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At least 73 records · Page 4Linked to original sources
PubMed1999

Correlation of urinary nickel excretion with observed 'total' and inhalable aerosol exposures of nickel refinery workers.

An investigation of the relationship between observed nickel aerosol exposures and urinary nickel excretion was undertaken at a Scandinavian nickel refinery. The goal of the study was to assess the impact of nickel aerosol speciation, the use of particle size-selective sampling instrumentation and adjustment of urinary levels for creatinine excretion on the usefulness of urinary nickel excretion as a marker for exposure. Urinary nickel measurements and paired 'total' and inhalable aerosol exposure measurements were collected each day for one week from refinery workers in four process areas. The mean observed urinary nickel concentration was 12 micrograms L-1 (11 micrograms of Ni per g of creatinine). The strongest relationships between urinary excretion and aerosol exposure were found when urinary nickel levels were adjusted for creatinine excretion and when exposure to only soluble forms of nickel aerosol was considered. No significant difference was observed between measures of 'total' and inhalable aerosol in the ability to predict urinary excretion patterns. In the light of these results, it is recommended that consideration be given to the chemical species distribution of nickel aerosol in the use of urinary nickel measurements as a screening tool for cancer risk in occupationally-exposed populations.

Adult↗
PubMed1990

Effects of temperature, and dietary magnesium and nickel levels on magnesium and nickel concentrations during the moult-cycle in Oniscus asellus (Porcellionidae, Isopoda, Crustacea).

Mean magnesium concentrations in intermoult Oniscus asellus, caged at 20 degrees C for 10 days, ranged from 1,059.15 +/- 51.9 ppm on diets containing 10 ppm nickel, to 6,827.6 +/- 314.1 ppm on a mixture of 500 ppm magnesium + 10 ppm nickel. Mean nickel concentrations ranged from 89.4 +/- 4.3 ppm on diets containing 500 ppm magnesium, to 314.0 +/- 14.8 ppm on a mixture of 500 ppm magnesium + 10 ppm nickel. At 30 degrees C, magnesium tissue concentrations ranged from 4,149.8 +/- 153.5 ppm on diets with 10 ppm nickel to 12,602.6 +/- 529.3 ppm on 500 ppm magnesium. Nickel concentrations at 30 degrees C varied from 156.8 +/- 6.7 in isopods in the control to 490.5 +/- 23.5 ppm on those on 500 ppm magnesium + 10 ppm nickel. Magnesium in intermoult isopods was mainly stored in other tissues, including the exoskeleton, and nickel in the hepatopancreas. Differences in both magnesium and nickel concentrations between males and females were not significant. Magnesium and nickel concentrations in postmoult isopods, on the average, amounted to 367.6 +/- 16.5 ppm and 18.7 +/- 0.7 ppm, respectively, at 20 degrees C, and 369.9 +/- 16.3 ppm and 30.9 +/- 1.3 ppm, respectively, at 30 degrees C. Differences between males and females, and between various treatments were not significant at P greater than 0.01. It is suggested that both hepatopancreas and other tissues, including the exoskeleton, are used as sinks to get rid of excessive tissue magnesium and nickel during the moult-cycle.

Animals↗
PubMed2002

A fluorescence-based sensing system for the environmental monitoring of nickel using the nickel binding protein from Escherichia coli.

A sensing system for nickel based on the nickel binding protein (NBP) from Escherichia coli is shown to be feasible. The versatility of NBP was demonstrated by its use in three different assay formats. When the NBP binds nickel, it undergoes a conformational change that can be used as the basis for an optical sensing system for nickel. The NBP gene was overexpressed in E. coli and the protein purified in a single step using perfusion anion-exchange chromatography. A unique cysteine residue at position 15 in the NBP was labeled with the fluorophore, N-[2-(1-maleimidyl)ethyl]-7-(diethylamino)coumarin-3-carboxamide (MDCC). In a spectrofluorimetric assay, there was a maximum of 65% quenching of the fluorescence signal produced by NBP-MDCC in the presence of nickel. A response curve for nickel using NBP-MDCC revealed a detection limit of 8 x 10(-8) mol L(-1). NBP-MDCC was also used to develop assays in microtiter plate and fiber optic bundle formats. Detection limits for nickel using these formats were also in the submicromolar range. Selectivity studies conducted with other divalent metals, including copper, cobalt, iron, cadmium, and manganese, showed that fluorescence quenching for cobalt was similar in magnitude but with a detection limit more than 10-fold higher than for nickel. The quenching responses were lower for the other metals, with detection limits at least 10 to 100 times higher than for nickel. These results suggest that fluorescently labeled NBP is potentially useful in the development of a sensing system for nickel.

