Статті в журналах: "Nickel Toxicology"

1

Morgan, L. G. "Nickel toxicology." Environmental Geochemistry and Health 11, no. 3-4 (December 1989): 75–76. http://dx.doi.org/10.1007/bf01758654.

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2

Zhao, Jinshun, Xianglin Shi, Vincent Castranova, and Min Ding. "Occupational Toxicology of Nickel and Nickel Compounds." Journal of Environmental Pathology, Toxicology and Oncology 28, no. 3 (2009): 177–208. http://dx.doi.org/10.1615/jenvironpatholtoxicoloncol.v28.i3.10.

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3

Waldron, H. "Progress in Nickel Toxicology." Occupational and Environmental Medicine 43, no. 3 (March 1, 1986): 216. http://dx.doi.org/10.1136/oem.43.3.216.

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4

Genchi, Giuseppe, Alessia Carocci, Graziantonio Lauria, Maria Stefania Sinicropi, and Alessia Catalano. "Nickel: Human Health and Environmental Toxicology." International Journal of Environmental Research and Public Health 17, no. 3 (January 21, 2020): 679. http://dx.doi.org/10.3390/ijerph17030679.

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Анотація:

Nickel is a transition element extensively distributed in the environment, air, water, and soil. It may derive from natural sources and anthropogenic activity. Although nickel is ubiquitous in the environment, its functional role as a trace element for animals and human beings has not been yet recognized. Environmental pollution from nickel may be due to industry, the use of liquid and solid fuels, as well as municipal and industrial waste. Nickel contact can cause a variety of side effects on human health, such as allergy, cardiovascular and kidney diseases, lung fibrosis, lung and nasal cancer. Although the molecular mechanisms of nickel-induced toxicity are not yet clear, mitochondrial dysfunctions and oxidative stress are thought to have a primary and crucial role in the toxicity of this metal. Recently, researchers, trying to characterize the capability of nickel to induce cancer, have found out that epigenetic alterations induced by nickel exposure can perturb the genome. The purpose of this review is to describe the chemical features of nickel in human beings and the mechanisms of its toxicity. Furthermore, the attention is focused on strategies to remove nickel from the environment, such as phytoremediation and phytomining.

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5

Forgacs, Zsolt, Peter Massányi, Norbert Lukac, and Zoltan Somosy. "Reproductive toxicology of nickel – Review." Journal of Environmental Science and Health, Part A 47, no. 9 (July 15, 2012): 1249–60. http://dx.doi.org/10.1080/10934529.2012.672114.

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6

Buxton, Samuel, Emily Garman, Katherine E. Heim, Tara Lyons-Darden, Christian E. Schlekat, Michael D. Taylor, and Adriana R. Oller. "Concise Review of Nickel Human Health Toxicology and Ecotoxicology." Inorganics 7, no. 7 (July 12, 2019): 89. http://dx.doi.org/10.3390/inorganics7070089.

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Nickel (Ni) metal and Ni compounds are widely used in applications like stainless steel, alloys, and batteries. Nickel is a naturally occurring element in water, soil, air, and living organisms, and is essential to microorganisms and plants. Thus, human and environmental nickel exposures are ubiquitous. Production and use of nickel and its compounds can, however, result in additional exposures to humans and the environment. Notable human health toxicity effects identified from human and/or animal studies include respiratory cancer, non-cancer toxicity effects following inhalation, dermatitis, and reproductive effects. These effects have thresholds, with indirect genotoxic and epigenetic events underlying the threshold mode of action for nickel carcinogenicity. Differences in human toxicity potencies/potentials of different nickel chemical forms are correlated with the bioavailability of the Ni2+ ion at target sites. Likewise, Ni2+ has been demonstrated to be the toxic chemical species in the environment, and models have been developed that account for the influence of abiotic factors on the bioavailability and toxicity of Ni2+ in different habitats. Emerging issues regarding the toxicity of nickel nanoforms and metal mixtures are briefly discussed. This review is unique in its covering of both human and environmental nickel toxicity data.

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7

Von Burg, R. "Nickel and some nickel compounds." Journal of Applied Toxicology 17, no. 6 (November 1997): 425–31. http://dx.doi.org/10.1002/(sici)1099-1263(199711/12)17:6<425::aid-jat460>3.0.co;2-r.

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8

Nicklin, Steve. "Nickel and the skin: Immunology and toxicology." Food and Chemical Toxicology 29, no. 4 (January 1991): 287–88. http://dx.doi.org/10.1016/0278-6915(91)90028-6.

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9

Barceloux, Donald G., and Donald Barceloux. "Nickel." Journal of Toxicology: Clinical Toxicology 37, no. 2 (January 1999): 239–58. http://dx.doi.org/10.1081/clt-100102423.

