The purpose of this study was to investigate the cytotoxicity of the nickel ion and provide with basic data for the biological evaluation of those medical devices containing nickel. Seven cell lines were chosen. They were L929, h9c2(2-1), 293[HEK-293], hFOB1.19, THLE-3, H9 and IM-9 respectively. According to the principle of biological evaluation of medical devices, MTT method was chosen to test the cytotoxicity in different concentrations of nickel ion. For each cell line, the relative growth rate (RGR) was obtained and the cytotoxic grade was classified. Besides, IC50 values were calculated. As a result, it was found that the sensitivity was different among all cell lines. H9 was the most sensitive one, while the L929 was the most tolerant one. The concentration which is not above 1.25 mg/L was safe for all seven cell lines, because the cytotoxicity for all cells exposed in this concentration were not higher than grade 1. According to the criteria for medical devices, the concentrations not above 5 mg/L were safe for L929 cells. This result helps us to roughly assess the cytotoxicity and systematic toxicity caused by nickel contained in medical devices.
Cell Line ; Equipment and Supplies ; HEK293 Cells ; Humans ; Ions ; toxicity ; Nickel ; toxicity

Objectives: To study the association between metals mixture exposure and DNA oxidative damage using mixture analysis methods, and to explore the most significant exposure factors that cause DNA oxidative damage. Methods: Workers from steel enterprises were recruited in Shandong Province. Urinary metals were measured by using the inductively coupled plasma mass spectrometry method. The level of urinary 8-hydroxy-2'-deoxyguanosine (8-OHdG) was determined by using the ultra-high performance liquid chromatography-mass spectrometry method. Bayesian kernel machine regression (BKMR), elastic net regression and quantile g-computation regression were used to analyze the association between urinary metals and urinary 8-OHdG. Results: A total of 768 subjects aged (36.15±7.40) years old were included in the study. BKMR, elastic net regression and quantile g-computation all revealed an overall positive association between the mixture concentration and increased urinary 8-OHdG. The quantile g-computation results showed that with a 25% increase in metal mixtures, the urinary 8-OHdG level increased by 77.60%. The elastic net regression showed that with a 25% increase in exposure risk score, the urinary 8-OHdG level increased by 26%. The BKMR summarized the contribution of individual exposures to the response, and selenium, zinc, and nickel were significant contributors to the urinary 8-OHdG elevation. Conclusion: Exposure to mixed metals causes elevated levels of DNA oxidative damage, and selenium, zinc, and nickel are significant exposure factors.
Humans ; Adult ; Nickel/toxicity* ; Selenium ; Bayes Theorem ; Metals/toxicity* ; 8-Hydroxy-2'-Deoxyguanosine ; Oxidative Stress/physiology* ; Zinc ; DNA Damage

OBJECTIVETo study the biological effects of nickel-refining dust.

METHODSThe cell phagocytosis, transformation activity, and cytotoxicity of the mouse NIH3T3 cells treated with nickel-refining dusts from two nickel-refining factories in China were observed, and the risk of carcinogenicity was studied.

RESULTS(1) Two samples of nickel-refining dusts could be phagocytosed by mouse NIH3T3 cells with different phagocytizing rates of 69.0% and 39.0% at 100.000 micro g/ml, and 78.0% and 47.0% at 200.000 micro g/ml respectively. The relative clone formation rates at 12.500 micro g/ml to 100.000 micro g/ml were 71.1% to 3.9% and 84.4% to 9.1%, respectively. The cytotoxicity expressed by clone formation rate was similar to that of Ni(2)O(3), but higher than that of TiO(2) and lower than the positive control of N-methyl-N'-nitro-N-nitroso-guanidine (MNNG). (2) MNNG, Ni(2)O(3) and the two samples of nickel-refining dusts could induce morphological transformation in NIH3T3 cells. The transformation rate at 12.500 micro g/ml to 50.000 micro g/ml were 1.9% to 3.6% and 0.9% to 2.5% respectively in a dose-dependent manner. (3) The NIH3T3 cells treated by MNNG and nickel-refining dusts could induce Con A agglutination, and may form as clone in soft agar. This finding proved the reliability of the transformed clone.