Bacterial Proteins↗
PubMed2006

Structural basis of the nickel response in Helicobacter pylori: crystal structures of HpNikR in Apo and nickel-bound states.

The survival of Helicobacter pylori in the human stomach critically relies on the availability and use of nickel, an absolute cofactor of the important virulence determinant urease. Nickel-responsive gene regulation is mediated by HpNikR, a protein belonging to the ribbon-helix-helix family of transcriptional regulators. Unlike its homologues, HpNikR acts as both a repressor and an activator within an acid adaptation cascade. We report the crystal structure of the full-length HpNikR in a nickel-free conformation and two nickel-bound structures obtained in different conditions: Ni1-HpNikR and Ni2-HpNikR. Apo-HpNikR shows the same global fold as its bacterial homologues although with an unusual closed trans-conformation and asymmetrical quaternary arrangement. The structure of Ni1-HpNikR in the presence of nickel has two different sides, one showing nickel binding similar to that of known NikRs and the other reflecting an intermediate state. The structure of Ni2-HpNikR obtained using a shorter exposure to nickel provides another snapshot of the nickel incorporation. Altogether, the three structures have allowed us to determine the route for nickel within HpNikR and reveal the cooperativity between the tetramerization domain and the DNA-binding domain. Experiments using point mutations of HpnikR residues involved in nickel internalisation confirm that these residues are critical for HpNikR functions in vivo.

Bacterial Proteins↗
PubMed2004

Reduced Fhit protein expression in nickel-transformed mouse cells and in nickel-induced murine sarcomas.

Nickel compounds are carcinogenic and induce malignant transformation of cultured cells. Since nickel has low mutagenic potential, it may act predominantly through epigenetic mechanisms, including down-regulation of tumor suppressor genes. FHIT is a tumor suppressor gene whose expression is frequently reduced or lost in tumors and pre-malignant lesions. Previously, we have shown that the phosphohydrolase activity of Fhit protein, associated with its tumor suppressor action, is inhibited by nickel. In cells, such effect would assist in carcinogenesis. The latter could be further enhanced if nickel also lowered cellular levels of Fhit protein itself, e.g. by down-regulation of FHIT gene. To test this possibility, we determined Fhit protein and Fhit-mRNA levels in a nickel-transformed mouse cell line and in nickel-induced murine sarcomas. In B200 cells, derived by nickel treatment of BALB/c-3T3 cells and exhibiting a malignant phenotype, Fhit protein levels were 50% of those in the parental cells, while Fhit-mRNA expression remained unchanged. A decrease of up to > 90% in Fhit protein levels was also observed in 22 local sarcomas (mostly fibrosarcomas) induced by i.m. injection of nickel subsulfide in C57BL/6 and MT+ (C57BL/6 overexpressing metallothionein) mice, as compared with normal muscles. Moreover, Fhit was absent in 3 out of 10 sarcomas from MT+ mice and in 1 of 12 sarcomas from C57BL/6 mice. The lack of Fhit protein coincided with the absence of the Fhit-mRNA transcript in these tumors. However, in the other tumors, the decreased Fhit levels were not always accompanied by reduced expression of Fhit-mRNA. Thus, the observed lowering of Fhit protein levels is mostly associated with changes in mRNA expression and protein translation or turnover rates, and rarely with a full silencing of the gene itself. Overall, the decline of Fhit in cells or tissues malignantly transformed by nickel may indicate possible involvement of this effect in the mechanisms of nickel carcinogenesis.

Acid Anhydride Hydrolases↗
PubMed2001

Reduced nickel sensitivity in young Danish women following regulation of nickel exposure.

In most western countries, nickel is the most common contact allergen among young women. In 1991, Denmark implemented a statutory order calling for the reduction of exposure to nickel in nickel-plated items in close contact with the skin. In a retrospective analysis, a comparison is made of the number of positive patch tests to nickel seen in a private practice of dermatology before and after this statutory order was implemented. From 1 January 1986 to 31 December 1989, 35 of 1135 (3.1%) men patch tested and 628 of 3024 (20.8%) women patch tested had positive reactions to nickel. From 1 January 1996 to 31 December 1999, 48 of 1104 (4.3%) men and 424 of 2193 (19.3%) women had positive patch tests to nickel. During the 1st period, 155 of 702 women under the age of 20 (22.1%) had positive patch tests to nickel, compared to 54 of 324 (16.7%) during the second period (p<0.05). The most likely explanations of this decrease in nickel sensitivity are reduced exposure to nickel and increased public awareness of the risk of nickel sensitization.