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10

Ptashynski, M. D., R. M. Pedlar, R. E. Evans, C. L. Baron, and J. F. Klaverkamp. "Toxicology of dietary nickel in lake whitefish (Coregonus clupeaformis)." Aquatic Toxicology 58, no. 3-4 (August 2002): 229–47. http://dx.doi.org/10.1016/s0166-445x(01)00239-9.

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11

Rizvi, Asim, Saima Parveen, Saniyya Khan, and Imrana Naseem. "Nickel toxicology with reference to male molecular reproductive physiology." Reproductive Biology 20, no. 1 (March 2020): 3–8. http://dx.doi.org/10.1016/j.repbio.2019.11.005.

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12

Emond, Christy A., Vernieda B. Vergara, Eric D. Lombardini, Steven R. Mog, and John F. Kalinich. "Induction of Rhabdomyosarcoma by Embedded Military-Grade Tungsten/Nickel/Cobalt Not by Tungsten/Nickel/Iron in the B6C3F1 Mouse." International Journal of Toxicology 34, no. 1 (December 28, 2014): 44–54. http://dx.doi.org/10.1177/1091581814565038.

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Continued improvements in the ballistic properties of military munitions have led to metal formulations for which little are known about the long-term health effects. Previously we have shown that a military-grade tungsten alloy comprised of tungsten, nickel, and cobalt, when embedded into the leg muscle of F344 rats to simulate a fragment wound, induces highly aggressive metastatic rhabdomyosarcomas. An important follow-up when assessing a compound’s carcinogenic potential is to test it in a second rodent species. In this study, we assessed the health effects of embedded fragments of 2 military-grade tungsten alloys, tungsten/nickel/cobalt and tungsten/nickel/iron, in the B6C3F1 mouse. Implantation of tungsten/nickel/cobalt pellets into the quadriceps muscle resulted in the formation of a rhabdomyosarcoma around the pellet. Conversely, implantation of tungsten/nickel/iron did not result in tumor formation. Unlike what was seen in the rat model, the tumors induced by the tungsten/nickel/cobalt did not exhibit aggressive growth patterns and did not metastasize.

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13

Outridge, P. M., and A. M. Scheuhammer. "Bioaccumulation and toxicology of nickel: implications for wild mammals and birds." Environmental Reviews 1, no. 2 (July 1, 1993): 172–97. http://dx.doi.org/10.1139/a93-013.

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The tissues of wild mammals and birds from uncontaminated environments generally contain from ~0.1 to 5 μg nickel∙g dry weight−1, whereas in Ni-polluted environments, tissues accumulate from -0.5 to 10 (mammals) and -0.5 to 80 (birds) μg nickel∙g dry weight−1. The highest concentrations in these ranges are usually associated with tissues directly exposed to the external environment (fur, feathers, skin). Bone frequently contains higher Ni concentrations than other internal tissues. Ni concentrations in the most commonly analysed internal organs (liver, kidneys) range from nondetectable to about 3 μg∙g dry weight−1, the kidneys often containing higher concentrations than the liver. There is some evidence that birds may tend to accumulate higher Ni burdens in polluted habitats than do mammals. For mammals, reduced growth and survival occur in response to chronic exposure to 500–2500 μg Ni∙g diet−1 (10–50 mg∙kg body weight−1∙d−1). Effects on reproduction and essential trace metal (especially iron) metabolism have been reported at levels as low as 5 μg∙g−1 in food or drinking water (0.2–0.4 mg∙kg body weight−1∙d−1), but these findings have not always been corroborated. Toxicological data on birds are more limited than those pertaining to mammals. Newly hatched chickens suffered reduced growth rates when fed ≥300 μg∙g diet−1, and chicks began to die when fed diets containing ≥500 μg∙g−1. In newly hatched mallard ducklings, chronic exposure to ≥800 μg∙g diet−1 resulted in ataxia, tremors, and significant mortality, whereas adult mallards fed 800 μg∙g−1 showed no evidence of systemic or reproductive toxicity. Tissue concentrations of Ni were not reliable indicators of potential toxicity in either mammals or birds, because significant effects, including mortality, frequently occurred in the absence of elevated tissue Ni concentrations. However, when there is evidence of elevated tissue Ni concentrations (>10 μg∙g−1 in the kidneys, and (or) >3 μg∙g−1 dry weight in the liver), Ni exposure sufficient to cause significant toxic effects should be suspected. Nickel has been reported in aquatic macrophytes and lower plants (but not in invertebrates or zooplankton) in the vicinity of Ni smelters in Canada in concentrations that approach or exceed dietary levels known to cause adverse effects in young animals. Sensitive species of wildlife ingesting this vegetation for considerable periods of time could experience Ni-related toxicity. In addition, wildlife food chains involving aquatic organisms (plants, invertebrates, fish) risk alterations in community structure in Ni-contaminated environments as Ni-sensitive taxa are eliminated or their abundance is reduced.Key words: nickel, toxicology, wildlife.

