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Articles de revues sur le sujet « Nickel Toxicology »

Auteur : Grafiati

Publié le 4 juin 2021

Mis à jour le 18 février 2022

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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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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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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 canc

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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,

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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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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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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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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 milita

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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 abou

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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-hy

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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 Ni3S

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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

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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 concen

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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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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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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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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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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 i

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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 intoxicat

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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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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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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 a

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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

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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 e

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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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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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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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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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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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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 t

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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 afte

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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

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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.

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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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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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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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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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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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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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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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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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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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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-modif

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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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