Adult↗
PubMed1999

Effects of repeated skin exposure to low nickel concentrations: a model for allergic contact dermatitis to nickel on the hands.

We studied the effects of repeated daily exposure to low nickel concentrations on the hands of patients with hand eczema and nickel allergy. The concentrations used were chosen to represent the range of trace to moderate occupational nickel exposure. The study was double-blinded and placebo controlled. Patients immersed a finger for 10 min daily into a 10-p.p.m. nickel concentration in water for the first week, and during the second week into a 100-p.p.m. nickel concentration. This regimen significantly increased (P = 0.05) local vesicle formation and blood flow (P = 0.03) as compared with a group of patients who immersed a finger into water. The nickel concentrations used also provoked significant inflammatory skin changes on sodium lauryl sulphate (SLS)-treated forearm skin of the patients, whereas inflammatory skin changes were not observed in healthy volunteers without hand eczema and nickel allergy, either on normal or on SLS-treated forearm skin. The present study strongly suggests that the changes observed were specific to nickel exposure. Standardized methods to assess trace to moderate nickel exposure on the hands, and the associated effects in nickel-sensitized subjects, are needed.

Adult↗
PubMed1996

Nickel dermatitis: how much nickel is safe?

The Nickel Directive will become law in the countries of the European Union in 1996. This directive states that the concentration of nickel in post assemblies (used after ear piercing) may not exceed 0.05%, that products which come into direct and prolonged contact with the skin, e.g. earrings, watchstraps or zippers, may not release greater than 0.5 microgram/cm2/week, and that nickel release from coated products will not exceed this level after 2 years of normal use. The data relating to the threshold for reacting to nickel and the levels of nickel release from nickel-containing objects, are considered in this review. Although the level of 0.5 microgram/cm2/week is one below which a minority of nickel-allergic subjects will react, it is not safe in every nickel-sensitive individual. This level of nickel release is currently exceeded by many nickel-containing alloys and jewelery items that are made from high-sulfur stainless steel, and manufacturers are going to have to change the composition of jewelery to comply with the directive.

Alloys↗
PubMed1979

Rhinoscopical findings in nickel workers, with special emphasis on the influence of nickel exposure and smoking habits.

Rhinoscopy and X-ray examination were performed on 318 nickel workers and 57 controls, to study the significance of these methods in detecting cancerous and precancerous mucosal changes. The clinical and radiological findings were compared with histopathological data and mucosal nickel concentrations determined in nasal biopsy material from the middle turbinate, with duration of nickel exposure, and with tobacco smoking habitl changes (43%) than the controls (26%), (0.01 less than P less than 0.02), mainly due to differences in frequency of hyperplastic rhinitis. Thirteen nickel workers (4%) had nasal polyps. Two of these cases, both employed at the nickel refinery for 28 years, appeared to have nasal carcinoma, according to histological examination. No distinct association was established between rhinoscopical findings and epithelial dysplasia found by histological examination. The explanatory values for the rhinoscopical findings of different factors, such as working category age, duration of nickel exposure, grams tobacco smoked per week, and nickel content of nasal mucosa, were evaluated by applying a stepwise multiple regression analysis. Number of years from first employment at the nickel refinery and tobacco consumption were the only explanatory factors that showed a statistically significant correlation to the rhinoscopical findings. The radiological examination revealed few characteristics findings. Chemical analysis of cigarettes handrolled by nickel workers showed high nickel concentrations compared with non-contaminated cigarettes.

Adult↗
PubMedDate not supplied

[Resistance of surface phosphohydrolases of barley root cells to nickel salts is one of factors of plant adaptation to excessive nickel in the environment].