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14

El Safty, Amal Mohamed Kamal, Aisha Mohamed Samir, Mona Kamal Mekkawy, and Marwa Mohamed Fouad. "Genotoxic Effects Due to Exposure to Chromium and Nickel Among Electroplating Workers." International Journal of Toxicology 37, no. 3 (March 19, 2018): 234–40. http://dx.doi.org/10.1177/1091581818764084.

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Using chromium and nickel for electroplating is important in many industries. This process induces variable adverse health effects among exposed workers. The aim of this study is to detect the genotoxic effects of combined exposure to chromium and nickel among electroplating workers. This study was conducted on 41 male workers occupationally exposed to chromium and nickel in the electroplating section of a factory compared to 41 male nonexposed individuals, where full history and clinical examination were performed. Laboratory investigations included measurement of serum chromium, nickel, 8-hydroxydeoxyguanosine (8-OHdG), and micronuclei were measured in buccal cells. In exposed workers, serum chromium ranged from 0.09 to 7.20 µg/L, serum nickel ranged from 1.20 to 28.00 µg/L, serum 8-OHdG ranged from 1.09 to12.60 ng/mL, and these results were statistically significantly increased compared to nonexposed group ( P < 0.001). Electroplaters showed higher frequencies of micronuclei in buccal cells when compared to nonexposed (ranged from 20.00 to 130.00 N/1,000 versus 2.00 to 28.00 N/1,000; P < 0.001). Linear regression models were done to detect independent predictors of 8-OHdG and micronucleus test by comparing exposed and nonexposed groups. The model found that exposure to chromium and nickel increases serum 8-OHdG by 4.754 (95% confidence interval [CI]: 3.54-5.96). The model found that exposure to chromium and nickel increases micronucleus by 35.927 (95% CI: 28.517-43.337). Serum 8-OHdG and micronucleus test in buccal cells were increased with combined exposure to chromium and nickel. The current research concluded that workers exposed to nickel and chromium in electroplating industry are at risk of significant cytogenetic damage.

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15

Waalkes, Michael P., Jie Liu, Kazimierz S. Kasprzak, and Bhalchandra A. Diwan. "Metallothionein-I/II Double Knockout Mice Are No More Sensitive to the Carcinogenic Effects of Nickel Subsulfide than Wild-Type Mice." International Journal of Toxicology 24, no. 4 (July 2005): 215–20. http://dx.doi.org/10.1080/10915810591000668.

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Metallothionein (MT) is a high-affinity metal-binding protein thought to mitigate the toxicity of various metals. MT may limit the toxicity of a metal by direct binding or through action as an antioxidant for metals that generate reactive oxygen species. Nickel compounds have carcinogenic potential in humans and animals, possibly by production of oxidative stress. The impact of MT deficiency on the carcinogenic effects of nickel is unknown. Thus, groups ( n = 25) of male MT-I/II double knockout (MT-null) or MT wild-type (WT) mice were exposed to a single treatment of nickel (0.5 or 1.0 mg Ni3S2/site, intramuscularly, [i.m.], into both hind legs), or left untreated (control) and observed over the next 104 weeks. There were no differences in the incidence of spontaneous tumors in MT-null and WT mice. Nickel induced injection site fibrosarcomas in a dose-related fashion to a similar extent in both WT and MT-null mice. Nickel-treatment had no effect on total lung tumor incidence, although some phenotypic-specific differences occurred in the proportion of benign and malignant pulmonary tumors. Overall, MT-null mice appear no more sensitive to the carcinogenic effects of nickel than WT mice. Thus, poor MT production does not appear to be a predisposing factor for nickel carcinogenesis.

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16

Faroon, Obaid M., Malcolm Williams, and Ralph O'Connor. "A Review of the Carcinogenicity of Chemicals Most Frequently Found at National Priorities List Sites." Toxicology and Industrial Health 10, no. 3 (May 1994): 203–30. http://dx.doi.org/10.1177/074823379401000309.

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Several studies have shown that numerous National Priorities List (NPL) sites have been contaminated with arsenic (747), cadmium (791), chloroform (596), or nickel (664). The National Toxicology Program (NTP, 1991) has classified these substances as known human carcinogens (arsenic and certain arsenic compounds) or as substances that may reasonably be anticipated to be carcinogens (cadmium and certain cadmium compounds, chloroform, and nickel and certain nickel compounds). The general population is probably exposed to low levels of these hazardous substances through drinking water, eating food, or inhaling contaminated air. People working or living near industries and facilities that manufacture and use chloroform, nickel, arsenic, or cadmium may be exposed to higher than background levels of these hazardous substances. Multiple pathways of exposure may exist for populations near hazardous waste sites. For example, high levels of chloroform (1,890 ppb) were found in well water near a waste site; high levels of cadmium exposure may exist for individuals living near cadmium-contaminated waste sites.