CONCLUSIONSThe present study for the first time demonstrate that nickel-refining dusts have cell transformation activity. The findings provide a new experimental evidence for the carcinogenic risk of nickel-refining dusts, and for the aetiology of lung cancer in nickel-refining workers.

Animals ; Cell Transformation, Neoplastic ; drug effects ; pathology ; Dust ; Mice ; NIH 3T3 Cells ; Nickel ; toxicity

Medical implantable stainless steels are widely used in medical field due to their excellent properties, besides its allergic response to human body, the nickel ion released from the steels due to corrosion has the harm of malformation and carcingenesis. The mechanical property, corrosion resistance and blood compatibility of a new nickel-free stainless steel (BIOSSN4) is researched in this paper. Compared with the traditional 316L medical stainless steel, BIOSSN4 shows wide future applications because of its better combination of strength and toughness, good corrosion resistance and biocompatibility.
Biocompatible Materials ; chemistry ; toxicity ; Corrosion ; Humans ; In Vitro Techniques ; Materials Testing ; Nickel ; chemistry ; toxicity ; Platelet Adhesiveness ; drug effects ; Stainless Steel ; chemistry ; toxicity ; Surface Properties

OBJECTIVETo study the effects of nickel-refining dusts on DNA damage in mouse NIH/3T3 cell.

METHODDNA damage of mouse NIH/3T3 cell induced by two nickel-refining dust samples was determined with single cell gel electrophoresis (SCGE) technique.

RESULTS(1) Under the condition of the same treatment time, the tailed cell (%) of NIH/3T3 cells increased with the increase in doses of nickel-refining dusts (35.5%, 69.7%, 85.2%, 41.3%, 75.7%, 89.2% respectively except for sample 2, 50 microg/ml, 24 h group), and DNA strand breaks reached the peak value at 4 h of exposure; (2) When we treated the NIH/3T3 cells with the same dose of nickel-refining dusts, the tail rate at 4 h was higher than those at 2 h and 24 h of exposure; (3) Both sample 1 and sample 2 with different doses of nickel-refining dusts could induce higher comet tail, DNA%, tail length (except for 12.5 microg/ml), extent of TM (except for sample 1, 12.5 microg/ml) than in control group (P < 0.05). The DNA damage range was significantly increased in different tested doses of nickel-refining dusts and the damage range reached the peak value when the cells were treated for 4 h.

CONCLUSIONNickel-refining dusts could induce different degree DNA damage in NIH/3T3 cells.

Animals ; Cell Cycle ; Cell Survival ; Comet Assay ; DNA Damage ; Dust ; Metallurgy ; Mice ; NIH 3T3 Cells ; Nickel ; toxicity

OBJECTIVETo study the effects of two kinds of nickel-refining fumes on DNA damage of NIH/3T3 cell and the difference.

METHODSNIH/3T3 cells were treated by two kinds of nickel fumes collected from smelting furnace and refining workshop of a nickel-smeltery, and PBS taken the place of nickel-smelting fumes was used as negative control. Several hours later, the cytotoxicity of on NIH/3T3 cells was detected with MTT colorimetric assay, and the DNA damage was also measured by comet assay (single cell gel electrophoresis).

RESULTWith the extension of exposure time and increasing of concentration, the living rate of NIH/3T3 cells was decreased; the tail rate, tail extent moment and tail DNA percent of NIH/3T3 cell induced by these two refining fumes were increased. After cells were treated with 100.00 microg/ml of nickel-smelting fume for 48 h, the living rate of NIH/3T3 cells was 24.5% and 26.5% respectively. The tail length of NIH/3T3 cell induced by these two refining fumes was not significant difference. Tail DNA percent of NIH/3T3 cell induced by smelting furnace fume was higher than negative control group (P < 0.05). The tail rate, and tail DNA percent (except 12.5 microg/ml and 50.0 microg/ml treated 2 h group) of NIH/3T3 cell induced by refining workshop fume was higher than negative control group (P < 0.05).