We studied the effect of nickel ions on the activity of ecto-phosphohydrolases (acid phosphatase and Ca-stimulated nucleotidase) from root surface of etiolated barley seedlings as well as from root microsomal fraction. The presence of nickel nitrate (25 microM) proved to stop root growth and insignificantly (on average by 20%) decreased specific hydrolytic activity of both enzymes determined on root surface as well as in the root microsomal fraction. At the same time, direct addition of nickel to the incubation mixture when measuring the substrate hydrolysis demonstrated high resistance of the microsomal fraction enzymes to the salts. A significant decrease in Ca-stimulated nucleotidase activity was observed only for nickel nitrate concentrations above 100 microM, reaching 50-60% for 3 mM Ni(NO3)2. The presence of an activator ion as well as extended duration of the microsomal fraction pretreatment with nickel nitrate (2.5 h) did not increase its effect on the enzyme activity. The pattern of nickel effect on acid phosphatase activity depended on the presence of magnesium ions in the mixture but did not change after extended duration of the microsomal fraction pretreatment (3 h). Inhibition of acid phosphatase activity in the presence of magnesium was observed only for nickel nitrate concentrations above 500 microM being no more than 20% for 3 mM Ni(NO3)2. Hence, the hydrolytic enzymes of the apoplast of plant root cells have different tolerance to to nickel salts. We propose that an insignificant decrease in specific activity of surface hydrolases of plant roots grown on a medium containing nickel salts in concentrations inhibiting growth processes (25 microM) is not related to direct effect of Ni on the apoplastic enzymes. The significance of hydrolytic enzyme resistance in plant adaptation to high nickel content in the soil is discussed.

Acid Phosphatase↗
PubMedDate not supplied

Treatment of nickel dermatitis. (The influence of tetraethylthiuramdisulfide (Antabuse) on nickel metabolism).

Nickel is the most common cause of allergic contact dermatitis in females. The dermatitis can be maintained both by direct contact and by ingestion of nickel. In 9 out of 17 patients suffering from dermatitis, a diet with a low nickel content has improved their condition. Eleven patients with chronic nickel hand dermatitis were given a daily dosage of 200 to 400 mg of tetraethylthiuramdisulfide (Antabuse). Antabuse is metabolized to the nickel chelating substance sodium diethyldithiocarbamate. In eight patients, the dermatitis cleared. Measurements of serum and urine nickel were performed in six patients. One week after the start of the Antabuse treatment, the urine nickel rose from 1 to 3.6 micrograms per 24 hours to 8.3 to 76.0 micrograms per 24 hours. The serum nickel rose from 0.26 to 0.80 micrograms per 1 to 2.0 to 7.7 micrograms per 1. In four patients the serum nickel exhibited a declining tendency during the treatment period. The results suggest that Antabuse is able to reduce the nickel deposits in man.

Dermatitis, Contact↗
PubMed1995

The nickel resistance determinant cloned from the enterobacterium Klebsiella oxytoca: conjugational transfer, expression, regulation and DNA homologies to various nickel-resistant bacteria.

Klebsiella oxytoca strain CCUG 15788, isolated from a mineral oil emulsion tank in Göteborg, Sweden, was found to be nickel-resistant (tolerating 10 mM NiCl2 in non-complexing mineral-gluconate media; inducible resistance). The nickel resistance determinants were transferred by helper-assisted conjugation to various strains of Escherichia coli and Citrobacter freundii and expressed to between 5 and 10 mM NiCl2. A 4.3 kb HindIII fragment was cloned from the genomic DNA of K. oxytoca. Ligated into the vector pSUP202, the fragment caused constitutive nickel resistance (of up to 3 or 10 mM Ni2+) in various E. coli strains. After cloning into the broad host range vector pVDZ'2 the fragment even expressed low nickel resistance in the transconjugant of Alcaligenes eutrophus AE104. With the 4.3 kb HindIII fragment as a biotinylated DNA probe it was shown by DNA-DNA hybridization that the nickel resistance determinant resides on the chromosome of K. oxytoca and not on its circular plasmid pKO1 (160 kb) or linear plasmid pKO2 (50 kb). Nickel resistance strongly correlated with the presence of the 4.3 kb HindIII fragment in the transconjugants. No homologies were detected when the nickel resistance determinants of other well-known nickel-resistant bacteria, such as A. eutrophus CH34 or A. denitrificans 4a-2, were used as target DNA. Among the 60 strains examined, positive signals only appeared with the 3.1 kb DNA fragment from A. xylosoxydans 31A and the genomic DNA of two enterobacterial strains (5-1 and 5-5) isolated from nickel-rich soil in New Caledonia.

Cloning, Molecular↗
PubMed1999

Nickel allergy and its relationship with local nickel pollution, ear piercing, and atopic dermatitis: a population-based study from Norway.