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17

Severa, J., A. Vyskocil, Z. Fiala, and M. Cizkova. "Distribution of nickel in body fluids and organs of rats chronically exposed to nickel sulphate." Human & Experimental Toxicology 14, no. 12 (December 1995): 955–58. http://dx.doi.org/10.1177/096032719501401204.

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1 Male and female rats were given 100 mg Ni L-1 (as nick el 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 absorp tion).

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18

Wong, P. K., and C. K. Wong. "Toxicity of nickel and nickel electroplating water toChlorella pyrenoidosa." Bulletin of Environmental Contamination and Toxicology 45, no. 5 (November 1990): 752–59. http://dx.doi.org/10.1007/bf01700997.

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19

Benson, Janet M., Edward B. Barr, William E. Bechtold, Yung-Sung Cheng, June K. Dunnick, William E. Eastin, Charles H. Hobbs, Christopher H. Kennedy, and Kirk R. Maples. "Fate of Inhaled Nickel Oxide and Nickel Subsulfide in F344/N Rats." Inhalation Toxicology 6, no. 2 (January 1994): 167–83. http://dx.doi.org/10.3109/08958379409029703.

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20

DUNNICK, J. K., M. R. ELWELL, J. M. BENSON, C. H. HOBBS, F. F. HAHN, P. J. HALY, Y. S. CHENG, and A. F. EIDSON. "Lung Toxicity after 13-Week Inhalation Exposure to Nickel Oxide, Nickel Subsulfide, or Nickel Sulfate Hexahydrate in F344/N Rats and B6C3F1 Mice." Toxicological Sciences 12, no. 3 (1989): 584–94. http://dx.doi.org/10.1093/toxsci/12.3.584.

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21

DUNNICK, J. "Lung toxicity after 13-week inhalation exposure to nickel oxide, nickel subsulfide, or nickel sulfate hexahydrate in F344/N rats and B6C3F1 mice." Fundamental and Applied Toxicology 12, no. 3 (April 1989): 584–94. http://dx.doi.org/10.1016/0272-0590(89)90031-6.

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22

Dunnick, J. "Comparative toxicity of nickel oxide, nickel sulfate hexahydrate, and nickel subsulfide after 12 days of inhalation exposure to F344/N rats and B6C3F1 mice." Toxicology 50, no. 2 (July 1988): 145–56. http://dx.doi.org/10.1016/0300-483x(88)90087-x.

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23

Dogra, S., A. K. Khanna, and J. L. Kaw. "Antibody forming cell response to nickel and nickel-coated fly ash in rats." Human & Experimental Toxicology 18, no. 5 (May 1999): 333–37. http://dx.doi.org/10.1191/096032799678840183.

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The potential of nickel as nickel chloride, native fly ash and Ni-coated fly ash to alter pulmonary and systemic immune response was evaluated upon intratracheal (I/T) exposure of rats. The animals were sensitised with sheep red blood cells (SRBC) through I/T and intraperitoneal (I/P) routes. Nickel exposure resulted in a decrease in the number of antibody forming cells (AFC) in lung associated lymph nodes (LALN) and spleen. In rats exposed to native fly ash there was a reduction in the number of AFC in LALN but not in spleen. The results did not demonstrate any significant difference in the immunosuppression of fly ash and Ni-coated fly ash exposed rats. The decrease in AFC formation in Ni-coated fly ash exposed animals was of a lesser magnitude than in rats exposed to Ni-alone.

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24

Menné, T., and H. I. Maibach. "Nickel Allergic Contact Dermatitis: A Review." Journal of the American College of Toxicology 8, no. 7 (December 1989): 1271–73. http://dx.doi.org/10.3109/10915818909009117.

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25

Ahmed, S., A. Rahman, M. Saleem, M. Athar, and S. Sultana. "Ellagic acid ameliorates nickel induced biochemical alterations: diminution of oxidative stress." Human & Experimental Toxicology 18, no. 11 (November 1999): 691–98. http://dx.doi.org/10.1191/096032799678839563.

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Nickel, a major environmental pollutant is known for its clastogenic, toxic and carcinogenic potentials. The present investigation shows that ellagic acid proves to be exceptional in the amelioration of the nickel-induced biochemical alterations in serum, liver and kidney. Administration of nickel (250 mmol Ni/kg body wt) to female Wistar rats, resulted in increase in the reduced glutathione (GSH) content [kidney (*P50.05) and liver (**P50.001)] and Glutathione-S-transferase (GST) and glutathione reductase (GR) activities [kidney and liver, (**P50.001)]. Ellagic acid treatment to the intoxicated rats leads to the formation of soluble ellagic acid-metal complex which facilitates excretion of nickel from the cell or tissue, thus ameliorating nickel-induced toxicity, as evident from the down regulation of GSH content, GST and GR activities with concomitant restoration of glutathione peroxidase (GPx) activity in liver and kidney. Our data shows that ellagic acid maintains cell membrane integrity through sequestration of metal ions from the extracellular fluid, as evident from the alleviated levels of serum glutamate oxaloacetate transaminase, (SGOT), serum glutamate pyruvate transaminase (SGPT) and lactate dehydrogenase (LDH) when compared to nickel treated group. Similarly, the enhanced blood urea nitrogen (BUN) and serum creatinine levels that are indicative of renal injury showed a reduction of about 45 and 40%, respectively. The data also show that treatment of ellagic acid after 30 min of nickel administration exhibits maximum inhibition in a dose-dependent manner. In summary, our data suggests that ellagic acid act as an effective chelating agent in suppressing nickel-induced renal and hepatic biochemical alterations.