CONCLUSIONNickel-smelting fume could depress the survival rate of NIH/3T3 cells, and induce different degree DNA damage of NIH/3T3 cell.

Animals ; Cell Survival ; drug effects ; Comet Assay ; DNA Damage ; drug effects ; Metallurgy ; Mice ; NIH 3T3 Cells ; Nickel ; toxicity

Animals ; Dose-Response Relationship, Drug ; Male ; Mice ; Mice, Inbred Strains ; Nickel ; toxicity ; Oxidative Stress ; physiology ; Testis ; drug effects ; metabolism

The purpose of this study was to investigate the NOAEL of the nickel ion and provide with basic data for the biological evaluation of those medical devices containing nickel. Five groups SD rats were repeatedly exposed during 14 d respectively to nickel at first stage doses of 4.9, 3.7, 2.5 mg/(kg.d), and the second stage doses of 1.2, 0.25 mg/(kg.d) by the intravenous route. The results showed that the NOAEL of nickel ion is 0.25 mg/(kg.d) for SD rats, and the result was verified by subchronic systemic toxicity test of nickel alloy. The threshold of toxicological concern (TTC) of nickel is 150 μg/d (based on application of 100-fold uncertainty factor and a body weight of 60 kg)deduced by these data.
Animals ; Equipment and Supplies/adverse effects* ; Nickel/toxicity* ; No-Observed-Adverse-Effect Level ; Rats ; Rats, Sprague-Dawley ; Risk Assessment

OBJECTIVETo determine the effects of water hardness on the toxicities of cobalt (Co) and nickel (Ni) to a freshwater fish, Capoeta fusca.

METHODSToxicity was investigated by static bioassay. Fish were exposed to cobalt (as CoCl(2)) and nickel (as NiCl(2)) for 96 h in waters with two levels of hardness ("hard" and "very hard", nominally 130 mg/L and 350 mg/L as CaCO(3), respectively).

RESULTSWater hardness had a significant effect on the acute toxicity of both elements. The 96 h LC(50) values for Co were 91.7 mg/L and 204.8 mg/L in hard and very hard waters, respectively, and for Ni the 96 h LC(50) values were 78.0 mg/L and 127.2 mg/L, respectively.

CONCLUSIONThe fish were more sensitive to Co and Ni toxicity in hard water than in very hard water; very hard water protects C. fusca against the toxicity of Co and Ni.

Animals ; Calcium Carbonate ; analysis ; Cobalt ; analysis ; toxicity ; Cyprinidae ; growth & development ; Environmental Monitoring ; Fresh Water ; analysis ; Iran ; Lethal Dose 50 ; Nickel ; analysis ; toxicity ; Toxicity Tests, Acute ; Water Pollutants, Chemical ; analysis ; toxicity

OBJECTIVETo provide evidence for illustrating the molecular mechanism of nickel carcinogenesis, and to identify the differential expression of protein in crystalline NiS-induced neoplastic transformation of human bronchial epithelial cell by proteomics technology.

METHODSTwo dimensional electrophoresis (2-DE) and the ImageMaster 3.10 software were used to analyze the differential expression of protein, matrix-assisted laser desorption/ionization-time of flight mass spectrometry (MALDI-TOF-MS) combined with database search was applied to identify protein peroxiredoxin 2 (PDX2) related to malignant transformation.

RESULTSThe good 2-DE pattern including resolution and reproducibility was obtained. Nearly 700 expressed proteins per 2-D gel were isolated with molecular weights (MW) ranging from 14,400 to 94,000 KD and pI 3 - 10. A protein PDX2 with MW 21,890 KD, pI 5.66, which was highly expressed in malignantly transformed cell, was identified using MALDI-TOF-MS.

CONCLUSIONPDX2 was involved in malignant transformation of human bronchial epithelial cell induced by crystalline nickel sulfide.

Bronchi ; cytology ; Cell Line ; Cell Transformation, Neoplastic ; chemically induced ; metabolism ; Epithelial Cells ; cytology ; drug effects ; metabolism ; Humans ; Nickel ; toxicity ; Peroxiredoxins ; metabolism ; Proteome