BACKGROUND: The north-Norwegian population of Sør-Varanger lives close to 2 Russian nickel smelters. OBJECTIVE: We studied the importance of the local nickel pollution, as well as ear piercing and atopic dermatitis, on the prevalence of nickel allergy in Sør-Varanger. METHODS: We patch-tested 1767 adults who were randomly selected from 2 different cross-sectional studies; in Sør-Varanger and the reference city of Tromsø, which has no nickel-polluting industry. RESULTS: Nickel allergy was diagnosed in 27.5% and 31.1% of the women in Sør-Varanger and Tromsø, respectively, and in 5.1% and 5.0% of the men. In women, ear piercing was a strong risk factor (relative risk = 3.30; 95% confidence interval = 2.01 to 5.43). A history of atopic dermatitis was not associated with nickel sensitization. We found no increased risk of nickel allergy in Sør-Varanger compared with Tromsø in adjusted multivariate analyses. CONCLUSION: The high prevalence of nickel allergy found in Sør-Varanger could not be attributed to pollution from the nearby nickel industry.

Adolescent↗
PubMed1999

Nickel concentrations in serum and urine of patients with nickel eczema.

This study is a part of the Biological Risk Assessment of Human Metal Sensitisation (BRAHMS) project with the aim of elucidating clinical and physiological effects of repeated exposures to low concentrations of metal allergens. Nickel allergic individuals (n = 35) with hand eczema and healthy controls (n = 30) were included in the study. Both groups had similar levels of nickel in urine, while the level of nickel in serum was significantly lower in nickel allergic individuals compared to controls. Nickel allergic individuals had a significantly lower intake of nickel-rich food items (chocolate, nuts, beans, porridge oats). Serum nickel levels correlated with intake of these foods, suggesting that the difference in serum nickel levels was caused by differences in dietary nickel intake.

Adult↗
PubMed2004

Molecular biology of nickel carcinogenesis: identification of differentially expressed genes in morphologically transformed C3H10T1/2 Cl 8 mouse embryo fibroblast cell lines induced by specific insoluble nickel compounds.

Inhalation of mixtures of insoluble and soluble nickel compounds by humans during nickel refining has been associated with excess lung and nasal sinus cancers. Insoluble nickel subsulfide (Ni3S2) and nickel oxide (NiO) are carcinogenic to rodents by inhalation. We previously showed that insoluble Ni3S2, crystalline nickel monosulfide (NiS), and green (high temperature, HT) and black (low temperature, LT) NiO, induced morphological transformation in cultured C3H/10T1/2 Cl 8 (10T1/2) mouse embryo cells. To understand molecular mechanisms of carcinogenesis by insoluble nickel compounds, we used random, arbitrarily primed-polymerase chain reaction (RAP-PCR) mRNA differential display and identified nine cDNA fragments that were differentially expressed between nontransformed and nickel-transformed cell lines in approximately 10.0% of the total mRNA. Expression of the calnexin gene (encoding a type I membrane protein/molecular chaperone), the ect-2 proto-oncogene, and the stress-inducible gene, Wdr1, was upregulated. Expression of six genes--the vitamin D interacting protein/thyroid hormone activating protein 80 (DRIP/TRAP-80) gene, the insulin-like growth factor receptor 1 (IGFR1) gene, the small nuclear activating protein (SNAP C3) gene, and three unknown genes, was down-regulated, in nickel-transformed cell lines. We hypothesize that these resulting aberrations in gene expression could contribute to the induction and/or maintenance of morphological transformation induced by specific insoluble nickel compounds.

Animals↗
PubMed2000

Lymphocyte subset changes in blood and gastrointestinal mucosa after oral nickel challenge in nickel-sensitized women.

This study investigates lymphocyte subsets in both the gastrointestinal mucosa and blood, in patients with nickel allergic contact dermatitis, after 10 mg oral nickel challenge (double-blind, placebo-controlled). 6 such patients with cutaneous symptoms induced only by skin contact with nickel (group A), 6 with a flare-up of cutaneous symptoms after food nickel ingestion (group B) and 6 healthy controls (group C) were enrolled. Blood lymphocyte subsets (CD4, CD45RO, CD8) were analyzed before and after 4 and 24 h from the challenge (test 1, 2, and 3), and intestinal biopsies were performed 2 days later. Challenges were positive in group B and negative in group A and controls. Serum and urine nickel levels significantly increased after nickel ingestion, with no differences between the 3 groups. At test 3, a significant decrease of the all CDs studied was found in group B. Biopsies of this group showed higher levels of CD45RO+ cells in the lamina propria and in the epithelium and lower levels of epithelial CD8+ lymphocytes. This study confirms that ingested nickel may induce flare-up of cutaneous reactions in some nickel-allergic patients, independently of the degree of sensitization and the intake of metal. In these patients, oral nickel stimulates the immune system, inducing maturation of T lymphocytes from virgin into memory cells; these latter cells seem to accumulate in the intestinal mucosa. The immunoreaction also involves CD8+ cells, whose role is not yet clear.