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26

Wong, C. K., P. K. Wong, and H. Tao. "Toxicity of nickel and nickel electroplating water to the freshwater cladoceranMoina macrocopa." Bulletin of Environmental Contamination and Toxicology 47, no. 3 (September 1991): 448–54. http://dx.doi.org/10.1007/bf01702209.

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27

Yokota, Shohei, Kazuichi Nakamura, and Ryo Kamata. "A comparative study of nickel nanoparticle and ionic nickel toxicities in zebrafish: histopathological changes and oxidative stress." Journal of Toxicological Sciences 44, no. 11 (2019): 737–51. http://dx.doi.org/10.2131/jts.44.737.

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28

Koizumi, Chisato, Kan Usuda, Satsuki Hayashi, Tomotaro Dote, and Koichi Kono. "Urinary nickel: measurement of exposure by inductively coupled plasma argon emission spectrometry." Toxicology and Industrial Health 20, no. 6-10 (July 2004): 103–8. http://dx.doi.org/10.1191/0748233704th201oa.

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Nickel is a rare earth metal and is widely used in modern industry. Its overexposure in human beings can provoke significant effects including lung, cardiovascular and kidney diseases. As an index of occupational exposure, urine is widely used for the monitoring of nickel concentration because it is a minimally invasive method. Recent studies have used atomic absorption spectrometry to measure nickel concentration. In this study, we introduced novel inductively coupled plasma argon emission spectrometry (ICPAES) which enables us to measure multiple elements simultaneously with smaller volume and with lower detection limits compared to conventional atomic absorption emission spectrometry, and we established the new measuring method by determining the appropriate wavelengths for nickel concentration. Furthermore, using the established new measuring method, we investigated the correlation between a single oral administration of nickel and urine elimination in rats. As a result, different concentrations of nickel standard solutions were measured by ICPAES, and among five specific wavelengths of nickel, 221.647 and 231.604 nm were chosen because they had the highest inclines of both signal to background ratio and emission intensity in simple linear regression analysis. Next, by using healthy human urine samples that had not been exposed to nickel, 231.604 nm was determined to be the most appropriate wavelength because it did not present abnormal intensity due to obstacle wavelength. Male Wistar rats received an oral administration of nickel ranging from 0.025 to 250 mg/kg, which is equivalent to 0.0015-15% of LD50, and during the following 24 h, urine samples were collected and the nickel concentration was measured by ICPAES. With a single oral administration of nickel, there was an increase in urine nickel concentration in a dose-dependent manner and the appropriate equation was developed. Acute renal failure was not observed in this dosage of oral nickel administration by analysing NAG, b2-microglobulin, urine albumin and urine protein. It was concluded that the obtained nickel reference values using ICPAES would be useful for the early diagnosis of nickel intoxication and in the assessment of the exposure to nickel.

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29

Vyskočil, A., C. Viau, and M. Čížková. "Chronic Nephrotoxicity of Soluble Nickel in Rots." Human & Experimental Toxicology 13, no. 10 (October 1994): 689–93. http://dx.doi.org/10.1177/096032719401301007.

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1 Male and female Wistar rats were given 100 mg L-1 of nickel (as nickel sulfate) in drinking water for 6 months. Lactate dehydrogenase, total proteins, N-acetyl-β-D-glucosaminidase (NAG), albumin and β2-microglobulin were measured in 24 h urine after 3 and 6 months of exposure. Body and kidney weights were also recorded. 2 After 6 months, urinary excretion of albumin in control and exposed rats was 354 and 1319 μg 24 h-1 for female rats (P<0.05) and 989 and 2065 μg 24 h-1 for male rats (P = non significant). Kidney weights were significantly increased in the exposed groups. No significant changes were observed in other parameters. 3 The results suggest that low-level oral exposure to soluble nickel either induces changes of glomerular permeability in female and possibly in male rats, or enhances the normal age-related glomerular nephritis lesions of ageing rats. The intake was probably not high enough to induce significant tubular changes. The female rat seems to be more sensitive to the nephrotoxic effect of nickel than the male rat.

