases. The Ni doses in workers with symptoms were estimated to range from 0.5 to 2.5 g. In 15 exposed workers who were tested on day 1 postexposure, serum Ni concentrations ranged from 13 to 1,340 micrograms/liter and urine Ni concentrations ranged from 0.15 to 12 mg/g creatinine. Ten subjects (with initial urine Ni concentrations greater than 0.8 mg/g creatinine) were hospitalized and treated for 3 days with intravenous fluids to induce diuresis, resulting in a mean elimination half-time (T1/2) for serum Ni of 27 hours (SD +/- 7 hour), which was significantly shorter (p less than .001) than the mean T1/2 of 60 hours (SD +/- 11 hours) in 11 subjects who did not receive intravenous fluids. Laboratory tests showed transiently elevated levels of blood reticulocytes (N = 7), urine albumin (N = 3), and serum bilirubin (N = 2). All subjects recovered rapidly, without evident sequellae, and returned to work by the eighth day after exposure.

Accidents, Occupational↗

PubMed2004

Mononuclear nickel(III) and nickel(II) thiolate complexes with intramolecular S-H proton interacting with both sulfur and nickel: relevance to the [NiFe]/[NiFeSe] hydrogenases.

Mononuclear, distorted square planar [Ni(II)(ER)(P(o-C(6)H(4)S)(2)(o-C(6)H(4)SH))](-) (ER = SePh (1), 2-S-C(4)H(3)S (2)) with a S-H proton directly interacting with both nickel and sulfur atoms were prepared by reaction of [Ni(CO)(SePh)(3)](-)/[Ni(CO)(2-S-C(4)H(3)S)(3)](-) and P(o-C(6)H(4)SH)(3), individually. The presence of combinations of intramolecular [Ni-S...H-SR]/[Ni...H-SR] interactions was verified in the solid state by the observation of an IR nu(SH) stretching band (2273 and 2283 cm(-)(1) (KBr) for complexes 1 and 2, individually) and (1)H NMR spectra (delta 8.079 (d) (CD(2)Cl(2)) and 8.39 (d) (C(4)D(8)O) ppm (-SH) for complexes 1 and 2, respectively) and subsequently confirmed by X-ray diffraction study. The exo-thiol proton (o-C(6)H(4)SH) in complexes 1 and 2 was identified as a D(2)O exchangeable proton from NMR and IR studies and was quantitatively removed by Lewis base Et(3)N to yield Ni(II) dimer [Ni(II)(P(o-C(6)H(4)S)(3))](2)(2)(-) (5). Instead of the ligand-based oxidation to form dinuclear Ni(II) complexes and dichalcogenide, oxidation of THF-CH(3)CN solution of complexes 1 and 2 by O(2) resulted in the formation of the mononuclear, distorted trigonal bipyramidal [Ni(III)(ER)(P(o-C(6)H(4)S)(3))](-) (ER = SePh (3), 2-S-C(4)H(3)S (4)) accompanied by byproduct H(2)O identified by (1)H NMR, respectively. The 4.2 K EPR spectra of complexes 3 and 4 exhibiting high rhombicities with three principal g values of 2.304, 2.091, and 2.0 are consonant with Ni(III) with the odd electron in the d(z)(2) orbital. Complex 3 undergoes a reversible Ni(III/II) process at E(1/2) = -0.67 V vs Ag/AgCl in MeCN.

Crystallography, X-Ray↗