Administration, Oral↗
PubMed1997

The HypB protein from Bradyrhizobium japonicum can store nickel and is required for the nickel-dependent transcriptional regulation of hydrogenase.

The HypB protein from Bradyrhizobium japonicum is a metal-binding GTPase required for hydrogenase expression. In-frame mutagenesis of hypB resulted in strains that were partially or completely deficient in hydrogenase expression, depending on the degree of disruption of the gene. Complete deletion of the gene yielded a strain (JH delta Eg) which lacked hydrogenase activity under all conditions tested, including the situation as bacteroids from soybean nodules. Mutant strain JH delta 23H lacking only the N-terminal histidine-rich region (38 amino acids deleted, 23 of which are His residues) expressed partial hydrogenase activity. The activity of strain JH delta 23H was low in comparison to the wild type in 10-50 nM nickel levels, but could be cured to nearly wild-type levels by including 50 microM nickel during the derepression incubation. Studies on strains harbouring the hup promoter-lacZ fusion plasmid showed that the complete deletion of hypB nearly abolished hup promoter activity, whereas the histidine deletion mutant had 60% of the wild-type promoter activity in 50 microM NiCl2. Further evidence that HypB is required for hup promoter-binding activity was obtained from gel-shift assays. HypB could not be detected by immunoblotting when the cells were cultured heterotrophically, but when there was a switch to microaerobic conditions (1% partial pressure O2, 10% partial pressure H2) HypB was detected, and its expression preceded hydrogenase synthesis by 3-6 h. 63Ni accumulation by whole cells showed that both of the mutant strains accumulate less nickel than the wild-type strain at all time points tested during the derepression incubation. Wild-type cultures that received nickel during the HypB expression-specific period and were then washed and derepressed for hydrogenase without nickel had activities comparable to those cells that were derepressed for hydrogenase with nickel for the entire time period. In contrast to the wild type, strain JH delta 23H cultures supplied with nickel only during the HypB expression period achieved hydrogenase activities that were 30% of those cultures supplied with nickel for the entire hydrogenase derepression period. These results indicate that the loss of the metal-binding area of HypB causes a decrease in the ability of the cells to sequester and store nickel for later use in one or more hydrogenase expression steps.

Amino Acid Sequence↗
PubMed1975

Nickel deficiency and nickel-rhodium interaction in chicks.

Nickel deficiency was produced in chicks under near optimal growth conditions. This judgment is based on the finding that chicks fed the experimental diet supplemented with nickel had a very satisfactory growth rate, over 600 g in 4 weeks. To induce nickel deficiency, chicks were raised in plastic cages located inside plastic isolators and were fed diets (containing 2-15 ng of nickel/g) based on dried skim milk, acid-washed ground corn, EDTA-extracted soy protein, and corn oil. In 2 experiments, controls were fed 3 mug of nickel/g as NiCl2-6H2O. In experiment 3, instead of 1 control group 25, 50, 250, and 2,500 ng/g of supplemental dietary nickel as NiCl2-6H2O were each given to separate groups of chicks. Nickel deprivation resulted in: ultrastructural changes in the liver with the most obvious abnormality in the organization of the rough endoplasmic reticulum; altered gross appearance, reduced oxidative ability, and decreased lipid phosphorus in the liver; altered shank skin pigmentation that was associated with a decrease in yellow lipochrome pigments; and lower hematocrits. Deficiency also tended to increase the thickness of the legs and size of the hock; decrease the length:width ratios of the tibias and femurs; and decrease the plasma cholesterol. None of the signs of deficiency were seen in chicks fed diets containing at least 52 ng of nickel/g. In one experiment, a group of birds was fed 50 mug of rhodium/g of diet as (ClRh(NH3)5)SO4 to ascertain whether rhodium is a metabolic antagonist of nickel. Supplemental rhodium increased the hematocrits and liver oxidative ability of both nickel-deficient and -supplemented chicks, and increased total liver lipids, liver lipid phosphorus, and liver cholesterol in the nickel-deficient chicks alone. Rhodium did not increase the signs of nickel deficiency.

Animals↗