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30

Maiti, Arpan Kumar, Nimai Chandra Saha, Goutam Paul, and Kishore Dhara. "Mitochondrial respiratory chain inhibition and Na+K+ATPase dysfunction are determinant factors modulating the toxicity of nickel in the brain of indian catfish Clarias batrachus L." Interdisciplinary Toxicology 11, no. 4 (December 1, 2018): 306–15. http://dx.doi.org/10.2478/intox-2018-0030.

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Abstract Nickel is a potential neurotoxic pollutant inflicting damage in living organisms, including fish, mainly through oxidative stress. Previous studies have demonstrated the impact of nickel toxicity on mitochondrial function, but there remain lacunae on the damage inflicted at mitochondrial respiratory level. Deficient mitochondrial function usually affects the activities of important adenosinetriphosphatases responsible for the maintenance of normal neuronal function, namely Na+K+ATPase, as explored in our study. Previous reports demonstrated the dysfunction of this enzyme upon nickel exposure but the contributing factors for the inhibition of this enzyme remained unexplored. The main purpose of this study was to elucidate the impact of nickel neurotoxicity on mitochondrial respiratory complexes and Na+K+ATPase in the piscine brain and to determine the contributing factors that had an impact on the same. Adult Clarias batrachus were exposed to nickel treated water at 10% and 20% of the 96 h LC50 value (41 mg.l−1) respectively and sampled on 20, 40 and 60 days. Exposure of fish brain to nickel led to partial inhibition of complex IV of mitochondrial respiratory chain, however, the activities of complex I, II and III remained unaltered. This partial inhibition of mitochondrial respiratory chain might have been sufficient to lower mitochondrial energy production in mitochondria that contributed to the partial dysfunction of Na+K+ATPase. Besides energy depletion other contributing factors were involved in the dysfunction of this enzyme, like loss of thiol groups for enzyme activity and lipid peroxidation-derived end products that might have induced conformational and functional changes. However, providing direct evidence for such conformational and functional changes of Na+K+ATPase was beyond the scope of the present study. In addition, immunoblotting results also showed a decrease in Na+K+ATPase protein expression highlighting the impact of nickel neurotoxicity on the expression of the enzyme itself. The implication of the inhibition of mitochondrial respiration and Na+K+ATPase dysfunction was the neuronal death as evidenced by enhanced caspase-3 and caspase-9 activities. Thus, this study established the deleterious impact of nickel neurotoxicity on mitochondrial functions in the piscine brain and identified probable contributing factors that can act concurrently in the inhibition of Na+K+ATPase. This study also provided a vital clue about the specific areas that the therapeutic agents should target to counter nickel neurotoxicity.

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31

Kasprzak, K. "Nickel carcinogenesis." Mutation Research/Fundamental and Molecular Mechanisms of Mutagenesis 533, no. 1-2 (December 10, 2003): 67–97. http://dx.doi.org/10.1016/j.mrfmmm.2003.08.021.

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32

Clemens, F. "Genotoxicity of Samples of Nickel Refinery Dust." Toxicological Sciences 73, no. 1 (March 25, 2003): 114–23. http://dx.doi.org/10.1093/toxsci/kfg070.

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33

Goodman, Julie E., Robyn L. Prueitt, David G. Dodge, and Sagar Thakali. "Carcinogenicity assessment of water-soluble nickel compounds." Critical Reviews in Toxicology 39, no. 5 (March 19, 2009): 365–417. http://dx.doi.org/10.1080/10408440902762777.

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34

RAOS, NENAD, and KAZIMIERZ S. KASPRZAK. "Allosteric Binding of Nickel(II) to Calmodulin." Toxicological Sciences 13, no. 4 (1989): 816–22. http://dx.doi.org/10.1093/toxsci/13.4.816.

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35

RAOS, N. "Allosteric binding of nickel(II) to calmodulin." Fundamental and Applied Toxicology 13, no. 4 (November 1989): 816–22. http://dx.doi.org/10.1016/0272-0590(89)90336-9.

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36

Novelli, Elb, NL Rodrigues, and BO Ribas. "Superoxide radical and toxicity of environmental nickel exposure." Human & Experimental Toxicology 14, no. 3 (March 1995): 248–51. http://dx.doi.org/10.1177/096032719501400303.

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Three nickel compounds were tested for pancreatic, hepatic and osteogenic damage in rats by a single i.m. injection Ni++ (7 mg kg-1). The nickel induced biochemical alterations included significantly increased levels of serum alkaline phosphatase in rats with NiS (75%) and NiO (50%). Amylase and aspartate transaminase were also increased, and lipoperoxide was increased in rats with NiO (5.6-fold) and NiS (3.4-fold). No serum changes were observed with NiCl 2. Daily injection of Cu-Zn superoxide dismutase (SOD) conjugated with polyethylene glycol pre vented the serum level changes, indicating that superoxide radical is an important intermediate in toxicity of nickel insoluble compounds.

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37

Mai, Weihua, Dongqing Lu, Xingwei Liu, and Ling Chen. "MCP-1 produced by keratinocytes is associated with leucocyte recruitment during elicitation of nickel-induced occupational allergic contact dermatitis." Toxicology and Industrial Health 34, no. 1 (November 13, 2017): 36–43. http://dx.doi.org/10.1177/0748233717738633.

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To investigate the expression profile of monocyte chemoattractant peptide-1 (MCP-1) by keratinocytes after nickel exposure and to identify its role for leucocyte migration during nickel-induced occupational allergic contact dermatitis (OACD), 26 workers diagnosed with nickel-induced OACD were enrolled. Skin biopsies from the positive nickel-challenged sites at different time points were assessed by immunohistochemistry (IHC) for MCP-1, CD68, CD45RO, and in situ hybridization (ISH) for MCP-1, using chronic periumbilical dermititis as controls. The expressions of MCP-1 in HaCaT cell culture after nickel treatment were quantified by enzyme-linked immunosorbent assay. The results showed that at positive nickel-challenged sites, strong expressions of MCP-1, both messenger RNA (mRNA) and protein, were detected in the basal keratinocytes during the early phase (24–48 h after nickel application), paralleled by the recruitment of CD68+ and CD45RO+ cells to the skin compartments. The expressions of MCP-1 declined gradually in the late phase (72–96 h after nickel application). Treatment with nickel sulfate at noncytotoxic concentrations (0.01–100 µM) induced a concentration-related elevation of MCP-1 expression by HaCaT cells compared to the untreated cells. The data indicated that a temporal expression pattern of MCP-1 produced by keratinocytes after nickel exposure was involved in the complex process of mononuclear cell infiltration during elicitation of nickel-induced OACD. Targeting MCP-1 might be a potential therapeutic strategy for OACD.

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38

Minigaliyeva, Ilzira A., Boris A. Katsnelson, Larisa I. Privalova, Vladimir B. Gurvich, Vladimir G. Panov, Anatoly N. Varaksin, Oleg H. Makeyev, et al. "Toxicodynamic and Toxicokinetic Descriptors of Combined Chromium (VI) and Nickel Toxicity." International Journal of Toxicology 33, no. 6 (October 28, 2014): 498–505. http://dx.doi.org/10.1177/1091581814555915.

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After repeated intraperitoneal injections of nickel and chromium (VI) salts to rats, we found, and confirmed by mathematical modeling, that their combined subchronic toxicity can either be of additive type or depart from it (predominantly toward subadditivity) depending on the effect assessed. Against the background of moderate systemic toxicity, the combination under study proved to possess a marked additive genotoxicity assessed by means of the random amplification of polymorphic DNA test. We also demonstrated that chromium and nickel reciprocally influenced the retention of these metals in some organs (especially in the spleen) but not their urinary excretion in this study.

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39

Joshi, Seema, M. M. Husain, Ramesh Chandra, S. K. Hasan, and R. C. Srivastava. "Hydroxyl radical formation resulting from the interaction of nickel complexes of L-histidine, glutathione or L-cysteine and hydrogen peroxide." Human & Experimental Toxicology 24, no. 1 (January 2005): 13–17. http://dx.doi.org/10.1191/0960327105ht493oa.

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L-histidine, L-cysteine, reduced glutathione (GSH) and other bioligands, which are ubiquitously present in biological systems, are recognized as antioxidants. Studies have shown that nickel (II) complexed with these ligands catalyzes the disproportionation of H2O2, leading to the generation of hydroxyl radicals (OH•). However, none of the studies could provide information regarding effective concentrations at which these ligands act either as pro-oxidant or antioxidant. Therefore, the observed paradoxical behaviour of biological antioxidants in nickel-induced oxidative response was evaluated. Benzoic acid (BA) is hydroxylated by OH• radical to form highly fluorescent dihydroxy benzoate (OH-BA). We used this model to study the effect of nickel complexes of L-histidine, GSH or L-cysteine on the hydroxylation of BA. The concentration-dependent effect of L-histidine, GSH and L-cysteine, or nickel on the hydroxylation of BA was studied. The hydroxylation of BA was significantly enhanced up to 1:0.5 molar ratio (Ni:hist or GSH). However, beyond 1:0.5 molar ratios, histidine/GSH inhibited the hydroxylation and complete inhibition was observed at 1:1 molar ratios. Sorbitol and caffeic acid, considered as scavengers of hydroxyl radicals, inhibited nickel-induced hydroxylation of BA. The present study demonstrates paradoxical behaviour of these bioligands. They act as pro-oxidant at lower ligand ratios and as antioxidant at higher ligand ratios. The redox properties of nickel complexes with histidine, GSH or cysteine reported here may be crucial for the toxicity of nlckel.

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40

Oller, Adriana R., Max Costa, and Günter Oberdörster. "Carcinogenicity Assessment of Selected Nickel Compounds." Toxicology and Applied Pharmacology 143, no. 1 (March 1997): 152–66. http://dx.doi.org/10.1006/taap.1996.8075.

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41

BENSON, JANET M., I.-YIIN CHANG, YUNG SUNG CHENG, FLETCHER F. HAHN, CHRISTOPHER H. KENNEDY, EDWARD B. BARR, KIRK R. MAPLES, and MORRIS B. SNIPES. "Particle Clearance and Histopathology in Lungs of F344/N Rats and B6C3F1 Mice Inhaling Nickel Oxide or Nickel Sulfate." Toxicological Sciences 28, no. 2 (1995): 232–44. http://dx.doi.org/10.1093/toxsci/28.2.232.

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42

Benson, J. "Particle Clearance and Histopathology in Lungs of F344/N Rats and B6C3F1 Mice Inhaling Nickel Oxide or Nickel Sulfate." Fundamental and Applied Toxicology 28, no. 2 (December 1995): 232–44. http://dx.doi.org/10.1006/faat.1995.1164.

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43

Nielsen, Gitte Dalsgaard, Ulla Søderberg, Poul J. Jørgensen, Douglas M. Templeton, Søren N. Rasmussen, Klaus E. Andersen, and Philippe Grandjean. "Absorption and Retention of Nickel from Drinking Water in Relation to Food Intake and Nickel Sensitivity." Toxicology and Applied Pharmacology 154, no. 1 (January 1999): 67–75. http://dx.doi.org/10.1006/taap.1998.8577.

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44

Cangul, H., L. Broday, K. Salnikow, J. Sutherland, W. Peng, Q. Zhang, V. Poltaratsky, H. Yee, M. A. Zoroddu, and M. Costa. "Molecular mechanisms of nickel carcinogenesis." Toxicology Letters 127, no. 1-3 (February 2002): 69–75. http://dx.doi.org/10.1016/s0378-4274(01)00485-4.

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45

Magaye, Ruth, and Jinshun Zhao. "Recent progress in studies of metallic nickel and nickel-based nanoparticles’ genotoxicity and carcinogenicity." Environmental Toxicology and Pharmacology 34, no. 3 (November 2012): 644–50. http://dx.doi.org/10.1016/j.etap.2012.08.012.

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46

Sunderman, F. William, Anterior Aitio, Lindsay G. Morgan, and Tor Norseth. "Biological Monitoring of Nickel." Toxicology and Industrial Health 2, no. 1 (January 1986): 17–78. http://dx.doi.org/10.1177/074823378600200102.

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47

Arsalane, K., C. Aerts, B. Wallaert, C. Voisin, and H. F. Hildebrand. "Effects of nickel hydroxycarbonate on alveolar macrophage functions." Journal of Applied Toxicology 12, no. 4 (August 1992): 285–90. http://dx.doi.org/10.1002/jat.2550120413.

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48

Muñoz, Alexandra, and Max Costa. "Elucidating the mechanisms of nickel compound uptake: A review of particulate and nano-nickel endocytosis and toxicity." Toxicology and Applied Pharmacology 260, no. 1 (April 2012): 1–16. http://dx.doi.org/10.1016/j.taap.2011.12.014.

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49

Guo, Xiaoqiang, Yanmin Zhang, Qiang Zhang, Pingping Fa, Yaoting Gui, Guoquan Gao, and Zhiming Cai. "The regulatory role of nickel on H3K27 demethylase JMJD3 in kidney cancer cells." Toxicology and Industrial Health 32, no. 7 (November 26, 2014): 1286–92. http://dx.doi.org/10.1177/0748233714552687.

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Nickel compounds are an important class of environmental pollutants and carcinogens. Chronic exposure to nickel compounds has been connected with increased risks of numerous cancers, including lung and kidney cancers. But the precise mechanism by which nickel compounds exert their carcinogenic properties is not completely understood. In this study, kidney cancer cells namely human embryonic kidney 293-containing SV40 large T-antigen (HEK293T) and 786-0 were incubated with various concentrations of nickel chloride for 24 h before analysing the expression of three histone H3K27 methylation-modifying enzymes and H3K27me3 using quantitative real-time polymerase chain reaction, Western blot and immunofluorescence analyses. Our results showed that incubation of nickel chloride upregulated the expression of H3K27me3 demethylase jumonji domain-containing protein 3 (JMJD3) in kidney cancer cells, which was accompanied by the reduction in the protein level of H3K27me3. Enhanced demethylation of H3K27me3 may represent a novel mechanism underlying the carcinogenicity of nickel compounds.

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50

Yao, Yixin, and Max Costa. "Toxicogenomic effect of nickel and beyond." Archives of Toxicology 88, no. 9 (July 29, 2014): 1645–50. http://dx.doi.org/10.1007/s00204-014-1313-8.

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